


y^i 



A TEXT-BOOK 



PRACTICE OF MEDICINE. 



J>0 



FOR STUDENTS AND PRACTITIONERS. 



BY 

HOBART AMORY HARE, M.D., B.Sc, 

PROFESSOR OF THERAPEUTICS IN THE JEFFERSON MEDICAL COLLEGE OF PHILADELPHIA ', PHYSICIAN 

TO THE JEFFERSON MEDICAL COLLEGE HOSPITAL ; ONE TIME CLINICAL PROFESSOR OF 

DISEASES OF CHILDREN IN THE UNIVERSITY OF PENNSYLVANIA ; AUTHOR 

OF "A TEXT-BOOK OF PRACTICAL THERAPEUTICS," AND 

"A TEXT-BOOK OF PRACTICAL DIAGNOSIS." 



SECOND EDITION. REVISED AND ENLARGED. 



ILLUSTRATED WITH 131 ENGRAVINGS AND 11 PLATES IN 
COLORS AND MONOCHROME. 




LEA BROTHEBS & CO., 
PHILADELPHIA AND NEW YORK. 

190 7. 



LIBRARY of CONGRESS 

Two Copies Received 

FEB 19 190r 

/"-Cepyritfit Entry M 

GLASS A' XXc, No, 

/fc *1xf. 

COPT B. 



O 



*°;** 



** 

r 



Sf 



Entered according to the Act of Congress, in the year 1907, by 

LEA BROTHERS & CO., 
In the Office of the Librarian of Congress. All rights reserved. 



DORNAN, PRINTER. 



PREFACE TO THE SECOND EDITION. 



In presenting the second edition of his text-book on the Practice of 
Medicine the author desires to express his appreciation of the cordial 
reception of the work since it first appeared, a reception which necessi- 
tated its being repeatedly put to press. 

The present volume, prepared for the physician and student of medicine, 
embodies the experience of more than twenty-two years of active hospital 
and private practice, during which time the author has been constantly 
teaching the subjects of clinical medicine and therapeutics. With this 
experience he has attempted to present the facts which the practitioner 
needs and which the student must thoroughly grasp if he is to be successful 
in gaining his degree and in practising his art. 

In the preparation of many portions of the work careful collections of 
statistics have been made, and these have not infrequently given results 
which add materially to our conception of the frequency of certain dis- 
eases at different periods of life, of the relative frequency of different 
symptoms, and the value of certain plans of treatment. 

Particular pains have been taken to present methods of treatment 
clearly and in such a way that they may be put in practice. 

Much information that might be included, which deals with subjects 
which are still uncertain and debatable, has been excluded. 

Warm thanks are due to my colleague, Dr. W. M. L. Coplin, Professor 
of Pathology in the Jefferson Medical College, for valuable suggestions and 
criticisms, in which he has shown not only a complete grasp of his own 
department of medical study, but intimate knowledge concerning the latest 
developments in clinical medicine. 

The author also desires to acknowledge the valuable suggestions, made 
during the preparation of this edition, of Dr. Aller G. Ellis, Demonstrator 
of Pathology, and Dr. Alfred Gordon, Instructor in Neurology in the Jeffer- 
son Medical College. 

The fact that the United States has, within the last few years, become 
possessed of territory in the tropics has greatly increased our interest in 
the many tropical diseases heretofore scarcely known by practitioners in the 
temperate zone, and the investigations by surgeons in the Army, Navy, and 

(iii) 



iv PREFACE 

the Public Health and Marine Hospital Service have thrown much light upon 
these affections. Further than this, the investigations by English physicians 
have broadened our views very greatly as to tropical disease. As troops 
returning from tropical service often bring with them manifestations of. 
these diseases, it behooves every practitioner to be able to recognize and 
treat such conditions. It seems appropriate, therefore, that a modern work 
on medicine should contain chapters on tropical medicine, the more so as 
lectures upon this subject are now given in many of the great medical 
schools. 

In the preparation of this second edition great care has been taken 
to embody the latest views that have received general acceptance as being 
scientifically and clinically correct, it being constantly borne in mind that 
the needs of the student and practitioner will be best met by excluding 
statements open to criticism and presenting facts which will prove useful 
in practice. 

H. A. H. 

Spruce and Eighteenth Streets, 
Philadelphia, January, 1907, 



CONTENTS 



INFECTIOUS DISEASES. 

PAGE 

Typhoid Fever . . . . . " . . . 17 

Paratyphoid Fever ........... 59 

Typhus Fever .... . ....... 61 

Relapsing Fever . . . . . . , . . . . .68 

Variola 70 

Vaccinia and Vaccination .......... 88 

Varicella 90 

Scarlet Fever 93 

Measles ............. 108 

Rubella 115 

Mumps 117 

Whooping-cough ............ 119 

Influenza . . ... . . . . . . . . . 125 

Dengue ............. 131 

Cerebrospinal Fever . . . . . . . . . . .134 

Croupous Pneumonia . . . . . . . . . . .143 

Diphtheria 171 

Gonorrhceal Infection . . . . . . . . . . .186 

Erysipelas 189 

Septicaemia and Pyaemia . . . . . . . . . .193 

Acute Rheumatic Fever . . . . . . . . . .196 

Cholera 204 

Yellow Fever 212 

Plague (Bubonic Plague) .219 

Climatic Bubo 226 

Dysentery .............. 227 

Epidemic Gangrenous Proctitis ......... 239 

Hill Diarrhoea 240 

Sprue (Psilosis) 242 

Nasha Fever . . . . . . . . . . ■ . 245 

Malta Fever . 245 

Beriberi 249 

Anthrax ............. 257 

Hydrophobia . . . . . . . . . . . . 261 

Tetanus 267 

Glanders 271 

Actinomycosis ............ 273 

Mycetoma (Madura Foot, Fungus Foot of India) ...... 275 

Syphilis . 276 

Hereditary Syphilis 286 

(v) 



vi CONTENTS 

PAGE 

Tuberculosis 290 

Acute Miliary Tuberculosis ......... 297 

Glandular Tuberculosis ......... 299 

Tuberculosis of the Serous Membranes ....... 301 

Pulmonary Tuberculosis ......... 309 

Tuberculosis of the Alimentary Canal ....... 334 

Tuberculosis of the Liver 338 

Tuberculosis of the Genito-urinary System ...... 338 

Tuberculosis of the Fallopian Tubes, Ovaries and Uterus .... 342 

Tuberculosis of the Heart ......... 343 

Tuberculosis of the Thyroid Gland 343 

Tuberculosis of the Brain and Cord ....... 343 

Leprosy ............. 344 

Febricula . 351 

Milk Sickness 352 

Weil's Disease 352 

Glandular Fever ............ 353 

Mountain Fever ............ 354 

Tick Fever 354 

Foot-and-Mouth Disease .......... 356 

Miliary Fever 356 

Japanese River Fever ........... 357 

Frambesia (Frambcesia Tropica, Yaws) ........ 358 

Verruga (Verruga Peruviana) . . . . . . . . . .360 

Kubisagari ............. 362 



DISEASES OF THE RESPIRATORY SYSTEM. 

Diseases of the Nose ........... 363 

Acute Coryza ........... 363 

Chronic Nasal Catarrh ......... 365 

Atrophic Nasal Catarrh . . . . . . . . . . 366 

Hay Fever . 367 

Epistaxis 369 

Diseases of the Larynx . . . . . . . . . . .369 

Acute Catarrhal Laryngitis . . . . . . . . .369 

Chronic Catarrhal Laryngitis ........ 371 

(Edematous Laryngitis ......... 372 

Spasmodic Laryngitis .......... 374 

Tuberculous Laryngitis ......... 375 

Syphilitic Laryngitis .......... 376 

Diseases of the Bronchi . . . . . . . . . . 377 

Acute Catarrhal Bronchitis ......... 377 

Chronic Catarrhal Bronchitis ........ 382 

Bronchiectasis ........... 383 

Fibrinous Bronchitis .......... 388 

Bronchial Asthma .......... 390 

Diseases of the Lungs ........... 397 

Bronchopneumonia .......... 397 

Metastatic Pneumonia .......... 408 

Pneumonoconiosis . . . . . . . . . .411 



CONTENTS vii 

Diseases of the Lungs: page 
Emphysema of the Lungs . . . . . « . . .413 

Compensatory or Acute Emphysema . . . . . .419 

Interstitial Emphysema . . . . . . . .419 

Small-lunged Emphysema ........ 420 

Gangrene of the Lung ......... 420 

Pulmonary Abscess .......... 423 

Congestion of the Lungs ......... 425 

Tumors in the Lungs .......... 428 

Diseases of the Pleura ........... 430 

Pleuritis 430 

Purulent Pleural Effusion or Empyema ...... 443 

Chronic Pleurisy ........... 448 

Hydrothorax ........... 448 

Pneumothorax, Hydropneumothorax, Pyopneumothorax .... 449 

Diseases of the Mediastinum ......... 452 

DISEASES OF THE CIRCULATORY SYSTEM. 

Diseases of the Pericardium .......... 457 

Pericarditis . . . . . . . . . . . 457 

Hydropericardium . . ....... 466 

Hsemopericardium .......... 467 

Pneumopericardium . . . . . . . . . . 467 

Pyopericardium ........... 468 

Diseases of the Heart ........... 468 

Hypertrophy and Dilatation of the Heart ...... 468 

Disease of the Myocardium ......... 473 

Cardiac Aneurysm ........ 479 

Wounds of the Heart . 481 

Endocarditis ........... 481 

Acute Endocarditis ......... 482 

Ulcerative Endocarditis ........ 485 

Chronic Endocarditis ......... 488 

Chronic Valvular Disease as a Result of Chronic Endocarditis . . 489 

Mitral Regurgitation ......... 494 

Mitral Stenosis .......... 499 

Aortic Stenosis .......... 504 

Aortic Regurgitation ......... 508 

Tricuspid Regurgitation ........ 513 

Tricuspid Stenosis . . . . . . . . .515 

Disease of the Pulmonary Valves . . . . . .515 

Neuroses of the Heart ......... 521 

Palpitation .......... 521 

Tachycardia .......... 521 

Bradycardia .......... 522 

Arhythmia .......... 522 

Angina Pectoris ........... 523 

Congenital Cardiac Defects ......... 527 

Diseases of the Arteries ........... 528 

Arteriosclerosis ........... 529 

Aneurysm ............ 534 

Aneurysm of Thoracic Aorta ....... 536 

Aneurysm of the Abdominal Aorta ...... 542 



viii CONTENTS 



DISEASES OF THE DIGESTIVE TRACT. 



I'AGE 



Diseases of the Mouth ........ 545 

Stomatitis .......... 54.5 

Catarrhal Stomatitis ........ 545 

Aphthous Stomatitis ....... 545 

Ulcerative Stomatitis ....... 546 

Thrush ......... 547 

Gangrenous Stomatitis, Cancrum Oris or Noma .... 548 

Eczema of the Tongue 549 

Leukoplakia Buccalis ........ 550 

Mucous Patches ......... 550 

Diseases of the Salivary Glands ........ 550 

Functional Disorders of the Salivary Glands ..... 550 

Ptyalism 550 

Dry Mouth ........... 551 

Inflammation of the Salivary Glands . . . . . . .551 

Ludvig's Angina ......... 552 

Diseases of the Pharynx . . . . . . . . . . . 552 

Acute Pharyngitis .......... 552 

Ulcerative or Phlegmonous Pharyngitis ...... 554 

Croupous Pharyngitis .......... 555 

Chronic Pharyngitis .......... 555 

Follicular Pharyngitis .......... 556 

Diseases of the Tonsils «... 556 

Acute Tonsillitis 556 

Chronic Hypertrophic Tonsillitis . . ... . . . . 558 

Diseases of the CEsophagus .......... 560 

Oesophagitis ........... 560 

Organic Stricture of the (Esophagus ....... 561 

Dilatation of the (Esophagus . . . . . . . . 561 

Spasms of the (Esophagus . . . 562 

Cancer of the (Esophagus . .563 

Diseases of the Stomach .......... 564 

Acute Gastric Catarrh 564 

Acute Toxic Gastritis .......... 565 

Phlegmonous Gastritis . . . ... . . . . . 566 

Diphtheritic Gastritis 568 

Mycotic Gastritis .......... 568 

Chronic Gastritis ........... 568 

Gastric Dilatation .......... 572 

Acute Gastrectasis ......... 578 

Gastric Ulcer ........... 579 

Cancer of the Stomach ......... 588 

Hypertrophic Stenosis of the Pylorus . 595 

Hour-glass Stomach .......... 598 

Gastric Neuroses ........... 601 

Cardiospasm .......... 601 

Pylorospasm .......... 602 

Gastric Hyperperistalsis ........ 602 

Merycismus .......... 603 

Nervous Eructation ......... 603 



CONTENTS ix 

Diseases of the Stomach : page 

Hyperesthesia .......... 603 

Gastralgia 603 

Bulimia 604 

Anorexia Nervosa ......... 604 

Nervous Disorders of Secretion ....... 604 

Hemorrhage from the Stomach ........ 604 

Cyclic Vomiting 607 

Diseases of the Intestines . . . . . . ... . . 608 

Diarrhoea 608 

Catarrhal Enteritis 609 

Ileocolitis of Childhood 609 

Cholera Infantum .......... 613 

Appendicitis ........... 613 

Intestinal Obstruction . . . . . . . . . . 623 

Congenital Malformation ........ 624 

Intussusception .......... 624 

Internal Strangulation . . . . . . . .626 

Volvulus 627 

Obstruction from Foreign Bodies ...... 628 

Duodenal Ulcer 628 

Enteroptosis 632 

Colitis 636 

Acute Colitis 636 

Mucous Colitis 637 

Folliculus and Croupous Colitis . . . . . . . 638 

Pseudomembranous Colitis ........ 639 

Dilatation of the Colon 639 



DISEASES OF THE PERITONEUM. 

Acute Peritonitis . . . ... . . . . . . 641 

Chronic Peritonitis ........... 647 

Chronic Adhesive Sclerotic Peritonitis ........ 648 

Cancer of the Peritoneum . ... . . . . . . 649 

Other Growths of the Peritoneum ......... 649 

Ascites 650 



DISEASES OF THE LIVER. 

Inflammation of the Liver . . . . . . . . . 653 

Acute Hepatitis or Hepatic Abscess ....... 653 

Cirrhosis of the Liver . . . . . . . . . . 658 

Atrophic Cirrhosis .......... 659 

Hypertrophic Cirrhosis ......... 663 

Syphilitic Cirrhosis .......... 664 

Perihepatitis (Capsular Cirrhosis) 665 

Affections of the Hepatic Bloodvessels 666 

Amyloid Liver ............ 667 

Fatty Liver 668 

Tumors of the Liver ........... 668 

Acute Yellow Atrophy of the Liver . . . . . . . . 670 



CONTENTS 



DISEASES OF THE BILIARY TRACT 



Acute Catarrh of the Bile-ducts, or Acute Cholangitis 
Chronic Catarrh of the Bile-ducts . 
Suppurative Inflammation of the Bile-ducts . 
Occlusion and Constrictions of the Bile-ducts 
Acute Cholecystitis ..... 

Cholelithiasis ...... 

Malignant Growths of the Gall-bladder and Biliary Passages 
Icterus Neonatorum ....... 



PAGE 

671 
673 
673 
674 
675 
677 
683 
686 



DISEASES OF THE PANCREAS. 

Pancreatitis ............ 687 

Acute Pancreatitis .......... 687 

Chronic Pancreatitis .......... 691 

Pancreatic Calculus ........... 693 

Pancreatic Cysts . . . . . . . . . . . . 694 

Pancreatic Tumors ........... 695 

Hemorrhages into the Pancreas ......... 695 

DISEASES OF THE KIDNEYS. 

Malformations of the Kidneys ......... 696 

Movable Kidney 696 

Circulatory Disturbances in the Kidney ........ 698 

Acute Hyperemia .......... 699 

Chronic Hyperemia .......... 699 

Acute Bright's Disease .......... 700 

Chronic Bright's Disease .......... 703 

Chronic Parenchymatous Nephritis ........ 704 

Chronic Interstitial Nephritis ......... 710 

Amyloid Disease of the Kidneys . . . . . . - . . . 718 

Uraemia . 720 

Pyelonephritis and Pyelitis . . . . . . . . . . 725 

Hydronephrosis ............ 728 

Cystic Disease of the Kidney ......... 730 

Tumors of the Kidney . . .732 

Nephrolithiasis ............ 733 

Perinephritic Abscess ........... 737 

Disorders of Urinary Secretion ......... 737 

Anuria 737 

Hematuria ........... 738 

Hemoglobinuria .......... 739 

Haematinuria . . . . . . . . . . . 739 

Albuminuria ............ 741 

Pyuria 744 

Chyluria 744 

Phosphaturia ........... 745 

Oxaluria ............ 745 

Indicanuria . . . . . . . . ... . 745 

Lithuria 746 

Melanuria ............ 746 

Myelopathic Albumosuria . . . . . . . . 746 



CONTENTS x i 



DISEASES OF THE DUCTLESS GLANDS AND LYMPHATIC 

SYSTEM. 

PAGE 

Diseases of the Thyroid Gland 749 

Goitre ..... 749 

Swelling of the Thyroid 750 

Tumors of the Thyroid Gland 751 

Exophthalmic Goitre . . . . . . . . . .751 

Myxcedema ........... 756 

Cretinism ............ 758 

Diseases of the Suprarenal Gland ......... 760 

Addison's Disease .......... 760 

Diseases of the Spleen . . . . . . . . . . 764 

Splenic Anaemia ...... «... . 765 

Banti's Disease ........... 767 

Hodgkin's Disease .......... 767 

Status Lymphaticus ... ..... . 770 

Diseases of the Thymus Gland ......... 772 



DISEASES OF THE BLOOD. 

Anaemia ............. 773 

Secondary Anaemia . . . . . . . . . 773 

Primary or Essential Anaemias ........ 775 

Chlorosis 775 

Pernicious Anaemia . . ...... 777 

Leukaemia ............. 780 

Splenomedullary Leukaemia . . . . . . . . .781 

Lymphatic Leukaemia .......... 782 

Chloroma 784 

Anaemia Infantum ........... 785 

Purpura ............. 785 

Haemophilia ............. 787 



DISEASES OF NUTRITION. 

Diabetes Mellitus 789 

Diabetes Insipidus ........... 806 

Gout 808 

Acute Gout ........... 813 

Chronic Gout 814 

Irregular Gout ........... 814 

Arthritis Deformans . . . . ... . . . . .818 

Chronic Rheumatism ........... 823 

Muscular Rheumatism . . . . . . , . . . . 824 

Rickets .... 825 

Scurvy . . 830 

Obesity 833 

Adiposis Dolorosa . .... r ..... . 836 



xii CONTENTS 

PAGE 

Acromegaly ...... 837 

Osteitis Deformans 839 

Hypertrophic Pulmonary Osteoarthropathy ....... 840 

Leontiasis Ossea ............ 840 

Scleroderma ............. 840 

Ainhum ............. 841 

INTOXICATIONS. 

Alcoholism 843 

Acute Alcoholism .......... 843 

Subacute and Chronic Alcoholism ....... 844 

Morphinism ............. 848 

Arsenical Poisoning ........... 850 

Lead Poisoning, or Plumbism . . . . . . . . .851 

Food Poisoning ............ 855 

Bromatotoxismus .......... 855 

Mytilotoxismus ........... 856 

Ichthyotoxismus . . ... . . . . . 856 

Kreotoxismus ........... 856 

Tyrotoxismus and Galactotoxismus ....... 857 

Pellagra (Maidismus) 857 

Lathy rism (Chickpea Disease; Lupinosis) . . . . . . . 859 

Atriplicism ............. 860 

Lacquer Poisoning . . . . . . . . . . . 860 



DISEASES DUE TO ANIMAL PARASITES. 

Malarial Fever 863 

Psorospermiasis . . . . . . . . . . . . 879 

Trypanosomiasis ............ 879 

Trypanosoma Fever .......... 880 

African Lethargy (Sleeping Sickness) . . . . . . .881 

Kala-Azar .883 

Nematodes ............. 884 

Ascariasis ............ 884 

Oxyuris Vermicularis .......... 885 

Trichina Spiralis . . . . . . . . . . 885 

Uncinariasis (Ankylostomiasis) ........ 887 

Filariasis (Filaria Sanguinis Hominis) ....... 892 

Filaria Nocturna .......... 893 

Elephantiasis . . . . . . . . . . 895 

Hsematochyluria . . . . . . . . . 895 

Lymph Scrotum ......... 897 

Guinea-worm Disease (Dracontiasis) ....... 897 

Strongyloides Intestinalis ......... 898 

Trichocephalus Dispar .......... 900 

Cestodes or Tapeworms ........... 900 

Trematodes 904 

Bilharzia Disease . . . . . . . . . . 905 

Distomatosis of the Lung ......... 907 

Distomatosis of the Liver (Liver Flukes) . . . . . . 908 



CONTENTS xiii 

PAGE 

Parasitic Infusoria ........... 909 

Dhobie Itch 909 

Chigger (Sand Flea) 911 

Myiasis . . • • . • . . • • • • .911 

Intestinal Myiasis . . . . . . . . . .912 

Dermatobia Cyaniventris 912 



DISEASES OF THE NERVOUS SYSTEM. 

DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN THE BRAIN 

AND ITS MEMBRANES. 

Hemorrhage into the Brain, Cerebral Thrombosis and Embolism . . . 913 

Infantile Cerebral Paralysis 925 

Little's Disease 929 

Aphasia ............. 930 

Tumors of the Brain and its Membranes 932 

Abscess of the Brain ........... 941 

Acute Cerebritis or Encephalitis 944 

Thrombosis of the Venous Sinuses ........ 946 

Cerebral Meningitis ........... 946 

Pachymeningitis . . . . . . . . . . . 947 

Pachymeningitis Interna ......... 947 

Leptomeningitis ........... 948 

Dementia Paralytica 950 

Disseminated Sclerosis ........... 954 



DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN THE SPINAL 
CORD OR ITS MEMBRANES. 

Locomotor Ataxia ........... 958 

Friedreich's Ataxia ........... 967 

Marie's Cerebellar Hereditary Ataxia ........ 970 

Acute Anterior Poliomyelitis ......... 970 

Chronic Anterior Poliomyelitis ......... 974 

Bulbar Paralysis ............ 977 

Lateral Sclerosis ............ 978 

Amyotrophic Lateral Sclerosis ......... 980 

Myelitis 983 

Acute and Subacute Myelitis ........ 983 

Chronic Myelitis . . . . . . . . . . 985 

Senile Paraplegia ............ 987 

Myelomalacia ............ 987 

Syringomyelia .......... i . 988 

Hemorrhage into the Spinal Cord ......... 990 

Hemorrhage into the Spinal Membranes . . . . . . 991 

Compression of the Spinal Cord ......... 993 

Spinal Meningitis ............ 997 

Chronic Spinal Meningitis ......... 999 

Acute Ascending Paralysis (Landry's Paralysis) ...... 1000 

Caisson Disease t . , . . T 1001 



xiv CONTENTS 

DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN THE NERVES. 

PAGE 

Neuritis 1003 

Special Forms of Neuritis .......... 1006 

Cervicobrachial Neuritis ......... 1006 

Obstetrical or Birth Neuritis 1007 

Multiple Neuritis 1007 

Diseases of the Cranial Nerves . . . . . . . . .1012 

The Olfactory Nerve . 1012 

The Optic Nerve 1012 

Optic Atrophy 1014 

Hemianopsia .......... 1015 

The Third or Oculomotor Nerve . . 1018 

The Fourth or Trochlears Nerve 1020 

The Fifth or Trifacial Nerve 1020 

The Sixth Abducens Nerve 1022 

Disturbances of Motility in the Ocular Muscles Depending on the 
Third, Fourth, and Sixth Nerves 1022 

Ophthalmoplegia; Paralysis of the Internal and External Muscles 

of the Eyeball 1023 

The Seventh or Facial Nerve . . . . . . . .1024 

Facial Spasm 1027 

The Eighth or Auditory Nerve 1028 

The Ninth or Glossopharyngeal Nerve 1030 

The Tenth or Vagus Nerve . . .1030 

Eleventh or Spinal Accessory Nerve ....... 1032 

Twelfth or Hypoglossal Nerve ........ 1034 

DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN THE MUSCLES. 

Muscular Dystrophies . . . . . . . . . . . 1035 

Pseudomuscular Hypertrophy ........ 1035 

Erb's Juvenile Muscular Dystrophy ....... 1036 

Landouzy-Dejerine Type of Muscular Dystrophy ..... 1037 

Muscular Atrophy of the Peroneal Type . . . . . . .1037 

FUNCTIONAL NERVOUS DISEASES AND DISEASES OF DISPUTED 

PATHOLOGY. 

Myotonia Congenita ........... 1038 

Paramyoclonus Multiplex .......... 1039 

Paralysis Agitans ............ 1040 

Chorea Minor t 1043 

Other Forms of Chorea 1046 

Huntington's Chorea . ......... 1046 

Dubini's Disease .......... 1047 

Hysteria 1047 

Epilepsy 1052 

Jacksonian Epilepsy . . . . . . . . . . 1061 

Petit Mai, or Minor Epilepsy 1061 

Eclampsia 1062 

Infantile Eclampsia .......... 1062 

Puerperal Eclampsia 1063 



CONTENTS xv 

PAGE 

Tetany 1064 

Latah 1066 

Amok (Running Amok) ........... 1066 

Astasia-abasia ............ 1067 

Neurasthenia ............ 1068 

Traumatic Neuroses 1070 

Occupation Neuroses ........... 1072 

Raynaud's Disease ........... 1075 

Angioneurotic (Edema ........... 1075 

Ervthromelalgia ............ 1076 

Migraine ............. 1077 

Sunstroke 1080 

Heat Exhaustion 1082 

Facial Hemiatrophy ........... 1083 

Periodical Paralysis 1083 



PRACTICE OF MEDICINE, 



DISEASES DUE TO A SPECIFIC IXFECTIOX 



TYPHOID FEVER. 

Definition. — Typhoid or Enteric fever, sometimes called Autumnal or 
Gastric fever, is an acute infectious disease due to the entrance into 
the body of a susceptible individual of the specific bacillus of Eberth, 
commonly known as Bacillus typhosus. The entrance of this organism 
into the system results, after a period of from one to three weeks in some 
persons, but not in all, in the development of fever, anorexia, headache, 
mental heaviness, and more or less severe pain in the bowels, back, and 
limbs. The tongue is coated, and the bowels are loose or constipated. 
With these symptoms are developed enlargement of the liver and spleen, 
and swellings and ulceration of the lymphoid structures of the small and 
large intestines, and a rose rash on the skin. 

History. — Typhoid fever for many years was confused with typhus fever 
and malarial fever, and its very name means "like typhus." In 1813 it 
was considered as a separate disease, but this separation was not generally 
known by the profession until Louis, of Paris (1829), first emphasized a 
number of its cardinal points. Not until 1837 was the identification com- 
plete, when Gerhard, of Philadelphia, published results achieved under 
the guidance of Louis which proved the malady to be a distinct entity. 
More than forty years later (1880) Eberth isolated the specific bacillus 
and proved it to be the sole cause of the disease. L^p to that time various 
causes had been thought to exist, but it had been recognized for many 
years as a "filth disease/' and, therefore, preventable to some degree. 

Distribution. — Enteric fever is one of the diseases which may be said to 
be pandemic, since it is found with some degree of constancy all over the 
world, its prevalence depending upon the introduction into the body of 
the specific bacillus usually with water or food. 

Etiology. — The cause of this disease, as just stated, is the specific bacillus 
of Eberth, a short, thick, actively motile bacillus, with rounded ends and 
flagella, growing readily in ordinary suitable media. It is killed by expo- 
sure to 60° C. (140° F.), but it can withstand a freezing temperature for many 
days. Exposed to sunlight it is slowly killed, but drying, except in very 
2 



18 DISEASES DUE TO A SPECIFIC INFECTION 

thin layers, does not destroy it. It remains alive for months, and even for 
years, in clothing and in soil, if the conditions are favorable. It is readily 
destroyed by the stronger germicides, such as carbolic acid (1:200) and 
bichloride of mercury (1:2000). The bacillus of Eberth bears a close 
resemblance to the Bacillus coli communis, which is always present in the 
intestine, and to the so-called paracolon bacillus and the Bacillus dysenteric. 

The second etiological factor in the development of the disease is the 
mode by which the bacillus gains access to the body. Almost invariably 
this access is through the mouth, stomach, and intestine, more rarely by 
inhalation of the bacillus in dust by the lungs. Infection takes place by 
the mouth in a host of ways, as by infected water, or milk diluted with 
infected water, or chilled by infected ice; by vegetables and oysters and 
clams, which, when eaten raw, are often the means of carrying infection. 
It has recently been proved at Ogdensburg, New York, that infected ice 
may transmit the organism after it has been stored in an ice-house for at 
least nine months. In still other instances persons nursing cases of this 
disease get the finger-tips infected and so, on putting the fingers to the mouth, 
introduce the organism into the body. Again, it has been proved beyond 
doubt that flies after lighting upon the discharges of a case of typhoid fever 
may carry the bacillus to otherwise pure food, and so spread the infection 
as long as twenty-three days after feeding on infected stools (Ficher). 
Stokes describes an epidemic in a factory employing 1500 women and 400 
men. As many as 200 of the women were ill at one time with typhoid 
fever, but none of the men fell ill. All the men drank beer at luncheon, 
whereas all the women used milk. The milk was found to have been in- 
fected by flies from a neighboring privy. Cockroaches may also spread 
the bacillus. 

Every great epidemic of the disease has been due to contamination of the 
water supply. In the Maidstone epidemic in England 1 person in every 17 
in the town was infected ; while in the Plymouth epidemic in Pennsylvania 
1 in every 7 was stricken, for there were 1200 cases in a population of 8000. 
As only a part of these 8000 persons used the contaminated water, the pro- 
portion of actual infection to exposure was far higher than 1 in 7. The 
influence of a bad and good water supply is shown in Figs. 1, 2 and 3. 

In 1888 the use of filtered drinking water was begun in the French army, 
as a result of which the morbidity of typhoid fever was diminished 49 per 
cent, in 1890, and the mortality 34 per cent. 

Prevention. — From what has just been said it is evident that typhoid fever is 
an entirely preventable disease, provided that the bacilli as they escape in 
the feces, the urine, the sputum, and, perhaps, in the sweat, are destroyed as 
soon as they pass from the patient's body. The destruction of the dis- 
charges and so of the bacilli is therefore absolutely essential, and in addition 
careful antisepsis on the part of the attendant as to personal cleanliness 
and the protection of the discharges from flies are to be enforced. As 
careless or ignorant persons do not disinfect the stools, the additional 
measures of prophylaxis are the boiling of all water that is to be placed 
in the mouth, and the use of nothing but well-cooked foods, which have 
not been exposed to flies or dust after cooking. The vessel which receives 



TYPHOID FEVER 



19 



the discharges of the patient should contain carbolic acid (1:200), corro- 
sive sublimate (1:2000), or chlorinated lime (a heaping teaspoonful to 
the pint). Formaldehyde solution (40 per cent.) may also be used. If the 



Fig. 1 



Fig. 2 



Fig. 3 




« « W * «J 

a a a a a 

« » 90 9D w 



» >• no a a 

» s» sa s> s» 

K 90 90 90 90 



1 






















1000 

1 






















2000 
1 






















3000 
1 






















4000 
1 






















5000 

1 






















6000 
1 






















7000 
1 






















8000 
1 






















9000 

1 






















ioooo m 



















Fig. 1. — Mortality in Chicago of typhoid fever. In 1891 and 1892 the water was contaminated with 
sewage and the death rate was about 1 to 450 to 1 to 1500. With a change in water supply the mor- 
tality has fallen to 1 to 6000 or even 1 to 9000. (Seibert.) 

Fig. 2. — Mortality of typhoid fever in Berlin before the supply of drinking water was filtered. In 
the decade 1843 to 1853 the average yearly mortality was 1 per 900 of inhabitants. 

Fig. 3. — Mortality of typhoid fever in Berlin after water was filtered. (Seibert.) 



stool is formed, it should be broken up by stirring it with a rod, so as to 
expose all the fecal matter to the germicide. 

Physicians and nurses are not careful enough about the destruction of the 
stools, and the average individual is willing to take his chances on the use of 



20 DISEASES DUE TO A SPECIFIC INFECTION 

unboiled water. Another of the difficulties is that patients may, when no 
longer kept in the house by the disease, continue to cast off bacilli in the 
urine or feces which are capable of infecting water supplies. This danger 
is of great importance, because at each urination or defecation the con- 
valescent patient may produce a new source of infection. Further, it is 
toward the close of the attack and during convalescence that the urine 
contains these specific organisms in pure culture and in enormous numbers, 
and they may remain persistently present, not only for days but for months. 
The patient should be told of this danger, should be directed to disinfect 
his discharges, and should receive daily doses of uritone or urotropin to 
destroy the bacilli in the urine before they are passed in that fluid. If he 
is also informed that bacilluria is a danger to himself, in that it may result 
in secondary diseases in his genito-urinary tract, he may be interested 
enough to aid the physician in arresting the spread of the bacillus by 
adhering to a plan of careful medication. 

All clothing, instruments, bedding, pillows, utensils, bath-tubs and ordi- 
nary wash-tubs, which may be contaminated by the discharges of a 
patient, should be disinfected thoroughly as soon as their function is per- 
formed. The hands of the nurses should be repeatedly disinfected. 

Another preventive of typhoid fever consists in the injection, or inocu- 
lation, of the individual with bouillon containing the toxins of Bacillus 
typhosus, the organisms themselves being destroyed beforehand by heat. 
Such an injection produces local swelling and some pain, a sense of nausea 
and depression, and some febrile movement, which symptoms speedily 
disappear, the patient at the end of twenty-four to thirty-six hours being 
well again. A fortnight later the individual is injected a second time. It 
is interesting to note that these injections increase the bacteriolytic power 
of the blood, cause in some degree the so-called Widal reaction, or agglutina- 
tion of the Bacillus typhosus, to take place when the serum of the injected 
person is used for this test, and in many hundred cases have probably served 
to act as a protective agent against infection, although the protection is by 
no means so complete as that afforded by vaccination against smallpox, 
nor has it been tried sufficiently widely to place its use upon a similar clinical 
basis. It has, however, had complete tests in the last few years. Thus, of 
29,650 individuals in South Africa, Egypt, Cyprus, India, and Ireland, who 
were similarly exposed to infection by typhoid fever, 7055 received pre- 
ventive inoculations. Of this number 333, or 4.72 per cent., contracted the 
disease; 34, or 1.03 per cent., died. Of the 22,595 who were not inoculated, 
2763, or 12.22 per cent., contracted the disease; 507, or 2.7 percent., died. 1 

It has been shown in the United States Government Laboratories at 
Washington and in the City Laboratory of Philadelphia that the intro- 
duction of so small an amount of sulphate of copper as 1 : 1,000,000, 
or even 1 : 4,000,000, will destroy the typhoid bacillus in a very few hours, 
and already this means has been successfully used in large reservoirs for 
the purification of the water supply of towns. It is said to be efficient, is 
very cheap, and entirely harmless to human beings who drink the water 

1 These statistics are compiled from the reports of Wright, Leishman, Luck, Fawcett, and Burt. 



TYPHOID FEVER 



21 



and to the fish in the water. How the copper acts is not known. If 
water containing typhoid bacilli is placed in burnished copper vessels for 
a few hours most of the typhoid germs are also destroyed. More recently, 
Gage and Clark have thrown doubt on this method, and its value must be 
considered sub judice. 

Frequency.— Typhoid fever affects males oftener than females, and occurs 
most frequently between fifteen and thirty years of age. It may, how- 
ever, affect infants or aged persons. It occurs more frequently in August, 
September, and October than any other quarter of the year, but is by no 
means limited to this period. (See Fig. 4.) 



Fig. 4 




Chart from the United States census, showing the period of the year when the mortality from 
typhoid fever reaches its maximum. 

Typhoid fever is becoming less and less frequent, and less severe all 
over the world. In Munich the mortality in the decade from 1851 to 
1861 ranged from 123 in 100,000 inhabitants to 453 in 100,000 inhabi- 
tants, whereas in the years from 1890 to 1897 the mortality was from 57 or 
14.8 in 100,000 people to 10 or 2.5 per 100,000; in Vienna it has fallen 
from 120 per 100,000 to 10 per 100,000; in Dantzig, from 100 per 100,000 
to 10.5. In Massachusetts the mortality from typhoid fever in 1901 was 
less than in any year since 1842. In 33 cities in that State it was only one- 
fourth of what it was thirty years ago. In Philadelphia a similar decrease 
is seen in both mortality and morbidity. (See Fig. 5.) The rise in mor- 
bidity in 1898 is due to the soldiers returning from the Spanish-American 



22 



DISEASES DUE TO A SPECIFIC INFECTION 



war, for the careless sanitation of large camps always makes it epidemic. 
Thus, in this war about 1 in every 5 of the soldiers in the United States 
army became infected, and nearly 87 per cent, of all the deaths in the army 





Fig. 5 


NUMBER 
OF 

CASES 




BETWEEN 




8100 — 7800 






7800 — 7500 


I 


± 1 


7500 — 7200 


t 


] 


7200 — 6900 






6900 — 6600 


7 


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6600—6300 


| 


I 


6300 — 6000 


I 




6000 — 5700 




::::::::::::::::::::::::::::::::]:::::::::::: 


5700 — 5400 




t 


5400 — 5100 


f 


, 


5100 — 4800 






4800—4500 


i 


21 :r::::t:::::::::::::::::::::::f::::;::::::7 


4500 — 4200 


90 -X * -i * 1 X- 


20 __L^_t_\ [ i._ 


4200 — 3900 


iq V \-i I— ■-* J 


19 >i_v— - -\X , I— 


3900—3600 


1r Al_ \ J /-— 


18 ___i_/l !l t /__._ 


3600 — 3300 


17 ^ l A V I - - I 


17 ____L_J h _4 * /S / r/ 


3300 — 3000 


ir—H-te-X V -V-4 -¥- 


10 * * r \ T 


3000—2700 


t *:::::::::::\::::::::::~::]::: ::::::::::::::: 


15 j_ .\-.\Z 


2700 — 2400 


1A \ x ' v'l 


14 _y^.___._ 


2400 — 2100 


to :/. 5Z a . 


id * * 7^ 


2100—1800 


19 - -^ * V 


13 v_ y_ v_ 


1800 — 1500 


u , \s -i. 


11 v 



Showing the decreasing mortality of typhoid fever in Philadelphia. Solid line, morbidity with sharp 
rise in 1898-99, due to returned soldiers of Spanish war. Broken line, mortality. 

were due to this cause. In Melbourne, Australia, there has also been a 
decrease in the mortality rate which is very noticeable, being over 50 per 
cent. This decrease is due chiefly to care in regard to water supplies. 



TYPHOID FEVER 



23 



The general mortality rate of the world may be said fifty years ago to 
have been almost universally 25 per cent., whereas it is now from 15 to 10 
per cent. 

With advancing years of age the morbidity decreases, but the mortality 
greatly increases. (See Fig. 6.) 

Pathology and Morbid Anatomy. — In studying the morbid anatomy of 
typhoid fever it must be remembered that it is not, when fully developed, 
a local infection, restricted to one or more foci from which the Bacillus 
typhosus distributes its toxin through the body. On the contrary, the 
typhoid infection is practically universal, and the bacillus may be found in 
varying numbers in every organ of the body, including the bone-marrow 
and skin. Contrary to general belief, they may not be demonstrable in 
the intestinal contents in large numbers until the disease is well advanced, 
and their presence in the stools depends largely upon the intensity of the 



Fig. 



AGE 


10 


11-16 


16-20 


21-25 


26-30 


31-35 


36-40 


11-45 


46-50 


51-55 


56-60 


61 


PER 
CENT 

50 

40 

30 

20 

10 













































































































































r 








































































/ 














































































































































J 
















































































































































/ 








































































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1 






































































t 








































































\ 








































































r 






































































7 






































































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_- 


-*■ 




















































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•" 


















































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\/ 


















































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' 














































































































































































































































































































































/ 






































































• 















































































































































Showing the increased mortality of typhoid fever with age. (Curschmann.) 



changes which take place in the intestinal glands. It is true, however, 
that the agminated glands (Peyer's patches) and the solitary glands of 
the small bowel are the parts oi the body which usually are the seat of 
the most evident and constant lesions. On the other hand, it is not to be 
forgotten that cases of undoubted typhoid fever occasionally occur in 
which no ulceration of the intestinal mucosa takes place. 

The alterations from the normal in the bowel may be discussed under 
three heads : (1) a diffuse catarrhal inflammation of the intestinal mucosa of 
varying severity, but usually resulting in desquamation of epithelium ; (2) 
hyperemia, swelling, endothelial hyperplasia, necrosis, and finally ulceration 
of the agminated glands or Peyer's patches; and (3) a similar change in the 
so-called solitary lymph follicles of the intestine, although the changes in the 
agminated glands are distinctly the more conspicuous. These changes begin 
in the very earliest stages of onset, and do not wait until the symptoms of the 



24 



DISEASES DUE TO A SPECIFIC INFECTION 



disease are well developed. If by some accident the patient comes to autopsy 
at this time, the intestinal mucosa will not only be found inflamed, but in 
addition the lymphoid structures just named will also be found swollen and 
reddened by hyperemia. Their edges are not well defined, and the entire 
gland is hyperplastic and spongy. A little later in the progress of the disease 
these areas become less red in hue and begin to look somewhat gray in 
color; they are firmer and project above the surrounding mucous membrane 
to a marked degree, so that they extend well into the lumen of the bowel. 



Fig. 7 




2 cm. 
Ulceration of a Peyer patch in typhoid fever, with associated swelling of solitary glands. 



Sometimes the hyperplasia within the gland is so great that its edges overhang 
the surrounding tissue. Still later the lymphatic tissue may become so infil- 
trated that neighboring patches of glandular tissue coalesce, and when 
they reach the stage of necrosis result in large areas of slough, so that 
the entire thickness of the intestinal wall may be involved (Fig. 7). The 
presence of so severe an ulcerative process naturally results in deep infil- 
tration of the bowel wall, and the inflammatory condition may extend to 
the peritoneal coat, so that this serous membrane is reddened or even grayish 



PLATE I. 




Showing Typhoid Ulcers in Small Bowel and near the 
Appendix. (Kast and Rumpler.) 



TYPHOID FEVER 25 

from exuded lymph. The severest forms of ulceration usually take place 
in the lower part of the ileum. 

While ulceration of the tissues composing Peyer's patches is the usual 
result of this infection, necrosis does not always ensue. The gland may 
become red and swollen and the inflammatory process go no farther, pro- 
ceeding from this state to that of resolution and healing. Not infrequently 
this agminated patch is not equally affected in all its parts, and this gives 
it an uneven appearance, which is emphasized when the portions which 
are most affected ulcerate, so that small ulcers are dotted over the sur- 
face of the swelling, which, if the process is severe, finally coalesce. In 
severe types of the disease the process is so well diffused that a huge 
slough forms which, when it drops off, leaves a swollen, ulcerated surface, 
the excavation being usually very deep. It is this type of necrosis that 
results in perforation, the opening in the bowel wall being usually found 
at a point directly opposite the mesenteric attachment. Rarely the perfor- 
ation takes place between the layers of the mesentery and causes a retro- 
peritoneal abscess. Harte states that in 140 cases out of 190 the perforation 
occurred in the small bowel within twelve inches of the caecum. If the 
patient survives the severer periods of the disease, the swelling of the 
glandular tissue gradually diminishes, granulations develop, new connective 
tissue largely takes the place once occupied by the gland, and the ordinary 
intestinal epithelium covers the exposed area. While it is true that the 
solitary glands are rarely so markedly affected as the agminated glands, 
they may suffer much more severely and be found diseased over a larger 
area than are the glands of Peyer. 

The number of ulcers in the bowel in typhoid fever varies greatly. Usually 
they are limited in number, but occasionally they cover very large areas. 
They may be more numerous in the csecum than elsewhere in the colon. Out 
of 577 autopsies upon cases of this disease in Hamburg and in Leipzig, the 
csecum was ulcerated in 510, or 88.39 per cent.; the csecum and appendix 
in 247, or 42.81 per cent.; the colon in 184 'cases, or 31.89 per cent.; the 
jejunum in 41 cases, or 7.10 per cent.; the rectum in 12 cases, or 2.08 per 
cent. The percentage of csecal lesions, in these statistics of Curschmann, 
just given, is much higher than is generally noted; 40 per cent, is more 
nearly correct. As already stated, the lower part of the small bowel is the 
area chiefly affected. 

Next to the changes in the intestine the most noteworthy alterations 
may be said to take place in the lymph nodes of the mesentery, which lie 
between the intestinal lesion and the general system. These tissues go 
through a similar process of hyperseniia, swelling, and endothelial prolifer- 
ation, which usually falls short of extensive necrosis. Small necrotic patches 
are not infrequent. More rarely large foci of softening or even suppuration 
may occur in these nodes, and as recovery takes place small septic areas 
are gradually walled off by lymph, become encysted, or are absorbed. 
Rupture of enlarged mesenteric nodes has been observed. 

The spleen, in addition to its swelling, which begins early and lasts for 
the first three weeks or more of the illness, is full and tense, and of a darker 
hue than normal. Later, as the attack wanes, it becomes soft and darker 



26 DISEASES DUE TO A SPECIFIC INFECTION 

in hue. The splenic blood sinuses are distended by erythrocytes, the endo- 
thelial cells proliferate, and the pulp here and there becomes the seat of 
small areas of coagulation necrosis. The splenic lesions may also consist 
in infarction and rupture, but the latter accident is very rare. 

Until a few years ago the presence of the typhoid bacillus in the blood 
was unknown, but we now know that this organism is present in this part 
of the body with great constancy during an attack of typhoid fever. 
It is usually present as early as the fifth day and persists until the close of 
the third week, or even longer than this. Rosenberger has recently collected 
535 cases of typhoid fever in which the blood was examined for the bacillus. 
It was found in 80 per cent, of these cases. The examination of the blood 
has therefore become of great importance in the early diagnosis of the 
disease. (See Diagnosis.) The bacillus probably gains access to the blood 
through the mesenteric glands. 

The liver is usually somewhat swollen, but the changes in its appearance 
are not peculiar to this disease. The hepatic cells manifest more or 
less cloudy swelling, and areas of coagulation necrosis containing endothelial 
cells are present. The cells lining the bile-ducts may be swollen, granular, 
and, in some cases, undergo a process of desquamation. Abscess of the 
liver may develop or gallstones may by their presence aid in the produc- 
tion of a cholecystitis, but more commonly typhoid fever probably induces 
gallstones. (See Complications.) 

The heart muscle nearly always suffers from typhoid infection in direct 
proportion to the severity of the toxsemia present. The myocardium is 
granular and may suffer from fatty or hyaline changes. Very rarely the 
endocardium becomes affected and the specific bacillus has been obtained 
from vegetations on the valves. 

The kidneys show no typical changes. They usually show cloudy swell- 
ing, and even an acute nephritis may be present. Sometimes as the result 
of a terminal infection multiple abscesses may form in the kidneys and a 
croupous exudate in the pelvis of these organs may develop. 

Reference is made elsewhere to the lesions of the respiratory tract which 
may complicate the course of the malady, such as laryngeal perichondritis, 
ulcerative laryngitis, hypostatic congestion, pneumonia in both its forms, 
pulmonary infarction, simple pleurisy, and empyema. (See Complications.) 

An endarteritis (which may be • a thromboendarteritis) has been shown 
to occur in a small percentage of cases, and it is reasonable to assume that 
the thrombotic processes occasionally observed in the veins depend upon 
a similar involvement of the lining membrane of these vessels. 

Longcope has shown that the lesions in the bone-marrow closely resemble 
the changes in the lymphoid tissues of the mesentery and of the bowel. 
There are present many lymphoid cells, large phagocytes and foci of 
necrosis. 

A very important factor to be recalled in the study of the pathology of 
typhoid fever is the presence of additional infecting micro-organisms 
which aid the Bacillus typhosus in producing severe lesions and often 
are equally responsible for a fatal termination. This view is, however, 
based on post-mortem findings, and is not supported by the results of 



TYPHOID FEVER 27 

ante-mortem examinations of the blood, for of 150 cases of typhoid fever in 
which the blood was examined during life Cole found but one in which 
mixed infection was present; the case was one of staphylococcemia, with 
multiple boils, and terminated in death. 

Incubation. — The period of incubation of the infection by typhoid fever 
is generally stated to be from one to three weeks. That the period of 
incubation may be much shorter than this would seem to be proved by the 
case reported by Duflocq and Voisin of a girl nineteen years of age who 
deliberately swallowed a virulent culture of the typhoid bacillus with the 
intention of committing suicide. She began to feel ill on the third day, 
had fever on the fourth day, rose spots on the fifth day, and the Widal 
reaction appeared on the sixth day. 

Symptoms. — Typhoid fever usually begins with a sense of wretchedness 
and general illness, no particular symptom being especially well marked, 
unless it be more or less severe frontal headache and aching in the back and 
limbs. The facial expression very early in typhoid fever usually becomes list- 
less and later stupid and heavy, and the patient is often a little deaf because 
his mental state is benumbed rather than because there is any actual trouble 
with the auditory apparatus. Not infrequently there may be a considerable 
amount of cough without expectoration, and there may be exaggeration 
of the sounds of bronchial breathing on auscultation. 

The tongue is somewhat coated, and very early its edges become clean 
and red, while the central coating remains. This appearance of the tongue 
is very characteristic, even in mild cases. 

Headache, thirst, and sleeplessness are usually prominent symptoms during 
the first week. A mild fever develops simultaneously and nose-bleed may 
occur repeatedly. Usually the liver and spleen become swollen toward 
the end of the first week, and the belly becomes somewhat tumid and 
tender. 

The characteristic enlargement of the spleen in enteric fever may be 
undemonstrable because of the distention of the stomach and intestine with 
gas; but while the presence of an enlarged spleen is of some importance in 
reaching a diagnosis of typhoid fever, inability to discover any increase in 
its size does not negative the diagnosis of typhoid fever in any degree. 

An undue amount of gurgling can be felt and heard in the right iliac 
fossa. 

Constipation is usual in the first week, but diarrhcea may be marked, and 
if loose the stools may be brownish, but later resemble okra-soup or pea- 
soup. 

The temperature in typhoid fever during the first week rises step by 
step. Each morning it is higher than on the previous morning, and each 
evening higher than on the night before, although the morning temperature 
is often lower than that of the preceding evening. (See Fig. 8.) Usually 
by the end of this week it reaches in the morning 102° or 103°, and at 
night 103° to 104°, and remains at this level until the fourteenth or 
twenty-first day. 

The pulse is more rapid than normal, ranging from 90 to 100 beats per 
minute, and it is usually soft and compressible; the pulse of debility, not 



28 



DISEASES DUE TO A SPECIFIC INFECTION 



of vigor. Often the pulse is a little dicrotic. As the disease progresses the 
pulse rate usually increases to about 110, but the pulse force distinctly 
diminishes. 

At about the seventh to the ninth day a very important diagnostic sign 
first makes its appearance, namely, the so-called rose spots, which usually 
develop on the skin of the abdomen and chest, sometimes on the back, and 
more rarely on the limbs. These spots are small, faint macules, usually 
scanty in number, which lose their color momentarily when pressed upon 
or when the skin on which they exist is stretched between the ringer and 
thumb of the physician. As a rule these spots are isolated, but very rarely 
they may be so profuse as to produce the appearance of an ordinary rash. 

Fig. 8 



x 

2 103' 



ivi] e|m| eJm! e|mI e|m[eTm|e|m|e|m|e|m|e|m| e[m e|m|e|m| e|m| eJmIemI em e mem] em e m e 



i 




90 TO 120-DICROTIO 



? 




Course of typhoid fever. (Modified from Musser.) 



The tongue becomes dry and it may be fissured, the mental stupor 
increases, diarrhoea is also active, and the moderate tympanites of the 
earlier days becomes more marked. If the patient has received little 
care, or if the case is essentially severe, his condition is manifestly one of 
profound toxaemia, and by the end of the second week he is evidently at 
the very acme of his infection. Death not infrequently takes place during 
this period as a result of profound toxaemia, hemorrhage, perforation, or 
pulmonary complications. 

Because of the toxaemia delirium may be marked, and it is usually of 
the low muttering type, the patient seems to be in a semi-stupor, the teeth 
are covered with sordes, and the tongue is foul and dry. 

These symptoms gradually carry the patient into his third week, with 
increasing diarrlwea, greater tympanites, deeper stupor, and more manifest 
signs of profound tox&mia, with muscular tremors or true subsultus tendinum. 
Emaciation by this time is marked and the skin dry and harsh. The heart 
is feeble, its sounds distant and muffled, and myocardial degeneration is 



TYPHOID FEVER 



29 



manifestly advanced. To the possibility of the appearance of the fatal 
complications named in the succeeding pages as appearing at the end of the 
second week are added at this time still greater danger of pulmonary hypo- 
static congestion and pneumonia. The patient may be so profoundly 
poisoned by the toxic products of the disease that he seems almost 
moribund. 

If the pathological process is not so severe that recovery is impossible, 
the first sign of the ending of the malady may develop at any time between 
the fourteenth and twenty-eighth day, according to the severity of the 



Fig. 9 



cf 

105 
104° 

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Part of a chart showing the period of steep curves from the fourteenth to the twentieth day 
of an attack of typhoid fever. 



disease. This consists in a slight modification of the temperature range 
and the development of a low morning temperature with a well-maintained 
high evening temperature, so that the daily range may amount to from 
2° to 3°. This is called the "period of steep curves/' and the appearance 
of these steep curves at this time in the course of the disease is usually a 
promise of approaching convalescence. An equally good description of this 
period is that of Murchison, who called it the "stage of changing fortunes," 
or that of Wunderlich, who described it as the " period of ambiguity." 



30 DISEASES DUE TO A SPECIFIC INFECTION 

The last stage of the acute febrile period having been reached, the 
temperature falls to normal during the next few days by lysis, and then 
may be subnormal until convalescence is well established, the patient 
being wasted and feeble, but usually ravenously hungry. 

Atypical Forms. — While the train of symptoms just described may be con- 
sidered typical of an attack of typhoid fever occurring under conditions favor- 
able for its full development, it is often so modified by various causes that a 
large proportion of cases do not present many of the most prominent and diag- 
nostic symptoms, but, in their place, manifestations so at variance with those 
of ordinary cases as to greatly perplex the physician. Thus, very marked 
variations in onset may occur and completely mislead the medical attendant 
if he be not on his guard. In some cases instead of manifesting itself grad- 
ually the disease has a sudden onset with a sharp chill followed, it may be, 
by a profuse sweat and a continued fever. This variation is perhaps most 
apt to occur in children. Headache may be so severe in the beginning as to 
rouse the suspicion of meningeal inflammation, and active delirium may 
be an early symptom, being severe enough to be maniacal in type. In other 
instances a pneumonia is the earliest sign of the malady, while in still others 
a severe choleraic diarrhea may begin the illness. It is also important to 
recall the fact that well-developed signs of appendicitis may appear, due 
to the swelling of the lymphoid tissues of the intestine and appendix by 
reason of the infection. This has frequently resulted in enthusiastic sur- 
geons removing the appendix only to find it slightly diseased as part of the 
general lymphatic change, the speedy appearance of the rose rash and per- 
sistent temperature soon showing the true character of the case. Rarely a 
severe attack of vomiting begins the illness, and still more rarely acute 
renal disease, nephro-typhoid, or the fievre typhbide h forme renale of the 
French observers, develops. 

Although diarrh&a was correctly considered at one time to be one of the 
most constant symptoms of enteric fever it is now absent in more than half 
the cases during the whole course of the disease, and splenic enlargement 
in many instances is too slight to be discovered, so that it is to be borne in 
mind that while these two symptoms possess a positive diagnostic value when 
present, their absence in no way contradicts the diagnosis of typhoid fever. 

In other instances the course of the fever greatly varies from that just 
described. It may rise very abruptly, and it may end equally suddenly, the 
lysis being completed in twenty hours. Sometimes the morning temperature 
is the higher of the two, although this is rare. The regular course of the 
temperature may also be greatly altered by intercurrent chills. (See Chills.) 
Very rarely, strange as it may seem, no febrile movement is present at any 
time in the course of the malady. 

The most important variations from what may be called the normal 
course of the temperature in the second and third week of this disease are 
those produced by free hemorrhage from an intestinal ulcer and by perfora- 
tion of the bowel. A sudden fall of several degrees should always arouse 
suspicion of one of these accidents, for the drop in the fever may be noted 
before any of the other signs of hemorrhage or perforation manifest them- 
selves. 



TYPHOID FEVER 



31 



Marked rises and falls of temperature are also often seen in patients 
who are markedly anaemic as the result of hemorrhage. Abortion also 
causes a marked fall of the 
fever. 

The course of the temperature 
may resemble that of remittent 
malarial fever, and it has fre- 
quently misled physicians into the 
belief that malarial infection and 
not typhoid infection was present. 
(See Chills.) Infectious complica- 
tions of the disease such as otitis 
media, phlebitis, f urunculosis,men- 
ingitis, and erysipelas may also 
cause sudden variations in tem- 
perature. And in cases which have 
been gravely ill it not rarely hap- 
pens that fever continues after the 
typhoid infection has run its course 
because of post-typhoidal septice- 
mia— that is, a multiple infection 
due to the presence of pyogenic 
organisms, which have found a 
favorable field for growth in a 
patient whose vitality has been 
impaired by the specific fever. 

As the stage of convalescence 
approaches, or when it is reached, 
a sharp return of active febrile 
movement may come on for a day 
or two, the temperature being as 
high or higher than ever before. 
It then returns to its ordinary level. 
This is called a recrudescence, and 
possesses no grave significance. It 
often follows mental excitement 
and the taking of improper or too 
much food. When this rise of 
temperature persists, it usually is 
indicative of some complicating 
malady, or of a relapse called an 
"intercurrent relapse" if it takes 
place during the continuance of 
the primary febrile period. (See 
Fig. 10.) After the fever has disap- 
peared there may be a prolonged 
continuance of a slight evening 
rise of temperature as the result S S S 2 S 3 - < 

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32 DISEASES DUE TO A SPECIFIC INFECTION 

of nervous irritability and anaemia, or it depends upon the abuse of strych- 
nine, with the mistaken idea that it is a valuable heart tonic at this time. 
In other cases a subnormal temperature for the entire twenty-four hours may 
persist for days. This is of no importance save that it indicates that the 
patient is feeble and needs good feeding and fresh air. The other variations 
met with depend upon the age of the patient. Old persons often have an 
irregular febrile movement, and children may have marked rises and falls of 
temperature which do not necessarily indicate any complications. 

Persistence of distinct febrile movement after the fourth week in any case 
of typhoid fever in which a relapse has not occurred nearly always means a 
complicating or secondary infection. The number of cases of rapid tuber- 
culosis called typhoid fever, until the persistent loss of flesh and fever forces 
the correct diagnosis upon the physician, is by no means small. The possi- 
bility of ulcerative endocarditis, cholecystitis with ulceration, with or without 
impacted gallstones, and septic infection due to suppuration as causes of 
fever are to be borne in mind and their presence carefully looked for. (See 
Complications.) 

That a patient with this disease may suffer not only from the infec- 
tion due to the bacilli of Eberth, but from multiple infections by other 
organisms which aid in decreasing his vital resistance should be borne in 
mind. 

Closely associated with the study of the temperature is that of chills. 
They may usher in an acute complicating inflammatory process, or be 
entirely without such significance. Sometimes they occur in cases which 
suffer from constipation, apparently as a result of the absorption of fecal 
poisons. (See Fig. 11.) In other cases they are due to a true coincident 
malarial infection, but it is a noteworthy fact that during the course of 
typhoid fever, even if the patient is also suffering from malarial infection, 
the latter usually remains in abeyance until the former has about run its 
course. It is better for the physician to regard such chills as being an indi- 
cation of some acute complication than to consider them as malarial, unless 
he can prove the existence of the last possibility by finding malarial 
organisms in the blood. 

The skin is sometimes covered by a fugacious scarlatiniform rash in 
the early stages. In certain cases it desquamates in large flakes or in 
fine, branny scales, the latter appearing oftenest in those who have been 
actively bathed and rubbed. 

Very commonly if sweating takes place, sudamina, or tiny sweat drops 
retained beneath the superficial epiderm are found on the abdomen, chest, 
or limbs. Herpes about the mouth is very rare in typhoid fever, but it 
does occur, notwithstanding the denial of this fact by some observers. 

Under the name of tache bleudtre or peliomata, faint blue or steel-gray 
spots of fairly good size are sometimes met with. They are not due to 
the disease, but are found only in those who are infested with lice. The 
so-called tache cerebrale is not characteristic of this disease, but is some- 
times seen during its course, and consists in a red line with white borders 
produced by drawing the finger-nail over the skin. It is probably due to 
vasomotor palsy of the cutaneous vessels. 



TYPHOID FEVER 



33 



Of the deeper lesions of the skin, we meet with bed-sores, which rarely 
occur in cases seen from the first and which receive proper care. They appear 
usually over the sacrum. Cases of superficial gangrene of the skin have 
been reported by Stahl and the author. Erysipelas occurs, usually of the 



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73 



34 DISEASES DUE TO A SPECIFIC INFECTION 

face, by reason of infection through fissures in the buccal or nasal mucous 
membrane. Sometimes erysipelas migrans develops. In very malignant 
cases petechia? may be present. 

Patients suffering from typhoid fever rarely suffer from other eruptive 
diseases, but instances of scarlet fever, chicken-pox, and measles occurring 
as complications are on record. In women in particular the hair often falls 
out freely during or after an attack. Boils are by no means rare lesions, 
and even carbuncles may develop as a result of multiple infection. 

The blood in typhoid fever suffers from an increasing degree of ancemia 
in respect to the number of the red cells and of their richness in haemoglobin. 
Indeed, the color-index is more markedly lowered than the corpuscular 
count. When an inadequate supply of liquids has been allowed the result- 
ing concentration of the blood may produce an apparent corpuscular richness 
not actually present. 

The bacteriolytic power of the blood in severe cases is probably always 
diminished. The leukocytes are slightly decreased in number, the large 
mononuclear and transitional cells are relatively increased, and, according 
to Thayer, the polymorphonuclear cells are decreased. Cabot asserts that 
a leukocytosis, non-inflammatory in origin, sometimes occurs. 

Complications and Sequelae. Circulatory Complications. — The heart, 
as already stated, is weakened, and if severely affected may develop em- 
bryocardia or fetal heart sounds. There are few, if any, diseases which 
do not have special predilection for the heart muscle or its valves, which so 
greatly interfere with this organ as does typhoid fever. A pulse rate above 
125 is ominous, and one of 130 or 140 dangerous. The danger is usually in 
direct proportion to the feebleness of the first sound of the heart. When 
the cardiac sounds are those of the foetus in utero (embryocardia), the prog- 
nosis is grave. A very rapid pulse and irritable cardiac action are sometimes 
seen in cases in which strychnine has been used to excess with the idea that 
it is a stimulant. A soft systolic murmur is occasionally audible, which 
may be hsemic in origin or due to relative insufficiency of the mitral valves. 
Rarely it may be due to endocarditis or pericarditis, but pericarditis is a 
very rare complication of typhoid fever. Gaudy and Gourand state that 
pericarditis arising during the course of typhoid fever occurs in two forms, 
namely, the fibrinous, which is characterized by an abundant pseudo- 
membranous exudation with only slight serous effusion, and the fibrino- 
purulent form, in which a considerable effusion may occur. Pericarditis 
may exist alone or may occur in connection with endocarditis, myocarditis, 
pleuritis, or pulmonary complications. As a rule, it develops very slowly 
and may remain latent, so that only most careful auscultation over the 
prsecordial region will reveal the presence of friction fremitus, and later 
careful percussion may be required to distinguish an effusion. The patho- 
genesis of this complication is obscure. The purulent form when it occurs 
may be due to secondary infection, although the fibrinous variety is prob- 
ably due to a direct infection with the Eberth bacillus. Typhoid fever 
complicated by purulent pericarditis is always fatal, but the existence of 
the serofibrinous pericarditis influences prognosis slightly if at all, unless 
the effusion be profuse. 



TYPHOID FEVER 35 

Sudden cardiac failure may occur as the result of myocarditis, or of 
embolism or thrombosis of the coronary arteries, from heart clot, throm- 
bosis of the cavfle and pulmonary veins or from pericarditis with effusion. 
Sometimes the cardiac failure is gradual when due to these causes. 

So far as the bloodvessels are concerned the most common lesion is 
phlebitis, which usually affects the veins of the left leg, especially the femoral 
vein. The frequency of involvement of the veins in the left leg depends 
upon the pressure exercised by the right common iliac artery upon the left 
common iliac vein, which tends to obstruct the flow of blood. Sometimes 
the tendency to the formation of a thrombus is greatly increased by a local 
infection of the endothelial lining of the vessel, and it is not uncommon for 
a severe chill or chills to mark the onset of the lesion. Wright and Knapp 
have recently shown that the tendency to the formation of a thrombus in 
typhoid fever is augmented by the increase of calcium in the blood. When 
milk is the exclusive diet the rise in the proportion of calcium oxide sup- 
plied to the body is very noteworthy. They also recommend that for the 
prevention of this state the physician add 20 to 40 grains of citrate of soda 
to each pint of milk taken by the patient in order to decalcify it. 

Thromboses of extraordinary size and number may form and extend from 
the femoral vein to the vena cava. When venous plugging seriously inter- 
feres with the circulation, the gangrene which results is usually moist, but 
in the vast majority of cases of phlebitis of the leg partial recovery takes 
place, although varicosity of the veins of the limb may persist after con- 
valescence is completed. The rarity of plugging of the veins of the upper 
extremity is remarkable. 

Arterial thrombosis is much more rare than is venous thrombosis. This 
complication usually develops after the second week of the fever, and is 
manifested by pain and tenderness along the course of the vessel affected. 
Usually the leg is the limb involved. After a temporary increase in the 
force of pulsation in the affected vessel the pulse becomes small and may 
be lost. The part becomes cold and discolored, and finally gangrene ensues. 
In other cases, in which the vessel which is involved is small, recovery takes 
place by the establishment of a collateral circulation. Even in the mild 
cases the patient suffers afterward from fatigue in the affected limb on 
exertion, and intermittent claudication may develop. The condition is due 
to an arteritis. 

Thayer has published statistics which seem to indicate that typhoid fever 
is prone to produce early senile changes in the bloodvessels in after years. 

Complications in the Alimentary Canal. — The complications in the 
upper digestive tract are pharyngitis, which is rarely severe enough to cause 
much discomfort, and oesophagitis, which is still more rare, although several 
observers have recorded ulceration of the oesophagus. Inflammation of the 
parotid gland is a rare complication of typhoid fever, and usually occurs 
about the third week in cases of severe infection. This inflammatory state 
may be due to infection of the gland from the mouth by ordinary pus 
organisms, or more rarely be due to the specific bacillus. Rarely parotitis 
occurs in the first week. In the only case the author has seen in which 
this complication developed at this time there was no pain or redness, and 



36 DISEASES DUE TO A SPECIFIC INFECTION 

the swelling disappeared in about ten days. It was also bilateral. In 
advanced typhoid fever it is usually bilateral; is often followed by ugly 
sloughing, and is a very dangerous complication. 

The stomach in typhoid fever is rarely much affected. Digestion in this 
viscus is, as a rule, feeble because in all fevers there is a lack of gastric 
secretion, and this is particularly true of typhoid fever. Vomiting may 
come on usually as a result of indiscretions in food and medicine. Some- 
times, however, late in the disease a persistent, pernicious vomiting develops 
which only ends with exhaustion and death. A few cases of gastric ulcer 
occurring in typhoid fever are recorded. 

When there are more than three or four stools a day diarrhoea is to be 
considered excessive. When a far greater number occur, it is usually 
the result of improper feeding. The stools are thin and resemble pea- 
soup save that they are apt to be a little more yellow. They are alkaline 
in reaction, offensive, and may contain particles of undigested food, as 
curds of milk, and also small shreds of lymphoid tissue from the sloughs 
of the bowel. The specific bacillus usually is not to be found in the stools 
until about the seventh or tenth day. The significance of active diarrhoea 
as to the gravity of the case has been much discussed, some believing that 
it is a sign of a severe infection. The real significance is not of severity of 
infection, but of severity of intestinal involvement, catarrhal or ulcerative, 
although in some cases even the latter state does not provoke active diar- 
rhoea. General diffuse pain in the bowels is often present early in the 
disease, but is apt to disappear later. 

Hemorrhage from the bowel in typhoid fever is one of the inevitable 
complications in a certain percentage of cases, and usually takes place 
after the second week of the disease. Very rarely slight loss of blood may 
occur in the first week. Proper treatment of the patient all through his 
attack may diminish toxsemia and prevent a fatal terminal infection, but no 
form of treatment so far devised has materially diminished the frequency of 
hemorrhage or the mortality from this cause, although the frequency of 
the occurrence and mortal effects vary greatly in different epidemics. The 
general average of its occurrence may be placed at 5 per cent. In 52,196 cases 
of typhoid fever collected from several series of cases reported by French 
and German physicians, and from the official reports of hospitals in the 
United States and Canada, England and Ireland, Germany, Austria, South 
Africa, and Australia, hemorrhage is stated to have occurred in 2725 cases, 
which gives a percentage of 5.22. The mortality in persons suffering from 
it is about 35 to 50 per cent., although in 271 cases of intestinal hemorrhage 
complicating typhoid fever, collected from the official reports of hospitals 
in the United States, Canada, England, and Germany, 71 cases proved 
fatal, which gives a percentage of 26.2. Hemorrhages usually arise from 
ulcers in the small intestine and are very rare in children. The symptoms 
consist of sudden fall in the temperature and it may be in the pulse rate, 
but this primary decrease is usually followed by a more rapid pulse than 
existed before the accident occurred. A diagnosis of hemorrhage is to be 
reached not only by the observance of the symptoms just described, but 
in addition by the presence of blood in the stools and by examining the 



TYPHOID FEVER 37 

blood to discover a paucity of haemoglobin. The gravity of a hemorrhage 
depends upon the relation of the quantity of blood lost to the vitality of 
the patient and the frequency with which the bleeding occurs. Thus a 
fairly profuse hemorrhage in a strong patient may be followed by no 
severe symptoms, whereas repeated small hemorrhages may greatly exhaust 
the most lusty individual. When the patient is at the end of a long and 
severe attack of the fever, even a comparatively small hemorrhage may be 
fatal. The existence of small losses of blood not sufficient in size to be 
manifest to the eye when the stools are examined, may be discovered by 
the tests for occult blood named in the Article on Gastric Ulcer. 

Perforation of the bowel, the most serious of all the complications of 
this disease that is commonly met with, has no relation to the severity of 
the general symptoms, for it occurs as often in mild as in severe cases. 
Indeed, in nearly 50 per cent, of recorded cases this accident occurred in 
mild cases. When perforation occurs the symptoms are apt to be ushered 
in by agonizing pain, usually felt in the appendicular region, which may be 
severe enough to rouse the patient from a considerable degree of stupor. 
If the patient is not too apathetic the pain is often described as being in 
the lower zone of the belly near the median line, and most commonly 
slightly to the right. The belly- wall is sensitive to palpation, speedily 
becomes tense and tympanitic, and all the symptoms of a general dif- 
fuse peritonitis may quickly ensue. The pain may, however, not be per- 
sistent, but pass away or become modified, as the peritoneal condition 
resulting from the escape of fecal matter into its cavity becomes more and 
more septic. The pulse becomes rapid and running, and collapse may 
speedily assert itself. When this occurs, death speedily comes on, the 
patient dying in a few hours, or, again, he may rally and survive for several 
days. Early death is, however, the more common result. Thus in the 
collection Of 34 cases made by Fitz, of Boston, 37.3 per cent, died on the 
first day, 29.5 per cent, on the second, and 83.4 per cent, in the first week. 
During the second week 9 died, in the third week 4 died, and 2 other cases 
lived thirty and thirty-eight days, respectively. If collapse does not ensue, 
the rally of the system results in a rise of the temperature to a point higher 
than before the accident, and this movement is often accompanied by 
chills and rigors. Usually by the second or third day the peritoneal symp- 
toms become more and more marked, the condition of the patient more 
and more asthenic and depressed, and death results by the fourth day 
from a general peritonitis with toxaemia from the absorption of toxic materials. 
In other cases the onset of the perforation is insidious; the belly before the 
perforation may have been moderately tympanitic, but now becomes intensely 
hard and rigid ; the pain, which in some cases is so severe, does not develop, 
but the great fall in fever followed by a rise, and this again by rigors, it 
may be, give evidence of the grave accident which has occurred. The 
pulse becomes increasingly rapid and running, and the respiration more 
and more costal and less and less diaphragmatic, until the patient sinks out 
of life, without much, if any, suffering, in generally the same manner as one 
sees death come to a case of diffuse septic peritonitis due to a pyosalpinx or 
to septic appendicitis. In such cases the perforation is usually very small, 



38 DISEASES DUE TO A SPECIFIC INFECTION 

and is so surrounded by adhesions that the escape of the intestinal con- 
tents is very gradual and insidious, infecting the peritoneum without the 
escaping fluid being copious enough at any one time to produce great pain 
or reaction. 

In this connection it is important to note that a sudden fall in temperature 
is not a symptom necessary to the diagnosis of intestinal perforation. On 
the contrary, there are many cases on record in which a rise of temperature 
has followed this accident. 

The diagnosis of perforation is to be reached by the following signs in 
addition to those just given: The hand of the physician, when lightly placed 
upon the abdominal wall, not only develops the fact that it is hypersensitive, 
but that its muscles are unduly tense. If the perforation has occurred 
very recently the rather swollen and tumid belly may be slightly scaphoid. 
Percussion may indicate the presence of gas in the peritoneal cavity, and 
the liver may be pushed away from the abdominal wall in such a manner 
that the ordinary area of liver dulness is largely decreased. Percussion of 
the right hypochondrium is, therefore, an essential procedure in the physical 
diagnosis of these cases. A fallacy underlying this test is the possibility of 
a portion of the colon, when greatly distended with gas, slipping up between 
the liver and the belly wall, and thus giving resonance; but this is a rare 
occurrence. 

In some cases, however, as intimated, the symptoms are so insidious that 
the absence of this sign does not negative the diagnosis of perforation. 
Indeed a positive diagnosis may not be possible, and cases are sometimes 
met with in which the perforation has not been suspected, and is found 
only at the autopsy. 

The diagnosis of peritonitis due to perforation is aided, but not confirmed, 
if an examination of the blood reveals a leukocytosis of polymorphonuclear 
cells. 

There are several conditions causing pain which must be carefully excluded 
before the physician can arrive at the diagnosis of perforation, even if the 
symptoms and signs just described are present. These are diaphragmatic 
pleurisy, pneumonia of the bases, appendicitis, iliac thrombosis, and intes- 
tinal obstruction. Further than this, peritonitis may develop from extension 
of the inflammatory process in the bowel or by reason of the migra- 
tion of micro-organisms through those parts of the bowel wall which 
have been impaired by the ulcerative process. In such cases the pain, 
swelling, and diaphragmatic paralysis may all be present without being 
due to perforation, and so closely may the symptoms of perforation be 
aped that operation has been performed, with the discovery that no perfora- 
tion had occurred; thus in a case under the care of Herringham, nothing 
was found at the section and the patient recovered. Perforation may also 
be simulated by suppuration and rupture of a swollen mesenteric gland. 
Other causes of peritonitis are necrosis of the mesenteric glands, infarc- 
tion of the spleen, or the development of abscess in an ovary or Fallopian 
tube. Very rarely peritonitis arises from cholecystitis or cholangitis, with 
or without gallstones. Liebermeister has recorded two cases in which 
rupture of the gall-bladder with escape of gallstones into the abdominal 



TYPHOID FEVER 39 

cavity took place. An ulcer in the appendix may perforate or an inter- 
current appendicitis may complicate the case. 

The percentage of frequency of occurrence of perforation is generally 
stated to be about 2.2, but in 30,966 cases of typhoid fever collected from 
several series of cases reported by French and German physicians, and 
from the official reports of hospitals in the United States and Canada, 
England and Ireland, Germany, Austria, South Africa, and Australia, 
perforation is stated to have occurred in 1144 cases, which gives a percentage 
of 3.69. The percentage of its mortality, when surgical interference is not 
resorted to at the most favorable time, is 90 to 95 per cent., and with 
operative interference it may be as high as 81 per cent. (See Treatment.) 

Perforation is very much more frequently seen in men than in women. 
Fitz in 444 cases found 71 per cent, in men and 29 per cent, in women. In 
21 cases of perforation in Basle, 15 were men and 6 were women; and 
Griesinger in 14 cases had 10 men and 4 women. Murchison also found 
in 24 cases 16 men and 8 women, although the general mortality of the 
disease among women was slightly higher than among men. So, too, 
Bristowe, of London, met with this accident in men in 11 of 15 cases, and, 
again, Nacke collected 106 perforation cases, of which 72 were in men 
and 34 were in women. 

Perforation is responsible for a large proportion of the deaths which occur 
from typhoid fever. Out of 1721 cases which came to autopsy the per- 
centage of deaths due to perforation was 11.3, according to Murchison. 
According to Holscher, it was found in 2000 Munich cases 114 times (5.7 
per cent.), and in 20 out of 80 of his cases which ended in death. In 4680 
cases tabulated by different writers, Fitz found the proportion to be 6.58 
per cent., which agrees with Holscher's statistics. Hoffman found that out 
of 250 deaths in typhoid fever 20 were due to perforation. 

Perforation takes place most commonly in the third and fourth weeks of 
the malady, but is by no means rare in the second week. It occurs most 
commonly in patients between twenty and thirty years of age. Elsberg has 
reported a case of a child of three and a half years who suffered from 
this accident, but whose life was saved by abdominal section. 

The relation of typhoid fever to appendicitis is one of great interest. 
It has been thought by some that appendicitis arising in typhoid fever was 
a mere coincidence; by others, that its origin depended upon a general infec- 
tious process; and, again, by others, that it was due to the direct infection of 
the appendix with the bacillus of Eberth. Probably all these views hold true 
in individual cases. The richness of the appendix in lymphoid tissue, and 
the fact that typhoid fever is particularly prone to attack such tissues, 
renders this organ peculiarly susceptible on theoretical grounds. That this 
view is correct is proved by the research of Hopfenhausen, who collected 
the appendices obtained from 30 cases of typhoid fever and studied them 
under Stilling in the University of Lausanne. She concludes that moderate 
changes in the appendix may be found in nearly all cases of this disease, 
that it is most marked in the earlier stages of the malady, and consists 
chiefly in cellular infiltration, specific lesions being rare and not suffi- 
cient to produce the more severe forms of appendicular disease. 



40 DISEASES DUE TO A SPECIFIC INFECTION 

True appendicitis complicating typhoid fever, in the sense of inflammation 
of the appendix severe enough to produce abscess, is undoubtedly a very 
rare affection. Hopfenhausen has collected statistics of 743 cases of appen- 
dicitis, of which 5 per cent, were due to typhoid fever. This must be a 
very much larger percentage than usually exists. 

It is a noteworthy fact that appendicular symptoms are not infrequent 
in early typhoid fever, and often disappear under rest in bed, and with 
the full development of the infection. Rarely the inflammation goes on 
to the formation of an appendicular abscess or perforation. The swelling 
of the lymph node in the mesoappendix and the presence of ulcers in the 
caecum explain why it is that pain in the appendicular area is by no means 
rare. (See Plate I.) Sudden pain in the lower zone of the abdomen may be 
indicative, not of appendicitis, but of the presence of an iliac thrombosis. 

Tympanites in typhoid fever is always present to some degree at some 
stage of the disease. When very marked, it is an evil symptom because 
it indicates active fermentation in the bowel, and the presence of intestinal 
atony, and because the gas presses on the abdominal thoracic viscera and 
disturbs their functions. By distending the intestine it may also predispose 
the patient to a hemorrhage or perforation by the strain on a severely ulcer- 
ated Peyer's patch. 

Hepatic Complications. — The liver and gall-bladder rarely show signs of 
active infection during the early part of an attack of typhoid fever. Jaundice 
is one of the rarest complications of this disease. Aside from some swelling 
and tenderness in the hepatic region, no symptoms in the hypochondrium are 
usually observable. It is, however, important to note that secondary involve- 
ment of the gall-bladder as a sequel of this malady is by no means rare, a true 
cholecystitis developing in a goodly proportion of cases as a result of infec- 
tion of this viscus by the bacillus of Eberth. This cholecystitis may be 
severe enough to result in empyema of the gall-bladder and perforation 
of its walls with symptoms resembling intestinal perforation. A still more 
interesting fact is that such a cholecystitis due to this organism may develop 
many years after the attack of typhoid fever, and again that the clumping 
of these organisms in the gall-bladder may give rise to the formation of 
gallstones. 

Louis, in his work on typhoid fever, published in 1836, states that changes 
in the bile and gall-bladder occur more frequently in typhoid fever than 
in other acute diseases, and cites 3 fatal cases in which cholecystitis, unrecog- 
nized during life, was found at autopsy. Grisolle and Andral mention 
similar cases. In 3 instances French found the gall-bladder of persons 
who had died of typhoid fever filled with turbid albuminous fluid, and 
Rokitansky speaks of having found "fibrinous exudations" in the gall- 
bladder of several patients who died from the disease. Murchison refers 
to the cholangitis and cholecystitis which may accompany typhoid fever, 
and reports a case of rupture of the gall-bladder, followed by general peri- 
tonitis. In 1876 Hagenmiiller reported 18 cases of cholecystitis complicating 
typhoid fever. He concluded that it was a more frequent complication 
than had generally been supposed. Holscher, in the 2000 Munich autop- 
sies, found empyema of the gall-bladder 5 times. 



TYPHOID FEVER 41 

In 1889 Bernheim suggested that typhoid bacilli might give rise to gall- 
stones by producing alteration or stagnation of the bile. In 1893 Defourt 
reported 19 cases of cholelithiasis, in which the first attack of biliary colic 
occurred at varying periods after typhoid fever. Osier has reported a case 
of hepatic colic occurring for the first time in the fifth week of typhoid 
fever. At operation nothing could be found to account for perforation 
of the gall-bladder, but nine months later a gallstone was discharged. 

Fournier found bacteria in 38 out of 100 gallstones which he removed 
at autopsies. The colon bacilli predominated, while the typhoid bacilli 
were found to be second in frequency. Milian, Chantemesse, and Horton 
Smith report similar experiences. 

Chiari found typhoid bacilli present in the gall-bladder in 19 out of 22 
cases, and obtained pure cultures from 15. In 9 out of 10 cases at St. 
Bartholomew's Hospital, London, Bacilli typhosi were found. Gushing 
mentions 5 cases of cholecystitis complicating typhoid fever, in which pure 
cultures of colon bacilli were obtained from the pus. Marsden reports a 
case in which cultures resembling Bacillus typhosus were obtained. Van 
Dungern obtained pure cultures of typhoid bacilli from pus surrounding 
the gall-bladder fourteen years and a half after an attack of typhoid fever. 
Pure cultures have often been obtained from six to eight months after the 
attack (Chantemesse, Dupre*). 

Mason thinks that the bacilli gain entrance through the biliary ducts. 
Councilman believes that they are carried through the blood, and that areas 
of necrosis in the liver afford them portals of entrance. Hagenmuller, Mayo 
Robson, and Mark Richardson believe that biliary complications, espe- 
cially cholecystitis, are due to ascending infection of the ducts. Marsden is 
of the opinion that the most important passage of bacilli into the gall- 
bladder is through the blood, the liver, and the biliary ducts. He is 
undoubtedly correct. 

Typhoid cholecystitis during the course of the fever is frequently latent. 
In more than one-half the recorded cases, either on account of latency of 
symptoms or typhoidal stupor, nothing unusual was observed during life. 

The two most constant symptoms are pain and swelling, the former being 
paroxysmal and most marked in the region of the gall-bladder and under 
the scapula. Maurice Richardson says that it may be in the epigastrium 
or over McBurney's point. According to Mayo Robson, if a line be drawn 
from the umbilicus to the ninth rib on the right side, there is almost always 
tenderness at the beginning of the second third of this line. Jaundice is 
rarely met with, but there may be repeated chills and sweats. 

Genitourinary Complications. — Albuminuria in typhoid fever is quite 
a constant condition, occurring as frequently as in 70 per cent, of all cases, 
and being most marked in the second week. Usually its presence is not asso- 
ciated with that of tube casts unless the patient is already a sufferer from 
nephritis prior to the attack. When casts are present, the albumin is usu- 
ally present in large amount. Albuminuria without casts is not a serious 
complication. Probably true nephritis is present in almost 20 per cent, of 
the cases, but this is usually not productive of renal symptoms. An ante- 
cedent nephritis may take on renewed activity and a true hemorrhagic 



42 DISEASES DUE TO A SPECIFIC INFECTION 

nephritis may occur, usually in severe cases only. The urine is apt to be 
scanty and of high specific gravity unless the physician insists upon the 
patient drinking freely of water. 

Pyuria in slight degree is common. Blumer says it occurs in 17 per cent., 
but it is a noteworthy fact that pyelitis due to typhoid fever is almost unknown. 
While this is true, it is also of interest to note that enormous numbers of 
the bacillus of Eberth are to be found in the urine after the second week 
of the disease, and often far into convalescence. Petruschky has estimated 
that 1 c.c. may contain 170,000,000 bacilli. A profuse polyuria is often 
present when the stage of convalescence is entered upon. 

Orchitis and epididymitis rarely occur as a result of a direct infection with 
the specific bacillus. They differ from the changes due to gonorrhoea in 
that they are less painful and more rapid in their course to suppuration or 
recovery. They are usually unilateral and the testicle is first affected. 
Typhoidal cystitis due to the presence of the bacillus of Eberth rarely occurs. 

Respiratory Complications. — The respiratory disorders met with in 
connection with the course of typhoid fever, aside from the bronchitis already 
mentioned, are quite numerous. In the later stages of the disease we may 
meet with severe laryngeal ulceration, which in turn may be complicated by 
perichondritis or oedema of the glottis. Hoffman found 28 cases of ulcer of 
the larynx in 250 autopsies in this disease, and Griesinger in 26 per cent, of 
those dying of the malady, so that it is by no means rare. Keen collected 
146 cases of severe laryngeal disease due to this cause, and found that 
necrosis of the laryngeal cartilages when it occurred was a very fatal 
complication, death occurring in 95 per cent, of the cases. 

Intense hypostatic congestion is one of the most constant pulmonary 
changes seen at autopsy; in some cases the blood may inundate the air 
vesicles, causing solidification. How often this change is agonal cannot be 
determined with any degree of certainty, but as it depends on more or less 
prolonged maintenance of one position aided by an enfeebled circulation 
the danger can be greatly lessened, if not avoided, by frequent changes 
in posture. 

Pneumonia develops in typhoid fever in three forms and in different stages 
of the disease: (1) As an acute lobar pneumonia ushering in the attack of 
enteric fever, and due to the Micrococcus lanceolatus, or, it is thought by 
some, to the infection of the lung by the bacillus of Eberth, the so-called 
''pneumotyphoid." True croupous pneumonia in the later stages is very 
rare. (2) Bronchopneumonia, probably arising from terminal infection or 
by hypostatic congestion due to the profound toxaemia and cardiac degenera- 
tion and feebleness, is more common. (3) Acute tuberculous pneumonia 
sometimes seizes the typhoid fever patient when he seems about to begin 
his convalescence. 

It is not to be forgotten that infarction of the lung may occur as the 
result of cardiac or venous emboli. Such an infarction may mislead the 
physician into a diagnosis of lobar or lobular pneumonia by reason of 
the dulness on percussion, the rise of temperature, and blood-tinged 
sputum. An infarction may, if the patient survives, result in pulmonary 
abscess or gangrene. 



TYPHOID FEVER 43 

Pleurisy arises very rarely as a primary lesion. It is usually secondary to 
infarction, pneumonia, or gangrene. Cases of empyema due to the specific 
bacillus have, however, been recorded. 

Nervous Complications. — The nervous disturbances vary very greatly. 
In the average case there is in the early part of the onset no mental change 
save that of unfitness for mental occupation, with dreamful sleep which is apt 
to be restless. Later the patient continually dozes off, yet awakens easily, and 
for a moment may be a little confused between the mental impressions left 
on his brain by the dream and the conditions he finds about him on returning 
to consciousness. Still later, if the infection is severe, he becomes more 
apathetic when awake, less easily aroused when asleep, and often delirious 
in his sleep, his dreams being evidently vivid, so that he keeps muttering 
the conversation he thinks he is actually having, or calls out loudly, as his 
dream seems to lead him to a point where an imperative call or sudden 
action is needed. Sometimes the delusions in the delirium amount to 
imperative conceptions, and the patient believes that he is away from home 
and must return there at once, or that he is being restrained by force, or, 
again, that some member of his family is in distress and needs his aid or 
is calling for him. Often this form of mental disturbance is painful to 
witness, difficult to overcome, and harassing to the patient. In these cases 
the hands may be moved continually in active motions, as if to illustrate 
the ideas of the patient. Such cases are apt to be grave if for no other 
reason than that they exhaust themselves if relief is not given. The 
more encouraging type of delirium is of the quiet, muttering form, as if 
the patient was gently "speaking in his sleep" as in health, and this may 
be taken as the natural form of delirium in the disease. Later the stupid 
condition becomes more and more marked in some cases, and absolute 
mental stillness is reached, in which only rough shaking or loud calling 
will arouse the patient. In severe cases with marked toxaemia we find at 
times a state of mental confusion, staring eyes, and semi-stupor, with per- 
sistent muttering, the so-called coma vigil. 

During convalescence mental aberration, depending usually upon exhaus- 
tion, may develop. The prognosis in such cases is usually good. 

Rarely in the course of typhoid fever symptoms of irritation or inflamma- 
tion of the meninges of the brain develop, and it is important to remember 
that these symptoms may arise from several causes. The most common of 
these is congestion and engorgement of the meningeal vessels without any 
true inflammatory process; the next most common form is that due to the 
extension of an infection from abscess in the middle ear; the third form is 
that in which there is infection with the streptococcus or pneumococcus, 
and very rarely the meningitis is due to the bacillus of Eberth. Cole 
has recorded three instances in which the typhoid bacillus was obtained 
from the cerebrospinal fluid by lumbar puncture in typhoid fever. In one 
the meningitis was serous, in another purulent; the character of the other 
is not stated. 

The frequency of this complication in the different periods of the disease 
when due to true typhoid infection of the meninges is in direct ratio to 
the length of the malady, namely, in the third or fourth week. In the 



44 DISEASES DUE TO A SPECIFIC INFECTION 

great majority of instances in which the complication has appeared the 
patient was under thirty years, and usually between twenty and thirty 
years. That is the period in which typhoid fever is most commonly 
seen. 

In every case of true typhoid meningitis, so far recorded, death has 
occurred, but this is a statement which does not possess as great prognostic 
value as would appear at first glance, since an absolute diagnosis of true 
typhoid meningitis can not be made during life, for the positive test is 
the bacteriological examination of the skull contents. Nevertheless, the 
presence of marked meningeal symptoms is of the gravest import in all 
cases. 

Sometimes, because of degenerative changes in the vessels, a hemorrhagic 
effusion into the meninges of the brain takes place, but this does not 
commonly produce marked symptoms unless it is profuse. 

Convulsions, generalized or localized, with coma and delirium may arise 
from thrombosis of the cerebral sinuses or of the cerebral arteries, but they 
are very rare from any cause. Murchison only met with them in 6 cases out 
of 2960. If due to the lesions named, they indicate a fatal termination 
in the near future. In Osier's case death followed convulsions, produced by 
thrombosis of the branches of the left middle cerebral artery, in twelve 
hours. If they occur in neurotic children or females, the outlook is not 
so gloomy, as they probably do not depend upon an actual lesion in the 
brain. 

Sometimes acute otitis media produces violent headache and finally 
symptoms of meningitis, but its presence is often unrecognized as a cause 
until a discharge takes place from the ear. 

Neuritis, generalized or localized, is met with occasionally in the later 
stages, producing wrist-drop or toe-drop, and sometimes causing severe 
pain. When there is a multiple neuritis the symptoms may closely resemble 
locomotor ataxia or anterior poliomyelitis. Sometimes the skin of the toes 
or of the whole foot becomes exquisitely sensitive. 

When hemiplegia occurs, which is quite rare, it results from cerebral 
embolism or thrombosis or very rarely from actual hemorrhage. 

Complications in the Bones, Joints, and Muscles. — Secondary 
disease of the bones, consisting of post-typhoidal osteomyelitis due to the 
specific bacillus or to infection by associated micro-organisms, may occur. 
The tibia and the ribs are the bones most commonly involved, and the 
changes are subacute or chronic rather than acute. So, too, arthritis may 
be due to pyogenic micro-organisms or to the Eberth bacillus, and is usually 
of a subacute or chronic type. Spontaneous dislocation of the hip may occur 
in very rare instances. 

Many years ago V. P. Gibney, of New York, described, under the name 
of typhoid spine, a condition in which there develops, often some days 
after the patient is up and about, and often only after some very slight jar 
or trauma, great tenderness of the spine, with pain in the back, and in the 
legs when they are moved. Usually it is held that this condition is not 
dependent upon a spondylitis, neuritis, or Pott's disease, and is probably 
a neurosis closely allied to the neuroses seen in cases of severe trauma. 



TYPHOID FEVER 45 

Fraenkel has recently shown that in fatal cases of typhoid fever the 
bacillus may be obtained from the cancellous tissue of the bodies of 
the vertebrae and some of these cases of so-called typhoid spine may be 
instances of osteomyelitis involving these structures. 

Sometimes in the stage of convalescence a curious state is developed in 
which the muscles of the lower extremities become painful, somewhat 
brawny, and even slight redness may appear in the skin covering them. 
Usually this is unilateral, but it may be bilateral. Most commonly it 
affects the calf of the leg, and pain is developed on pressure or on move- 
ment, active or passive. This is due to a myositis. It should not be 
confused with phlegmasia dolens due to thrombosis. 

Typhoid Fever Complicating Pregnancy. — In a very large number of 
cases of typhoid fever complicating pregnancy, abortion or premature labor 
comes on. Corbin collected 364 cases of typhoid fever occurring in pregnant 
women, and Fellner, of Vienna, has added 7 others to this number, making a 
total of 371 cases. Of these 371 cases 228, or 61 per cent., ended in prema- 
ture births, and in 202 cases pregnancy terminated before the sixth month. 
Most of the full-term children were born dead, and those who were born 
alive were weak and did not long survive. The mortality in the mother 
under these circumstances is about 16 per cent. 

Diagnosis. — The diagnosis of typhoid fever is to be based on the char- 
acteristic ascent of the temperature, the general malaise of the patient, the 
peculiarly coated tongue with red edges, the tumid belly, and the develop- 
ment of the rash about the seventh to the ninth day. If to these symptoms 
are added an enlargement of the spleen and liver, the diagnosis becomes 
still more certain, and is confirmed if the laboratory tests mentioned on 
the following pages are positive. The laboratory aids to diagnosis are 
the Widal or agglutination test; the isolation of the bacillus from the 
blood, from the stools, from the urine, and from the rose spots, and 
the diazo reaction. The objection to these tests is the difficulty as to 
technique for the general practitioner, and, more important still, the fact 
that some of them are obtainable in many instances so late in the course 
of the disease as only to confirm the clinical diagnosis already made. (See 
page 48.) 

Typhoid fever must be separated from a number of maladies which 
closely resemble it. Pure typhoid infection may result in the production 
of a fever which closely follows the remittent or intermittent malarial 
types, and which is often associated with so much gastric disturbance and 
vomiting and so lacking in the more prominent typhoid symptoms usually 
seen that the picture of remittent malarial fever is clear, while the true 
picture of typhoid fever is clouded. Again, there can be no doubt that 
cases of true malarial infection occur in which the symptoms so closely 
resemble those of typhoid fever that a purely clinical diagnosis is almost 
impossible if an epidemic of typhoid fever is in full swing at the time. 
Finally, there can also be no doubt that it is possible for the patient to have 
a double infection with the bacillus of Eberth and the plasmodium of 
Laveran, in which case, however, the malarial manifestations are usually 
dwarfed by the typhoid poison, and only are marked at the onset of the 



46 



DISEASES DUE TO A SPECIFIC INFECTION 



enteric fever and at its termination. To this mixed infection the term 
typhomalarial fever may be correctly applied to indicate not a separate 
disease, but a double infection. Etymologically, this term might also be 
used to define a condition of malarial fever in which, because of profound 
debility, the patient was in a typhoid state — that is, in a condition of which 
typhoid fever is a type. Practically, however, it should be discarded or 
limited in its use to the double infection just described. 

How far constant fever occurring day after day and associated with 
manifestations of general loss of strength and debility can be relied upon 
in the diagnosis of typhoid fever is hard to determine. Certain it is that if 
a physician makes a diagnosis of enteric fever upon these symptoms alone, 
without bearing in mind the fact that similar conditions are equally well 
developed under other forms of infection, he will find himself in error in 
not a few instances. Chief among these conditions may be mentioned 
tuberculosis of the lungs or peritoneum, that form of influenza in which 
the chief symptoms are abdominal, cases of ulcerative endocarditis, septi- 
cemia, and pyaemia, and those of cholecystitis with ulceration, as from 
impacted gallstones. It must not be forgotten, too, that syphilitic fever 
may in very susceptible persons resemble typhoid infection. The febrile 
movement, rose rash (if it be scanty), malaise, and signs of general infection 
in this disease may readily mislead the physician. Again, in the more 
advanced, or tertiary, stages of syphilis a prolonged low, septic fever may 
be present. Any case of so-called typhoid fever which lasts more than 
four weeks without the attack being prolonged by a relapse is almost 
certainly suffering from another disease, often tuberculosis. 

It is not to be forgotten that trichiniasis may resemble typhoid fever, 
for in it we have fever, pains in the limbs and back, headache, stupor, and 
nausea, with pain in the belly and diarrhoea. 

The differentiation of typhoid from other fevers is aided by a study of 
the following table: 



Typhoid Fever. 
Onset gradual. 
Face dull and apathetic. 

Delirium a late symptom. 

Coma a late symptom. 

Eruption very late. 

Eruption chiefly on trunk, well defined, and 

appears in several crops of small rose-red 

spots. 
Leukocytes decreased. 
Widal test positive. 
Bacilli of Eberth in blood. 

Typhoid Fever. 
Rash appears in crops. 
Profuse sweats rare. 
Temperature curves regular. 
Pulse rarely over 100. 
Bacillus of Eberth in blood. 
Widal test positive. 
No eye changes. 
Respirations slightly increased. 
Cyanosis rare. 



Typhus Fever. 

Onset abrupt. 

Face livid, anxious, swollen, conjunctiva red- 
dened. Pupils contracted. 

Delirium an early symptom. 

Coma an early symptom. 

Eruption early. 

Eruption over trunk and limbs and ill- 
defined. Does not appear in crops, and is 
dusky red or petechial in character. 

Leukocytes increased. 

Widal test negative. 

Bacilli absent. 

Acute Miliary Tuberculosis. 
Rash, if present, not in crops. 
Profuse sweats constant. 
Temperature curves irregular. 
Pulse usually rapid. 
Absent from blood. 
Negative. 

Choroidal tubercles. 
Greatly increased. 
Cyanosis common, 



TYPHOID FEVER 

Typhoid Fever of the Cerebral Type. Cerebral Meningitis. 



47 



Regular temperature. 
No marked blood change. 
Herpes very rare. 
Rose rash on trunk chiefly. 
Cerebrospinal fluid negative. 



Irregular temperature. 

Increase in polynuclear white cells. 

Very common. 

Petechia? over whole surface. 

Positive for the specific bacillus. 



Typhoid Fever. 

Onset gradual. 
Fever gradually rises. 
Chills rare in onset. 
Unaffected by quinine. 
Heavy facial expression. 

Herpes rare. 

Early delirium rare. 

Anaemia moderate. 

Moderate reduction in leukocytes. 

Rose rash. 

Bacilli in blood. 



JEstivo-autumnal Fever. 

Onset acute. 
Fever rises irregularly. 
Severe chills common. 
Improved by quinine. 

Anxious facies with slightly icteroid conjunc- 
tiva. 
Herpes common. 
Early delirium common. 
Anaemia marked. 
Great reduction in leukocytes. 
No rash. 
Plasmodium in blood. 



Typhoid Fever. 



Onset gradual. 
Enlarged spleen. 
Rose rash. 
Prostration gradual. 
Lasts several weeks. 



Influenza. 

Onset sudden. 

No enlargement of spleen. 

No rash. 

Prostration rapid. 

Lasts a few days. 



Typhoid Fever. 

Onset gradual. 

Nervous symptoms moderate. 

No leukocytosis. 

Widal test positive. 

Bacilli in blood. 

Lasts weeks. 

Disease of youth. 



Typhoid Pneumonia. 

Onset more rapid. 
Nervous symptoms severe. 
Marked leukocytosis. 
Widal test negative. 
None in blood. 
Lasts a shorter time. 
Disease of old age. 



Typhoid Fever. 



No cardiac murmurs. 
Regular temperature. 
Sweats rare. 
No leukocytosis. 
No cardiac dyspnoea. 
No petechiae. 
No infarctions. 
No leukocytosis. 
Widal test positive. 
No retinal emboli. 
No chills. 
Bacilli in blood. 



Ulcerative Endocarditis. 

Cardiac murmurs. 

Irregular septic temperature. 

Sweats common. 

Marked leukocytosis. 

Cardiac dyspnoea. 

Petechiae. 

Infarctions. 

Leukocytosis. 

Negative. 

Retinal emboli. 

Repeated chills. 

No bacilli in blood. 



Typhoid Fever. 



Rose rash. 
Face not swollen. 
Muscles normal. 
Eosinophiles decreased. 
A common disease, 



Trichiniasis. 



No rash. 
Face swollen. 
Myositis. 

Eosinophiles numerous, 
A rare disease. 



48 DISEASES DUE TO A SPECIFIC INFECTION 

For the diagnosis of paratyphoid fever from typhoid fever, see the article 
on that disease. 

Tests. — The so-called Widal test depends upon the fact that if a small 
amount of blood, or blood serum, or even the breast milk or tears from a 
patient having or recently having had typhoid fever, are brought in proper 
dilutions in contact with living typhoid bacilli these organisms soon cease 
to move, that is, lose their motility, and gradually come together in clumps, 
or, in other words, agglutinate. 

Nahrt and Bolton have found that agglutinating properties are trans- 
mitted from mother to child by means of the milk, and that the typhoid 
bacillus, when present in the foetus, produces agglutinins in its blood. 
They were unable to determine whether agglutinins were transmitted from 
mother to foetus through the placenta. 

The typhoid bacilli to be employed in the test are not such as have been 
recently isolated from a case of typhoid fever, but those which have been 
modified by repeated transplantation on artificial media. These bacilli are 
kept in sealed tubes of nutrient agar-agar in an ice-chest; from such a stock 
culture inoculations are made, and when the test is to be used are placed 
in broth-bouillon, incubated for twenty-four hours at a temperature of 37° C, 
and then employed for the test. It is essential that it be proved beforehand 
that this culture is composed of organisms reacting to known typhoid 
serum and not to healthy serum. From this test culture a proper dilution 
is made by adding the bacilli to blood diluted with normal salt solution. 
A hanging drop is now placed under the microscope and examined with 
a magnifying power of about 800 diameters. The bacilli should appear as 
actively motile organisms which do not clump. 

The finger-tip or lobe of the ear is pricked, and by means of the "white 
pipette" of a blood-cell counting apparatus the blood is drawn up to the 
mark 0.5. Then the pipette is dipped in distilled water and the water is 
drawn up till the figure 11 is reached. This gives us a dilution of 1:20. 
One drop of the mixture of bacilli in salt solution and one drop of the diluted 
blood are then placed on a cover-glass, which is inverted over a hollow slide 
and the drop examined. A positive reaction consists in an absolute immo- 
bilization of all the bacilli and of a clumping of a majority of them. This 
reaction should occur in five minutes if the dilution of blood has been 1 : 20, 
and in thirty minutes if it has been 1 : 40, and in two hours if the dilution 
has been 1 : 60. A rapid clumping with a weak dilution is to be regarded 
as a very positive test. On the other hand, it is to be remembered that a 
dilution of blood in the proportion of 1 : 10 may give a reaction even if nor- 
mal blood is used. An exact estimate of the strength of the solution and of 
the time of reaction is therefore of importance. 

This test is an exceedingly accurate one, if properly employed. The chief 
difficulty about it is that the reaction is often absent until the seventh or 
even the twelfth day of the disease. Out of over 8000 cases reported by a 
number of observers, the test was positive in 94 per cent. A negative result 
is unimportant if it is obtained prior to the third week. But cases have been 
recorded in which bacilli have been isolated from the blood during life and 
at autopsy the lesions were those of typhoid fever, but at no time during 



TYPHOID FEVER 



49 



the course of the disease did the blood yield the agglutinative reaction. 
Repeated tests should also be made before it is decided that the blood does 
not give the reaction. When dried blood is used its volume as near as may be 
should be restored by the addition of distilled water, and from this the proper 
dilution is to be prepared and the resulting dilution used as already indi- 
cated. The fallacies of this test lie in the possibility that the patient may 
have had typhoid fever at some previous time and so give the reaction, 
and in mistaking irregular and delayed clumping as true agglutination or 
as a partial reaction. 

This test has now been brought within the reach of everyone by the use 
of an agglutometer which has been placed on the market by a well-known 
house. (See Fig. 12.) 



Fig. 12 




Agglutometer for the agglutination test for typhoid fever. 

This apparatus is designed to obviate the use of the microscope and the 
fresh live culture of typhoid bacilli necessary in the Widal test when made 
in the old way. Laboratory experiments have shown it equal in delicacy 
to the former method. The limits of the reaction are more distinct than in 
the old process. 

One bottle of a sterile permanent suspension of typhoid bacilli is fur- 
nished, together with four test tubes, one lancet and tube for collecting 
blood, one vial for diluting the serum, one small pipette for distributing 
the diluted serum, and one large pipette with two graduations (each cor- 
responding to ten drops of the size delivered by the small pipette) for 
filling the tubes with suspension. The three tubes labelled 50, 100, and 
200, are to be used for the test; the fourth is a control tube to which no 
serum should be added. 

Let blood flow into the blood tube until the bottom is covered with a 
layer one-eighth to one-fourth inch thick. The blood will flow much more 
4 



50 DISEASES DUE TO A SPECIFIC INFECTION 

rapidly if the lobe of the ear is squeezed intermittently between the thumb 
and index finger. 

Cork the tube and replace in an upright position. 

In a short time (an hour) the serum will have separated, or may be readily 
made to do so by carefully loosening the edges of the clot with the lancet. 

After the serum has separated, insert the pipette into the blood tube, the 
point resting in the lateral depression, and incline both slightly, when the 
serum will readily enter the pipette. 

Add one drop of serum to ten drops of clear water in the diluting tube, 
and shake well. If the diluted serum is cloudy, let it clear by standing 
a few minutes before distributing to the tubes of suspension. 

By means of the large pipette put 20 drops (two graduations) of the 
suspension of typhoid bacilli in each of the four test-tubes. 

Add the serum dilution to the typhoid suspension in the following amounts: 
four drops added to the tube marked 50 gives a dilution of 1 : 50 ; two drops 
added to the tube marked 100 gives a dilution of 1 : 100 ; one drop added to 
the tube marked 200 gives a dilution of 1 : 200. 

No serum should be added to the control tube. 

After adding the serum dilution, cork the tubes and shake well. Put 
away in a warm place. 

Examine the tubes at the end of one and four hours, and again on the 
following day. The rapidity of the reaction depends both upon the agglu- 
tinating power of the blood serum and the temperature at which the tubes 
are kept. The reaction may be seen with the greatest distinctness when one 
stands near the middle of the tod n facing a window. The tubes should be 
held on a level with the eye and inclined slightly away from the observer. 

When the reaction is positive, floccules appear in one or more of the 
tubes, depending upon the agglutinating power of the serum tested. 
These flakes are small at first and disseminated through the fluid. They 
gradually increase in size and settle to the bottom of the tube. 

In a complete reaction the supernatant fluid is perfectly clear. 

In a positive but incomplete reaction, floccules are seen in the still cloudy 
fluid. 

In a negative reaction the fluid in the tubes remains uniformly clouded, 
as in the control. 

All apparatus and corks should be thoroughly washed before using a 
second time. 

The diazo reaction, sometimes called Ehrlich's reaction, depends upon 
the fact that in typhoid fever the urine of the patient contains a chromogen 
which, when treated with diazo-benzene-sulphonic acid and ammonia, pro- 
duces a distinct red hue in the urine, which may be as deep as garnet red. 
Other diseases give this reaction, such as tuberculosis and some cases of 
pneumonia, but it is of considerable value in determining the presence of 
typhoid fever if taken in conjunction with other signs. It is usually present 
as early as the sixth day, and lasts until about the eighteenth day. The test 
itself consists in using two solutions. One of these consists of a 5 per cent, 
solution of hydrochloric acid to which has been added sulphanilic acid in 
the proportion of 1 gram for each 100 c.c. The other is a 0.5 per cent. 



TYPHOID FEVER 51 

solution of sodium nitrite. When the test is to be made the two solutions 
are mixed in the proportion of 40:1. Equal parts of urine and this mix- 
ture are then shaken together and rendered alkaline by the addition of 
ammonium hydrate, which is allowed to flow down the side of the tube, 
forming the layer above the mixture just named. At the dividing line 
between these two fluids the reaction appears. If typhoid fever is present 
a garnet-red hue develops. If it is not present, only an orange tint is 
seen unless one of the other maladies which give this test is present. After 
the test tube containing these liquids has stood for some time a green 
sediment forms, which Ehrlich considers very characteristic of a true 
reaction. 

Another method of reaching a positive diagnosis is the examination of 
the blood itself for the specific bacillus, which, as already stated, is present 
in this fluid in nearly all, if not all, cases of typhoid fever. While it is 
true that this examination is not possible for one who is not trained in its 
technique from the bacteriological standpoint, it is also a fact that this test 
is not open to the fallacies of the Widal test, and that the bacilli are often 
found as early as the fifth day, whereas the Widal test is frequently not 
positive till the ninth day, or even later. The urine and stools may be 
examined for the specific infecting micro-organism, but they are rarely dis- 
coverable in these discharges early enough to aid the diagnosis. 

The Widal test and the discovery of the bacillus of Eberth in the blood 
enable us to differentiate true typhoid fever from paratyphoid fever. 

Finally, it is to be remembered as a valuable diagnostic fact that the 
fever of the first stages of typhoid fever is more resistant to the cold bath 
than in any other malady, although it yields readily enough later on in 
the course of the malady to this therapeutic measure. 

Prognosis. — The prognosis in typhoid fever depends upon several important 
factors. One of these is the time at which the patient comes under medical 
care, not because active medication is of great advantage, but rather because 
patients that go to bed late in the onset of the disease usually become more 
seriously ill than those who conserve their vital forces by rest from the very 
beginning of the malady. Patients who travel long distances in the early 
stages of typhoid are wont to have severe attacks, and if, after the disease 
is well developed, travelling is resorted to the illness nearly always increases 
in violence. Another factor is the state of the patient at the beginning of 
the malady, as to his vital resistance and general health. Fat persons usually 
do not withstand it well. Children nearly always recover from typhoid 
fever in its uncomplicated forms, and aged persons, while rarely affected, 
succumb when attacked in direct proportion to their years. (See Fig. 6.) 

A third factor is the degree of toxaemia which develops in severe cases, 
particularly if they are not treated skilfully at first. 

Aside from these general considerations it is impossible to make an 
accurate prognosis as to the severity of the attack or probable recovery of 
the patient in the first week of the disease, because the malady develops 
slowly and because a fatal termination is nearly always due to some 
intercurrent complication which cannot be foreseen. Even when the 
disease is ushered in with violence of all the symptoms, particularly an 



52 DISEASES DUE TO A SPECIFIC INFECTION 

exceedingly high temperature, it often happens that it follows a very short 
and fairly mild course, so that a severe onset justifies the physician in 
expecting a speedy recovery in many instances. When, however, compli- 
cating conditions such as pulmonary, cerebral, or meningeal manifestations 
develop, the prognosis is of course correspondingly grave. 

Recovery in typhoid fever, under the modern and favorable methods of 
treatment, takes place in about 93 per cent, of cases in the best types of 
private practice and in hospitals in which the patients are received early 
and in fairly good condition. In private practice among the poor it is much 
lower. In army practice the mortality may vary from 2 or 3 per cent, in 
time of peace to 50 per cent, in time of war, illustrating very well the fact, 
already stated, that early rest in bed, perfect quiet of mind and body, and 
proper nursing are most favorable in their influence, whereas an absence 
of these aids to recovery is most harmful. Under the cold-bath treatment 
of typhoid fever, when it is instituted early, the mortality of about 7 per cent, 
is largely due to those unavoidable accidents, hemorrhage and perforation 
of the bowel. 

Much depends in all cases upon the severity of the infection. In some 
widespread epidemics the mortality is singularly low even when the care 
of the patients is not in many cases very skilful; in others it is corre- 
spondingly high. In the United States army in the Spanish war it was 
only 7 per cent., a remarkably low rate for war time; whereas in the 
Boer war the English troops suffered from a death rate of nearly 21 
per cent. 

Sudden death sometimes occurs in typhoid fever without the autopsy 
revealing any adequate cause, the real cause being in all probability an 
acute cardiac dilatation. 

Treatment. — The following is the plan pursued by the author in the 
treatment of this disease. As soon as the patient comes under observation, 
unless his bowels have already been moved by the aid of calomel, he is given 
1 to 2 grains of this drug in quarter-grain doses every hour. If his bowels are 
not moved in twelve hours, a movement is produced by the aid of a large 
rectal injection of soap and water, and if need be by the ingestion of a Seid- 
litz powder. Twelve hours later he receives 5 to 10 minims of dilute hydro- 
chloric acid with a teaspoonful of essence of pepsin ; this is repeated regu- 
larly every six hours throughout the disease after food. 

Hydrotherapy. — An order is given that if the temperature rises as high as 
102.5° the patient is to be rubbed with tepid, cool, cold, or ice-water, or even 
with a piece of ice, according to the degree with which his temperature resists 
the bath and according to the degree of toxaemia present. If toxaemia is very 
great, it is often necessary to give a thorough, brief and brisk, rub-off with a 
small piece of ice, not so much to reduce the fever as to cause reaction and 
arouse the patient's vitality. With this application of cold, in different degrees 
according to the needs of the case, there must be employed by another 
nurse, or by the free hand of the nurse who uses the cold, active friction to 
the skin as the cold comes in contact with the integument, because friction 
increases the heat loss 50 per cent., aids in producing those most essential 
conditions, reaction and equalization of the capillary circulation, and prevents 



TYPHOID FEVER 53 

the patient from being chilled. It is a cardinal rule that if the patient has 
been ill so long that reaction does not occur under the bath, it is contra- 
indicated and we must endeavor by gentle measures and the use of tepid 
or even of hot water to redevelop the power of the body to react. In 
other words, that temperature of water should be used which is necessary 
when combined with active friction to reduce the temperature at least 2° 
in fifteen to twenty minutes, provided reaction can be produced. Without 
reaction we simply increase internal congestions by the use of cold water. 
It is interesting to note that Hirschfeld has treated over 1000 cases with 
tepid immersion baths of 80° to 90° with a mortality of only 3.4 per cent. 

Whenever cold is used, an ice-bag or cold cloth should be applied to the 
head to prevent cerebral congestion. 

While the method of bathing just described is that nearly always pursued 
by the writer, it is proper to give definite information concerning the so-called 
Brand method of cold bathing, a plan which was introduced by Brand, of 
Stettin, many years ago, but which has only received its full share of credit 
during the past fifteen years. This plan consists in immersing the patient, 
when his temperature reaches 102° or 102.5°, in a tub of water the tempera- 
ture of which is 70°, and keeping him there with active friction for fifteen 
or twenty minutes, until the temperature is reduced to 100°. In order to 
combat chilling and aid the circulation it is customary to give the patient 
one-half to one ounce of whiskey before, during, or after the bath. The bath 
is repeated whenever the temperature rises to 102°. Usually it is needed 
every two or three hours. In order that the patient's strength may be 
conserved he should be lifted into and out of the tub. When cold is prop- 
erly used it should, after the first week of the disease, produce changes in 
the temperature, as shown in the following chart (Fig. 13). 

This so-called plunge bath, or Brand bath, is a remedy of the greatest 
possible value, but is not needed in every case as a matter of routine. 
When used it is essential to produce reaction and to use friction, and to 
apply ice to the head. The indications for its use are identical with 
those just named. It is actually contraindicated in the very young and very 
old, in whom it is often difficult to produce reaction, and if the case comes 
under treatment so late as the beginning of the third week, since reaction to 
cold is usually then lost. The presence of a complicating pneumonia also 
contraindicates it. Other disadvantages are that the back cannot be rubbed, 
although the muscles in that part of the body contain much heat and the 
skin is most prone to suffer from bed-sores, and that the patient must 
be lifted or raise himself out of the tub. The temperature of the plunge 
bath when its use is deemed wise should not be placed at a tepid level and 
then reduced while the patient is in the water, as this does not administer 
a stimulating and awakening shock to the system, but simply chills the 
patient, thereby doing no good, for the object in using water in typhoid 
fever is to produce reaction, eliminate poisons, and reduce temperature, and 
the means by which this is best accomplished can be determined in each 
case by the physician. 

Personally the writer has never failed to successfully accomplish all 
these results by cold rubbing, with friction, if it is properly given, but 



54 



DISEASES DUE TO A SPECIFIC INFECTION 



many physicians prefer to follow the method of Brand as a routine 
practice. An enormous array of statistics prove its value as a life-saving 
agent. 1 

Some form of bath at least once a day is absolutely necessary even if the 
temperature never exceeds normal, to establish cleanliness and equalize the 
circulation everywhere, and he who treats typhoid fever without resort to 
efficient hydrotherapy, if it can be used, is not doing all for his patient that 
can be done. 

The use of hydrotherapy greatly lowers the mortality, saving about 10 in 
every 100 cases, but it does not diminish the frequency of perforation or 
hemorrhage, and it apparently increases the frequency of relapse. This 
may be due to the fact that more are saved to run the chance of relapse, 



Fig. 13 



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Chart showing the falls in temperature and reactions following the use of cold spongings in a case of 
typhoid fever. The dotted lines show the fall The broken, nearly horizontal line shows the morn- 
ing and evening range unaffected by sponging. Thirty-four baths were given in eight days. 

but also may depend upon the fact that mild cases are more prone to 
relapse than severe ones. Hydrotherapy does not shorten the duration of 
the fever, but it often shortens the length of the illness by preventing 
complications. 

Diet.— The diet consists of milk in the first week and often for most of the 
second week, about a quart to a quart and a half a day being given, so 
divided that the patient gets it every three or four hours. It is followed 
by the acid and pepsin already named, unless the stomach is irritable, when 
a little lime-water may be given as- a substitute, or a little Celestins Vichy 
water may be used. When the digestion of milk is difficult it is well to 
add to it hot water or to dilute it with an alkaline or carbonated water. 
If the taste of the milk is unpleasant to the patient, it may be flavored 

1 See article by the author in Therapeutic Gazette for March, 1898. 



TYPHOID FEVER 55 

by the addition of vanilla, nutmeg, coffee, tea, or cocoa in small amounts. 
After the first week or ten days the patient is allowed from one to two soft- 
boiled eggs each day, so soft that they can better be taken as a drink than 
eaten with a spoon, and flavored with a little salt. Well-boiled rice strained 
through a fine sieve, and even thin cornstarch or barley-gruel, if well 
cooked, may be given at this time with advantage, particularly if at the 
same time a little taka-diastase is used to aid their digestion. The author 
is firmly convinced that by this means terminal infections and general 
feebleness can be largely avoided and the patient brought to the stage of 
convalescence ready for speedy return to health and with greater vital 
force. Broths and other liquid animal soups are inadvisable, for they are 
good culture-media, and often tend to increase tympanites and diarrhoea. 
They are largely used by many physicians, but never by the writer. When 
curds appear in the stools, the quantity of milk should be diminished or it 
should be peptonized, or its digestion aided by the use of pancreatin given 
after it is taken. The use of 5 to 10 grains of citrate of soda in the milk 
will also prevent the formation of curds. 

The use of cows' milk in large amounts for a considerable time has been 
shown to increase the coagulability of the blood, as cows' milk contains 
an excess of calcium salts. Wright has suggested that this is one of the 
reasons why thrombosis is so common in typhoid fever. To prevent the 
increase in coagulability a mixed diet should be given and a few grains of 
citric acid be administered daily for a few days at intervals of a week. 

Medicines. — Drugs are not to be given if they can be avoided — that 
is, they are not to be used unless they are certainly needed to combat some 
definite condition which should be alleviated. In the great majority of 
cases, if not in all, the so-called antipyretic drugs are not only useless but 
harmful, and particularly harmful if their use is resorted to simultaneously 
with bathing. Their only justifiable use in a case which can be properly 
nursed and bathed is for the purpose of relieving headache and backache, 
when they may be given in small doses, such as 2 grains of acetanilid three or 
four times a day. Quinine is of little, if any, value except as a tonic in 
small doses. 

Stimulants are to be used when the pulse is actually weak and the car- 
diac first sound distant or feeble. The best of them is whiskey or brandy, 
diluted with milk or water, and given in doses of half an ounce every three 
to six hours as needed. Many cases do better without any stimulation, 
whereas others need much larger doses of alcohol than those just named. 
Digitalis is rarely of any service because it does not act well in the presence 
of fever, rarely supports the degenerated muscle fibres of the heart, and is 
apt to disorder the stomach. When the cardiac condition is desperate, 
Hoffmann's anodyne in drachm doses every two hours in cool water is 
very valuable. When profound adynamia develops and the patient is 
critically ill, much good may result from the injection hypodermically of 
\ grain of camphor in 30 drops of sterilized olive oil every eight hours 
for five or six doses. Another method of value when the vascular system 
is relaxed and the patient adynamic is the use of hypodermoclysis, adding 
to the pint of a 0.9 per cent, saline solution 1 drachm of adrenalin chloride 



56 DISEASES DUE TO A SPECIFIC INFECTION 

solution of the strength of 1 : 1000. Strychnine may also be used, but it is 
a mistake to employ it for more than a few doses in the active stage of this 
disease. It is better to keep it in reserve for attacks of sudden circulatory 
failure. 

Antisepsis. — Absolute intestinal antisepsis can not be produced by any 
known means, although it is possible to modify very materially the growth of 
micro-organisms in the bowel by the use of proper remedies. If the physician 
takes the ground that by the use of these substances he destroys the Bacillus 
typhosus and so benefits the patient, he is largely in error, and his use of them 
is not rational because the bacillus in the early stages at best is not free in the 
bowel, and in the later stages is widely distributed in every part of the body. 
If, on the other hand, these remedies are given to combat intestinal fer- 
mentation, as shown by foul-smelling stools and tympanites and other 
evidences of an excessive growth of the non-specific bacteria which throng 
the bowel during the progress of this disease, his use of them is rational in 
that by this means other toxic materials are prevented from being gene- 
rated in excess. So far as we know, the most active and harmless intes- 
tinal antiseptic is acetozone given in the daily dose of 30 grains dissolved in J 
gallon of pure water flavored with some one of the volatile oils, but not 
with sugar. This quantity may be given the patient as a drink in the 
course of one or two days. Another is the sulphocarbolate of zinc in the 
dose of 2 to 3 grains in pill form three or four times a day. Still another 
drug of far older use is turpentine in emulsion in the dose of 10 to 20 drops 
three or four times a day. The latter I prefer. In many of these cases also 
the use of a few small doses of calomel or salol is advantageous. 

Tkeatment of Special Symptoms. — Constipation is to be relieved pref- 
erably by the use of enemata of soap and water, to which may be added 
in obstinate cases a teaspoonful or two of glycerin. Many of these patients 
have no constipation in the sense that the ileum or colon is sluggish; but, 
on the other hand, the sigmoid flexure becomes packed with hardened 
feces, and mechanical obstruction occurs. The use of purgatives by the 
mouth is therefore useless unless very strong drugs are used, which are dan- 
gerous. If it is thought that the bowels are really sluggish a little cascara 
sagrada (20 to 30 minims of the non-bitter extract) may be given each evening. 

Diarrhoea, if excessive — that is, more than three or four stools a day — 
may be controlled by 5 to 10 drop doses of aromatic sulphuric acid in simple 
elixir or by adding to these two ingredients a half drachm of fluid extract of 
hsematoxylon. If much fermentation is present, an intestinal antiseptic 
should be used, such as zinc sulphocarbolate or acetozone. 

Vomiting is to be primarily prevented by regulating the diet as already 
referred to. If it persists, as little food and drink should be given as pos- 
sible for a few hours to let the stomach rest; and if there be much nervous 
irritability, 60 grains of sodium bromide in a little starch-water should be 
given by the rectum to quiet the vomiting centre. Counterirritation should 
be applied over the epigastrium in the form of a mustard plaster or turpentine 
stupe. If alcohol is being used as a stimulant its use must be stopped, or, 
if this is impossible, then a very old brandy or wine should be substituted 
for the whiskey and given in very small quantities. 



TYPHOID FEVER 57 

For tympanites a turpentine stupe is to be placed over the belly, if possible, 
before the gas accumulates in any amount, and if it persists a rectal injec- 
tion of the emulsion of asafcetida, with or without a drachm or two of tur- 
pentine, should be given. The efficiency of this injection may be much 
increased in the way of expelling gas, and if marked adynamia is present, 
by adding half an ounce of Hoffmann's anodyne to the injection. Turpen- 
tine in the dose of 10 drops, in emulsion or capsule, may also be given by 
the mouth for this condition. When the gas fails to come away, its passage 
may be aided by the introduction of a long rectal rubber tube. 

Hemorrhage from the bowel does not offer very much opportunity for 
direct rational treatment. In the majority of instances the best we can do 
in the way of real benefit to the patient is the maintenance of body heat 
by the application of hot bottles; and if the circulation becomes markedly 
feeble, the employment of normal salt solution by hypodermoclysis, a pint 
of it being given once, twice, or thrice in the succeeding twenty-four hours, 
according to the needs of the patient. Bandages may be applied to the 
limbs to limit the circulation to the vital parts, and the foot of the bed 
be raised for a similar purpose. The large number of remedies which 
have been suggested for the direct control of the hemorrhage indicate how 
feeble they all are. There is no more reason for supposing that astringents 
given by the mouth can check hemorrhage from an ulcerated vessel in the 
bowel than that they can check a hemorrhage from a branch of the anterior 
tibial artery; and when they are given and hemorrhage ceases, the arrest 
is due more to coincidence than to the effect of any drug. If any remedy 
of this type is of value, it is probably MonsePs salt (ferri subsulphas), 
which should be given in a hard pill or compressed tablet enclosed in a cap- 
sule, with the hope that it will escape from the stomach into the intestine 
without being dissolved, and thereby exert its styptic influence. Of course, 
if it is dissolved in the stomach, its chemical characteristics are altered. 
Many physicians apply a small ice-bag over the centre of the belly to influ- 
ence the circulation in the small intestine, with the hope that in that way 
hemorrhage will be controlled. There is no objection to this plan of treat- 
ment, and the author often resorts to it; but it should be used with caution, 
if the hemorrhage is severe, lest it aid in devitalizing the patient by abstract- 
ing heat. Simultaneously with the application of the ice-bag to the belly, 
hot bottles should be applied to the other parts of the body, for it is to be 
remembered that the loss of bodily heat is an important factor, not only 
because the vital processes can not be well performed at a low temperature, 
but also because the sudden reduction of temperature caused by the hemor- 
rhage deprives the heart and other organs of the stimulating effect of the 
fever which has been present for days. Another popular method of treat- 
ment is the administration of a pill containing a grain of opium and a grain 
of acetate of lead; the opium being expected to diminish peristalsis and so 
aid clotting, and the lead to act as a styptic. The opium is probably of 
value, but it is doubtful if the lead ever reaches the bleeding spot without 
becoming altered by the gastric and intestinal juices. When there seems 
to be continued oozing of blood from a large intestinal ulcer without free 
hemorrhage, the administration of turpentine and the use of adrenalin 



58 DISEASES DUE TO A SPECIFIC INFECTION 

chloride is to be seriously considered, as there is reason to believe that they 
both control capillary hemorrhage. Wright and his co-laborers have 
shown that the hypodermic use of calcium lactate and the internal use 
of calcium chloride increase the coagulability of the blood and these salts 
may be used. (See Purpura.) After the hemorrhage has ceased, particularly 
as convalescence is begun, small doses of iron should be administered to 
combat the anaemia. 

The treatment of 'perforation of the bowel from a medical point of view 
consists in giving opium to relieve pain, and employing heat and stimulants 
to combat shock. If a skilled abdominal surgeon can be obtained, all 
such cases should be operated upon at once, since the mortality under 
operation is less than with no operation. Statistics seem to show a mor- 
tality of about 80 per cent, with operation and 95 per cent, without it. My 
colleague, Dr. Keen, has published 158 cases, which were all he and Dr. 
Tinker could find in literature up to January 1, 1900. They gave a recovery 
percentage of 23.41. I have collected 54 cases which have been reported 
since January 1, 1900, and find that 35 of the number were followed by 
recovery. This gives a recovery percentage of 61.54, which is far too high 
for the general run of cases. Harte and Ashhurst place the recovery after 
operation at 26 per cent. Among children the results have been excel- 
lent. Out of 25 cases collected by Elsberg 16 recovered, a postoperative 
mortality of only 36 per cent. These figures are of value as showing 
that recovery may take place, but they do not give the real percentage 
of deaths, for most of the cases that are operated upon and die are not re- 
ported. I have seen 3 of these within a year. To be successful the 
operation ought to be performed at the earliest possible moment after 
perforation, although if the patient when seen is profoundly shocked 
it may be necessary to rally him by stimulation before the operation is com- 
menced or even postpone operation until sufficient time has elapsed to allow 
him to rally. 

Statistics clearly prove that the prospect of recovery from perforation 
treated by operation steadily diminishes with each hour that passes after 
the accident occurs. Cases are on record, however, and I have seen more 
than one, in which perforation took place and recovery occurred without 
operation. 

Persistent insomnia is rarely a troublesome symptom in typhoid fever. 
Although patients complain of wakefulness at night, careful observation 
will usually show that they get sufficient sleep in twenty-four hours. In 
some cases, however, when they are wakeful, largely because of active 
delirium, and are rapidly exhausting their vital forces by continued nervous 
activity, life can be saved by the hypodermic injection of \ grain of 
morphine, to which may be added T \-$ grain of nitroglycerin to prevent 
secondary nausea and depression. 

The application of an ice-bag to the head throughout the attack will 
usually prevent ordinary delirium from becoming excessive. 

Bed-sores are usually prevented by the friction applied to all portions of 
the skin in the baths which are given every few hours. If they appear over 
the sacrum, the patient should lie as much as possible on his sides, all bony 



PARATYPHOID FEVER 59 

prominences on which the patient rests being protected from contact with 
the bed by circular air-cushions. When the skin first reddens the irritation 
may be allayed by painting it with a solution of nitrate of silver, 20 grains 
to the ounce. If the bed-sore has begun to form, a useful dressing consists 
in equal parts of powdered chloretone and boric acid. If the slough becomes 
large, all that portion which is actually dead should be cut away, the part 
thoroughly sprayed with peroxide of hydrogen, dried by the gentle application 
of soft lint, and then dressed with the dusting-powder just named. 

The treatment of the other complications of typhoid fever will be found 
under the headings of the respective diseases, such as Pneumonia, etc. 

During convalescence the patient should be fed with increasing quantities 
of nutritious, easily digested food, but stimulants if possible should be 
avoided. If the patient is out of bed care should be taken that food is 
not ingested until after he has lain down to rest, in order that he may not be 
tired and so lack nervous energy during the progress of the digestive 
processes. 

As already pointed out when discussing the prevention of typhoid fever, 
urotropin or uritone should be given in doses of 5 grains three times a day 
in water, to destroy the bacilli which are usually present in the urine. 

The ordinary diet should not be restored until from two to three weeks 
after all fever has ceased. The author has often been impressed with the 
fact that the use of green vegetables, such as lettuce, spinach, asparagus, 
and similar substances, seem to exercise a most valuable influence in con- 
valescence in typhoid fever, perhaps because they antagonize scorbutic 
tendencies. 

PARATYPHOID FEVER. 

Paratyphoid fever is a disease caused by infection with paratyphoid 
bacilli, and presents a symptom-complex closely resembling or indistin- 
guishable from that of typhoid fever. 

Bacteriology. — The paratyphoid bacilli belong to a group of organisms 
intermediate between the Bacillus typhosus and Bacillus coli communis. 
Buxton has shown that by appropriate methods organisms occupying this 
position may be divided into several groups; one resembling the colon 
bacillus, for which he proposes to use the name paracolon; another group 
closely allied to the typhoid bacillus, called the paratyphoid, and pro- 
ducing the condition termed paratyphoid fever. The last-named group 
may by appropriate cultural methods be further divided into a species cul- 
turally unlike the paracolon type, and a second distinct species resembling 
the paracolon group. 

Pathology. — Differing anatomically from typhoid fever in essential 
details, this disease possesses no characteristic morbid anatomy, resembling 
in this respect the other forms of septicaemia. The most constant change 
is splenic enlargement, which was present in all of the cases coming to 
autopsy. In 3 cases ulcers were present in the intestine, but they resem- 
bled the ulcers of dysentery more than those of typhoid; in 2 cases the 
ulcers were numerous; in 1 case with abundant hemorrhage the most 



60 DISEASES DUE TO A SPECIFIC INFECTION 

extensive ulceration was observed. The patches of Peyer and the solitary 
follicles are but slightly if at all changed. The mesenteric glands are but 
slightly altered; focal necroses, not containing endothelial cells, occur in 
the liver. The proliferative and phagocytic endothelial changes of typhoid 
are practically absent. There are no constant changes found in other 
organs, although toxaemia in severe cases may induce its usual anatomical 
changes. Giitig examined the blood of six paratyphoid patients and found 
that the neutrophiles are diminished during the early stages of the disease. 
The lymphocytes also are diminished at first, but become increased later 
in the disease, and in convalescence they constitute more than half the 
entire number of white cells. The eosinophiles disappear from the blood 
during the fever, but reappear just before or shortly after the temperature 
becomes normal. 

The bacilli have been found in the heart's blood, in a cardiac thrombus, 
in the liver, lungs, spleen, adrenal bodies, cerebral cortex, and in the fluid 
of pericardial and pleuritic effusions. 

Cases have been reported from France, Germany, Holland, Roumania, 
England, the United States, and the Philippine Islands. The disease 
affects chiefly young adults, and, like typhoid fever, is more prevalent in 
autumn than at other seasons of the year. V. Sion and V. Negal and 
De Feyfer and Keyser found that the epidemics under their observation were 
produced by drinking infected water. Hunermann traced several cases 
occurring among children to one of their number who had suffered from a 
mild infection. Of the other recorded cases nothing definite concerning 
the mode of infection is known. 

Symptoms. — The disease may be mild or severe. The onset is gradual, and 
the symptoms of invasion are the same as those met with in typhoid fever, 
namely, headache, lassitude, and slight bronchitis. During the course of 
the disease the spleen becomes enlarged, rose spots may appear, and the 
patient develops the typhoid state. In Cushing's case a relapse occurred. 
Johnston states that diarrhoea and termination of the fever by crisis are of 
more frequent occurrence than in typhoid fever. Brion found diarrhoea 
in 18 per cent, of the recorded cases. In uncomplicated cases no leuko- 
cytosis has been observed. Hemorrhage from the bowel occurred in 5 
per cent. 

Complications. — Pratt has published a list of complications which includes 
all that have occurred in the 84 recorded cases. He divides them into three 
categories, viz.: 1. Those occurring in cases caused by Bacillus para- 
typhosus a. 2. Those occurring in cases caused by Bacillus paratyphosus /9. 
3. Those occurring in cases in which the species of the causative organism 
was not determined. He has shown that the complications of paratyphoid 
fever are of about the same character and frequency as those of true typhoid 
fever. 

Diagnosis. — The diagnosis depends upon the isolation and cultivation 
of a paratyphoid bacillus from the patient's blood, urine, or feces, or from 
a localized lesion. Bacilli thus obtained should be agglutinated by the 
patient's blood serum, and the latter should agglutinate known paratyphoid 
bacilli. In case an organism cannot be recovered Pratt thinks a diagnosis 



TYPHUS FEVER 61 

of paratyphoid is justifiable if the patient's blood serum agglutinates known 
strains of paratyphoid bacilli. While the Widal reaction is usually nega- 
tive, or positive only in very low dilution, Johnston believes that all cases in 
which it is negative must not be regarded as cases of paratyphoid rather than 
true typhoid fever. 

Prognosis. — The prognosis would seem to be favorable, as only 3 deaths 
have occurred in 83 undoubted cases of the disease, and 1 of these was a 
mixed infection with the Bacillus typhosus. 

Treatment. — This is identical with that of true typhoid fever. 



TYPHUS FEVER. 

Definition. — Typhus fever is an acute, infectious, self-limited disease of 
sudden onset which is characterized by fever, mental apathy, and the develop- 
ment of a rash which does not recur in crops as does the rose rash of typhoid 
fever. It is particularly prone to attack large numbers of persons in unhealthy 
surroundings, and is distinctly a disease of starvation or overcrowding. The 
period of incubation of typhus fever as a rule varies from eight to fourteen 
days, but there can be no doubt that many cases have been attacked within 
seven days after exposure. A few cases are said to have developed as early 
as the fourth day. Typhus fever is one of the most contagious of the acute 
infectious maladies. 

Some confusion has arisen in the past between typhus and typhoid fever, 
but at present, they are clearly differentiated, although it is worthy of note 
that the symptoms of enteric fever are so much like typhus fever in their 
degree of adynamia that it is called "typhoid" or like typhus, while German 
writers of the present day still call typhoid fever " ileotyphus." 

Typhus fever is sometimes called Spotted Fever, Ship Fever, Putrid 
Fever, or Hunger Typhus. 

The infection probably reproduces itself solely in the body of the infected 
patient, and is spread by direct contact with the patient or by his garments 
or discharges. It is not transmitted any great distance through pure air. 

History. — Typhus fever was first described as occurring in 1083 by Corradi, 
but it was not fully recognized as a distinct malady till 1546, when Fracas- 
torius wrote of the affection as he had seen it in Verona in 1505 and 1508. 
Several epidemics are reported as having occurred during the last half of 
the sixteenth century, in the eighteenth century, and in the early part of the 
nineteenth century in various parts of Europe; a most virulent epidemic 
ravaging Ireland and England in 1846. In America it first appeared in 
the New England States in 1807, and in Philadelphia in 1812, where it is 
said to have existed in isolated cases until 1836. 

Distribution. — Typhus fever seems to occur in all parts of the world if the 
conditions favorable to its development are present in the sense of unhealthy 
surroundings and provided the necessary germ is introduced. Because of 
its intimate association with unsanitary conditions it has been epidemic in 
great armies, during famine, and on ships in which the crew or passengers 
often were huddled together for long periods of time. On the continent 



62 DISEASES DUE TO A SPECIFIC INFECTION 

of Europe it spreads usually from east to west and is disseminated chiefly 
by the poorest classes when they travel from place to place. Persia, 
China, Hungary, and Turkey are never free from typhus fever, and small 
epidemics occasionally arise from these sources. Sometimes small epidemics 
or sporadic cases arise without it being possible to find any source of infec- 
tion. The disease is exceedingly rare in the United Stares, but the possi- 
bility of its occurrence must always be borne in mind by quarantine officers 
and physicians in charge of large hospitals in crowded cities. 

Etiology. — As already stated, typhus fever is a malady which depends upon 
a specific cause and the presence of unsanitary conditions for its develop- 
ment. The specific contagion, whatever it may be, retains its virulence for 
long periods of time in garments and in furniture. Much difference in its 
infectiousness also exists, for in some epidemics nearly everyone exposed is 
taken ill, whereas in others but few are affected. Kelsch has advanced 
the theory that the micro-organism of the disease is one which is usually 
benign, but may become malignant under favorable states. The specific 
micro-organism has never been isolated, although several investigators 
have claimed its discovery. 

Exposure for a considerable period of time to the atmosphere of a room 
which is poorly ventilated and which contains typhus patients is the most 
effective way of contracting the disease, whereas if ventilation is good and 
the exposed person in perfect health there is much less danger of infection. 
When a large number of cases of typhus fever are grouped together in 
a ward, the infection becomes very virulent and both the attendants and the 
physicians are extremely prone to contract the disease. Now that vaccination, 
antidiphtheritic serum, and antiplague inoculations protect the physician 
and nurse from these infectious diseases, there is no malady so apt to 
attack them and against which there is so little prophylactic aid as typhus. 

The most infectious period of the disease is in the early stages and at the 
height of the fever, although Moore asserts that it is most contagious during 
convalescence. It is also infectious even during the stage of incubation. 
Mild cases are probably as capable of spreading the infection as severe ones. 
After the febrile condition has passed away there is reason to believe that 
the patient ceases to be a direct source of infection, and if an attendant 
who comes in contact with him for the first time now contracts the disease, 
it must be from the poison which has found lodgement in the clothing of 
the patient during his illness. So far as we know, the most common 
means by which infection gains access to the body is by the organs of res- 
piration and perchance by the skin. Indeed, some clinicians of experience 
assert that actual contact between the body of the patient and that of the 
attendant is necessary for infection to take place, but this is not generally 
conceded. Certain it is that a very brief period of exposure is sufficient for 
the transmission of the disease. The infectious agent or agents of typhus 
fever is rarely if ever carried by water or other liquid media. Lowered 
vitality of the individual naturally increases his susceptibility. The influ- 
ence of age and sex is very slight, for all ages, after early infancy, seem 
equally susceptible, the greater predominance of the malady between twenty 
and forty probably being due to increased opportunities for exposure. 



TYPHUS FEVER 63 

The influence of climate and season upon the spread of typhus fever is 
only an indirect one, in that the poor ventilation of the houses of the lower 
classes during the winter months aids in the dissemination of the disease 
among the occupants, whereas in summer the better supply of fresh air 
and the greater amount of out-door life tends to diminish the danger of 
infection. 

Prevention. — There is no disease in the prevention of which fresh air 
plays so large a part as it does in typhus fever. Indeed, it may be stated 
that if a healthy man be supplied with plenty of fresh air while in the pres- 
ence of the sick he will have a fair chance of escape, whereas if the air of the 
room be impure infection is almost certain, for, as already stated, typhus fever 
is a malady of darkness and poor ventilation. Practical experience seems to 
indicate that the various disinfectants usually employed have little value in 
preventing its spread unless they are used in concentrated form upon the 
garments which have been infected. By far the best means of preventing the 
spread of typhus fever are the admission of a plentiful supply of fresh air and 
sunshine, the application of steam or scalding water to all woodwork and 
clothing, or the use of dry heat if steam heat cannot be employed. The 
bed-clothing and mattresses should be destroyed by fire. The value of 
formaldehyde gas as a disinfectant is still undecided for preventing the 
spread of this disease. 

Pathology and Morbid Anatomy. — Typhus fever, unlike typhoid fever, has 
no peculiar morbid anatomy, and it is therefore impossible from autopsy 
findings alone to determine that the cause of death has been typhus. The 
skin, it is true, may show very soon after death numerous petechia?, and 
early decomposition constantly occurs after death from this disease. The 
body is usually not greatly emaciated because the disease lasts so short a 
time. The muscles, which are somewhat dry, may also show, when exam- 
ined under the microscope, signs of granular or fatty degeneration just as 
they do in typhoid fever. 

The respiratory passages may be inflamed or congested. Thus there 
may be laryngeal ulceration as in typhoid fever and a considerable degree 
of bronchitis. Often hypostatic congestion of the lungs is present. In 
other instances a true lobar pneumonia occurs. Indeed, Curschmann says 
it occurred in 15 per cent, of his cases. The heart muscle is friable and 
surfers from the form of myocarditis seen in all infectious diseases, and 
the blood is found to be darker and more liquid than normal. It is a note- 
worthy fact that the intestines show no lesions whatever either in Peyer's 
patches or in the solitary glands. If such lesions are present the disease is 
typhoid, not typhus, fever. The liver is usually swollen and is found to be 
the seat of cloudy swelling, while the spleen is also enlarged to some degree 
but very soft. It may contain infarcts. The kidneys are also the seat of 
cloudy swelling. 

Symptoms. — The symptoms of typhus fever are quite characteristic. 
Unlike those of typhoid fever, the invasion is usually abrupt, the patient 
suddenly feeling ill about twelve days after exposure, and being seized by a 
chill or series of chills, with headache, backache, and general prostration. 
The fever rises rapidly, reaching its acme it may be as early as the second 



64 DISEASES DUE TO A SPECIFIC INFECTION 

day, but as a rule it rises steadily during the first four or five days, and 
during this period of rise the characteristic morning remissions of typhoid 
fever do not occur to so marked a degree. By the fifth day the temperature 
often reaches 105° or even 107°, but when the infection is not severe it 
may not go above 103°. After having reached its highest point it remains 
fairly constant with a slight decrease each morning, the evening tem- 
perature, however, remaining high until the period of crisis, at about the 
fourteenth day. In cases characterized by severe infection the tempera- 
ture may continue to rise until it reaches as high as 109°, when death usually 
occurs. To those cases in which the temperature reaches this very high 
point within the first few days of the illness the term Typhus Siderans is 
usually applied. 

The pulse is full and rapid, but usually not so feeble as in the early 
stages of typhoid fever. The face is deeply flushed the conjunctiva con- 
gested, and the expression one of apathy, although in some cases delirium 
varying from mild wandering to actual maniacal violence may be met with. 
Sometimes the delirium is wild (delirium ferox), sometimes it is like that 
of delirium tremens, and sometimes it is low and muttering — the typho- 
mania of Galen. If the toxaemia is severe extreme prostration and feeble- 
ness may ensue by the tenth day. 

In from three to five days the eruption appears upon the abdomen and 
chest, and soon spreads to the legs, arms, and face. It possesses two pecu- 
liar characteristics. In the first place it is papular, as in typhoid fever, but 
the spots are rarely as rosy as they are in that disease, and may finally 
become as dark as actual petechias, which indeed they really are. The 
second peculiarity is that there seems to be a subcuticular eruption or area 
of congestion, or mottling, so that the skin is marbled or mottled. Unlike 
the rash of typhoid fever, that of typhus does not disappear on pressure, 
and is distinctly manifest after death. Even if the case is mild the petechial 
character of the rash is present. In some instances the skin is said to give 
off a peculiar, musty or mouse-like odor. In children the rash may be so 
profuse as to resemble an attack of malignant measles. 

As the disease advances to the second week the evidences of toxaemia 
become more marked. The active delirium which perchance was present 
at first is replaced by stupor and coma vigil with subsultus tendinum, the 
tongue is dry and heavily coated, the teeth covered with sordes, and the 
heart's action rapid and feeble. The respirations are quickened but shallow, 
and diarrhoea may be marked. This stage is called the "putrid," "malig- 
nant," or "typhoid" stage of the malady. It is essentially one of profound 
toxaemia, and the patient lies in a state of deep prostration, indifferent to 
all sounds and objects in the immediate vicinity, mumbling a few disjointed 
sentences, his tongue being so coated and dry that it is almost impossible 
for him to move it. The pupils are often strongly contracted and the ten- 
dons twitch, while there may also be carphologia, or picking at the bed- 
clothes. Finally, if the illness becomes more severe, the patient lies with 
open eyes, gazing into space, with dilated pupils, a thready, imperceptible 
pulse, and a cold, clammy skin, which heralds the approach of death, which 
is due to the toxaemia, asthenia, and hypostatic pulmonary congestion. 



TYPHUS FEVER 65 

If the patient survives the early stages of attack, the fever usually ends 
by the twelfth or fourteenth day and the temperature undergoes much more, 
rapid defervescence than it does in typhoid fever. Indeed, it is generally 
thought that the fever ends by crisis; so that the patient passes, during a 
prolonged sleep, from a state of severe illness with a clouded mind to early 
convalescence with a clear mind, a critical fall of temperature taking place. 
This remarkable change in the aspect of the case has been alluded to by 
some authors as quite pathognomonic of typhus fever, but the statement that 
the fall of the temperature is always by crisis is not universally conceded 
to be correct. Thus, Moore, of Dublin, states that the end is by crisis; 
while Curschmann asserts that in the great majority of cases it ends by 
lysis, although he admits that a critical fall occasionally takes place, covering 
a period of from two to three days. This is hardly a crisis in the usual 
acceptation of the term. 

Whatever may be the true method of the fall of temperature, it is certainly 
a fact that convalescence is rapidly established; so that the patient pro- 
ceeds to complete recovery more rapidly than after typhoid fever, health 
being completely restored, it may be, by the end of a month. 

Relapse in typhus fever very rarely takes place, and in the vast majority 
of cases one attack produces immunity against further infection. 

The complications of typhus fever are those which we would expect to 
meet with in the presence of any severe infection. Bronchopneumonia or 
lobar pneumonia may occur. In very poorly nourished individuals noma 
may develop, and symptoms of generalized paralysis develop as the result 
of neuritis. So, too, septic arthritis and infection of the parotid glands may 
occur. 

Diagnosis. — Several characteristics of typhus fever have already been 
emphasized. The most noteworthy of these are: the sudden accession of 
the disease, the rapid rise of temperature without morning remission, the 
development of a peculiar rash between the third and fifth day, the dusky 
appearance of the face, the musty odor of the skin, and the early appear- 
ance of active delirium or profound apathy. All these symptoms are quite 
different from those met with ordinarily in typhoid fever, but it is not to 
be forgotten that sometimes typhoid fever begins suddenly and presents 
manifestations closely resembling those of typhus; so that during the pres- 
ence of an epidemic of typhus or typhoid fever cases of either one of these 
diseases may readily be overlooked. In the differentiation the early devel- 
opment of the rash (third to fifth day) in typhus fever is of great practical 
value, and the distribution of the rash is still more helpful in aiding a 
decision; for the rash of typhus fever, if profuse, involves the extremities 
as well as the trunk, whereas that of typhoid fever is chiefly limited to the 
body; a profuse and dusky rose rash on the hands and legs is therefore 
distinctly in favor of typhus fever. Again, the rash of typhus fever is con- 
stant, whereas that of typhoid fever fades and recurs in crops. Sometimes 
however, the rash of typhus fever, like that of typhoid fever, is very scant, 
only a few rose spots being present. Indeed, the disease may occur without 
any exanthema being manifest. 

As the illness progresses much additional differential information 
5 



66 DISEASES DUE TO A SPECIFIC INFECTION 

can be gained if the case be one of typhoid fever by the discovery of 
the Widal reaction, the recovery of the Bacillus typhosus in the blood and 
in the rose spots. Then, too, typhoid fever does not end so abruptly nor 
so early as does typhus fever. Malignant measles and variola may in 
their earliest stages resemble typhus, but their later course clearly separates 
them. 

Relapsing fever is separated from typhus fever by the clear mental con- 
dition of the patient notwithstanding his high temperature, by the lack of 
petechia?, and the absence, as a rule, of severe initial symptoms. 

Prognosis. — The prognosis in typhus fever varies greatly with the pre- 
vious condition of the patient, and also to some degree with the severity of 
the epidemic. Usually the mortality rate varies from 10 to 20 per cent, in 
young adults, but in children it is often much less than this. In advanced 
years the mortality is very high. 

Curschmann has stated that "old age makes itself felt as early as the 
fortieth year and that after fifty almost 50 per cent, die." The accompanying 
chart, Fig. 14, made from the statistics of Murchison, Guttstadt, and 
Curschmann indicates further the influence of age on the prognosis. 

Death in typhus fever rarely occurs before the second week. After the 
end of the second week it seldom takes place except as the result of some 
untoward complication. 

Treatment. — The treatment of typhus fever is in many respects identical 
with that now recognized as useful in typhoid fever. The patient should 
be isolated, of course, and provided with an abundance of light and air. 
As already stated, in no disease are these aids to health more essential for 
recovery. As the course of the malady is one toward profound asthenia, 
easily assimilated or predigested foods should be given as freely as the 
patient can utilize them. Milk to which is added a little pancreatin and 
sodium bicarbonate, barley- and rice-gruel in which is placed some taka- 
diastase, and copious draughts of water to flush the kidneys and aid in the 
elimination of poisons are to be administered. The fever is to be treated 
by cool or cold bathing as the patient lies in bed, according to the directions 
given under typhoid fever, and cold is to be kept applied to the head con- 
tinuously. The coal-tar antipyretics are not to be used if they can be 
avoided. When signs of cerebral and pulmonary hypostatic congestion 
manifest themselves the patient may be immersed in a bath of about 90°, 
and cold water at 60° poured over his head and shoulders as a douche, 
active friction of the body and limbs being performed by the nurse for 
several minutes before the sick man is returned to his bed. Should the cir- 
culation fail, alcohol in the form of whiskey or brandy, well diluted with 
water, is to be employed for the purpose of supporting the heart and nervous 
system. Camphor in \ grain doses is useful for this purpose. If the nervous 
restlessness of the patient is sufficient to endanger life by the resulting 
exhaustion, a hypodermic injection of morphine may be given to produce 
sleep or nervous quiet. 

The bowels should be kept open by the use of gentle laxatives, or be 
evacuated by a saline purge if obstinately confined. The activity of the 
kidneys must also be maintained by the use of alkaline diuretics and sweet 



TYPHUS FEVER 



67 



spirit of nitre and by the free administration of a pure drinking water. 
As retention of urine often occurs, the state of the bladder must be care- 
fully watched. 



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age from the statistics of Murchison, Guttstadt, and Curschmann. 



68 DISEASES DUE TO A SPECIFIC INFECTION 



RELAPSING FEVER. 

Definition. — Relapsing fever, as its name indicates, is characterized by 
an attack of fever which lasts about six days, this in turn is followed by a 
period in which fever is absent, and this again by a recurrence of a period 
of fever. These alternating periods may be repeated three or four times. 
It is due to a specific micro-organism, the so-called spirillum or spirochete 
of Obermeier. Sometimes it is called Febris Recurrens, " Seven Days' 
Fever," and " Famine Fever." 

History. — The history of relapsing fever is, when compared to some other 
infectious diseases, fairly modern, for the first descriptions of it occurred 
in medical literature about 1729, although it was not until 1739 that Rutty 
gave a clear description of its course. After this for nearly a century no 
reports of its existence are to be found, but between 1842 and 1852 it 
appeared over a wide area, occurring in England, Ireland, Scotland, Ger- 
many, and finally in America, to which country it was brought by a ship- 
load of immigrants who came from Liverpool and landed in Philadelphia 
in 1844. It became epidemic in the United States in the decade from 1861 
to 1870, and it is interesting to note that as the American, Gerhard, first 
aided in the differentiation of typhoid fever from typhus in Philadelphia, so 
Pepper, Rhoads, and Parry, of the same city, have contributed to medical 
literature the best account of the disease as it has appeared in this country, 
having observed a larger number of cases than any other clinicians. 

Distribution. — Relapsing fever has occurred in almost all parts of the 
civilized world. 

Etiology. — It has been claimed that filthy surroundings and bad food 
are active in the development of relapsing fever, but they probably exercise 
a general influence by lowering vitality rather than by directly aiding infec- 
tion. Sex, age, and nationality exercise no influence, and it is doubtful if 
any one season of the year increases the prevalence of the disease. The 
actual cause of relapsing fever, as already stated, is a spirillum known as 
the spirillum of Obermeier, which is constantly found in the blood of patients 
suffering from the disease during the stage of fever. It is absent from the 
blood in the intermissions, although small, glistening bodies, said to be 
spores, can be seen. The disease is contagious, that is it requires contact 
with the patient or with his garments for the infection to be spread. Patients 
may be infected by insects, for example by bed-bugs which have previously 
bitten patients suffering from relapsing fever. That the disease is ever 
conveyed by the air is doubtful. 

Pathology and Morbid Anatomy. — The changes produced in the body by 
relapsing fever are not only not marked, but not at all characteristic. The 
spleen and liver are swollen and engorged, as in nearly all febrile infectious 
diseases, and the voluntary muscles may undergo granular degeneration. 
Similar changes may be found also in the heart muscle. Sometimes multiple 
infarctions and hyperplasia of the bone-marrow are present and ecchymotic 
spots, which are found ante-mortem, are seen in the skin and subcutaneous 
tissues. 



RELAPSING FEVER 



69 



Symptoms. — As a rule about six or seven days after exposure to the dis- 
ease the infected person is abruptly seized by a severe chill, or more rarely by 
headache and vomiting. The face becomes flushed, but the expression is 
not dull and apathetic as it is in typhus or typhoid fever, unless the infection 





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is very severe, when typhoid symptoms may soon develop. A moderate 
degree of jaundice also is present in many cases. No characteristic eruption 
appears on the skin, although small petechias or ecchymotic spots may 



70 DISEASES DUE TO A SPECIFIC INFECTION 

occur in severe cases. Many observers have recorded the presence of a 
disagreeable, musty odor about the patient. 

The febrile movement is the most notable manifestation of the disease. 
The fever begins to rise while the stage of chill is still young, and reaches 
102° or 103° in the first twenty-four hours and 104° or 106° in the next 
twenty-four hours. During the febrile stage of about six days this level 
of temperature is fairly constantly maintained, although irregular remis- 
sions of 1° or 2° may occur. Sometimes the fever reaches 108°. In some 
cases the primary febrile period lasts only two days. While the febrile 
movement just described is characteristic, its ending is more so, for a crit- 
ical fall of temperature takes place with a suddenness and completeness 
which is rarely met with in any other disease unless it be croupous pneu- 
monia (Fig. 15). Not rarely it falls 6° in three hours, although a fall of 
1° an hour is more common. The rapid fall may carry the temperature 
a little below normal. After a few days of no fever the relapse takes 
place with the same sudden onset as occurred with the primary attack. 
It runs a course in all respects like the original seizure, but it more com- 
monly ends by lysis than does the first paroxysm. The third and fourth 
attacks, if they occur, are usually milder than the first two. The duration 
of the period of intermission varies from one to ten days, although 
it is usually six days or a week, and the duration of the entire illness 
may vary from eighteen to ninety days, according to the number of 
relapses. 

The pulse during the early attacks is rapid, and it may be bounding, 
but if the patient be enfeebled by prolongation of the illness it may be 
small and compressible. Severe frontal and occipital headache is often 
experienced by the patient in the first attack, but delirium is rare except it 
be due to serious complications or to very high fever. 

Prognosis. — The prognosis as to ultimate recovery is quite good, the 
mortality of the disease usually being about 4 per cent. 

Treatment. — There is no specific treatment for relapsing fever. Good 
nursing, careful feeding, and the use of stimulants, if the patient is feeble, 
are of course needful. The action of the bowels and kidneys, as in all infec- 
tious diseases, should be carefully attended to. No results from the use of 
hydrotherapy in relapsing fever have been published so far as the writer is 
aware, but the course of the febrile movement scarcely indicates this plan 
of treatment. 

VARIOLA. 

Definition. — Variola, or smallpox, is an acute infectious disease affecting 
the entire body, but manifesting itself chiefly by the development upon the 
skin, more particularly that of the face and forearms, of an exanthem which 
is at first macular, then papular, then vesicular, pustular, and finally 
umbilicated. 

History. — Smallpox is one of the ancient diseases, for records exist which 
show it to have occurred many centuries before the time of Christ. The 
first authentic medical record of the malady did not appear, however, 



VARIOLA 71 

before the tenth century, when Rhazes, of Bagdad, wrote his Treatise on 
Smallpox and Measles. It is generally considered that smallpox did not 
gain entrance to Europe till about a.d. 710, when the Arabs conquered 
the Spaniards. It reached Germany about the tenth century, at which time 
it also appeared in England. At times since the tenth century it has swept 
away thousands of persons in a single epidemic, and very few escaped 
its ravages. Indeed, a large part of the population of London were at one 
time pock-marked. It was first introduced into Mexico in 1520, and into 
Massachusetts in 1633. Until the introduction of vaccination it was one 
of the most death-dealing maladies known to man. (For the influence of 
vaccination in diminishing smallpox see article on Vaccinia.) 

Distribution. — Smallpox has occurred in all parts of the civilized world, 
from the Arctic to the Tropics, and is of equal virulence in very cold and 
in very warm climates. 

Etiology. — Variola is believed by some to be due to a parasite named by 
Guarnieri, in 1892, the Cytoryctes variolas, and carefully studied by Wasie- 
lewski in 1901. Its evolution has been more fully known by the labors 
of Councilman, Magrath, and Brinckerhoff in 1903 and Brinckerhoff and 
Tyzzer in 1905, the latter being an extensive investigation of experimental 
variola and vaccine in Philippine monkeys. These in every respect con- 
firm the previous findings in human beings. Basing his views upon pre- 
viously accomplished work, but especially upon the study of Councilman 
and his students, Calkins has attempted to formulate the different stages 
in the life history of the parasite. A full review of these and previous 
inquiries into the nature of the specific organism of variola and vaccinia 
will be found in the Journal of Medical Research, February, 1904, vol. 
xi., No. 1, pp. 8-360 and January, 1906, vol. xiv., No. 2, pp. 209-359. (For 
the process of the development of this organism see Pathology and Morbid 
Anatomy.) 

The disease affects persons who may be exposed to it at all ages, 
and remarkably few people who are unvaccinated are able to resist the 
infection, not more than from 1 to 5 per cent. The negro race is peculiarly 
susceptible, and in this race the rate of mortality from the disease is 
usually very high. Smallpox affects males more frequently than females. 
It is more common in the winter and spring than in the summer, per- 
haps because of the crowding in the homes of the poor during the cold 
months. 

The contagion of smallpox is spread in several ways — viz., directly, that 
is, by contact with the patient's body and his clothing; and indirectly, by 
the air. Stokes has recently published a paper indicating that the infec- 
tion usually enters the body through the lungs. A nurse may convey the 
disease from a patient to a healthy individual, and rats, mice, and flies 
may do likewise. The patient ill of smallpox is capable of infecting a 
healthy person from the initial stage of the disease to the moment when, 
recovery having occurred, every particle of pustule or desquamating skin 
has been cast off. The most contagious periods are, however, those of 
vesication, pustulation, and exfoliation. 

The fact that the disease is spread by aerial convection is never to be 



72 



DISEASES DUE TO A SPECIFIC INFECTION 



forgotten, and it may be carried in this way from a few feet to several yards 
(Fig. 16). Much difference of opinion, however, exists among those who 
have studied the question of aerial convection. Power, of Fulham, and 
Barry, of Sheffield, England, found a noticeable influence exercised by the 
propinquity of a smallpox hospital, but Savill, from investigations carried 
on at Warrington, came to the conclusion that aerial currents influenced the 
spread of the disease but little. It must be remembered, moreover, that 
before we accept these figures as to aerial convection we must be sure that 
the contagion was actually carried by the air and not by insects or animals. 
I know of one smallpox hospital from which flies, mice, rats, and cats 
passed freely, and surrounding which smallpox was almost constantly 
present. 

Fig. 16 
4000 feet. 




0.02 per cent. 
Diagram showing the percentage of aerial convection of smallpox. (Moore.) 

Bodies dead of smallpox can also spread the disease among those who 
handle them. 

The severity of the infection depends not so much upon the violence of 
the disease in the giver as in the susceptibility of the receiver of the malady. 
A mild case may therefore be provocative of most virulent epidemic. 

Incubation. — The period of incubation of smallpox varies from five to 
twenty days, but as a rule it is about twelve days. Cases occurring in less 
than five days after exposure are very rare. 



VARIOLA 73 

Prevention. — There is one measure above all others to be used in the 
prevention of smallpox, and that is vaccination, which by its beneficent 
influence has changed smallpox from a common and fearful scourge of man- 
kind to a disease so rare that many physicians practice a lifetime without 
seeing a case. (See Vaccine and Vaccination). 

It is very important to bear in mind the clinical fact that vaccination 
not only protects the patient who may be subsequently exposed to small- 
pox, but also that it protects the patient who, having been so exposed, is 
subsequently vaccinated. Even if the vaccination be performed so long 
after the exposure that smallpox nevertheless develops, the severity of the 
disease will be modified, the degree of modification being in direct ratio to 
the length of time between vaccination and the appearance of the variola. 

A most interesting illustration of this has been sent me most kindly by 
Dr. Allan Warner, of the Borough Isolation Hospital, Leicester, England. 
The history of the cases is as follows: 

A boy, aged fourteen years, unvaccinated, sickened with smallpox on 
April 14. He was removed to the hospital on April 18, where he had a 
severe confluent attack. The father consented to his wife and three children 
being vaccinated, stating that personally he would not be vaccinated, but 
would be a "test," to see if there was anything in it. Ten days later his 
daughter, aged three years, developed a smallpox eruption; she had less 
than one hundred spots and never appeared ill. No other person in the 
house suffered from smallpox except the father, vaccinated in infancy, his 
eruption appearing fourteen days after the son had been removed to the 
hospital. A photograph of the father and daughter, taken on the twelfth day 
of the father's eruption, may be seen in Fig. 17, and requires no comment. 

In cases of urgency it is generally held that humanized virus is more valu- 
able than calf virus, but as humanized virus is often difficult to obtain it 
is better to vaccinate the patient in different places with glycerinated vac- 
cine made by different manufacturers, since in this way there is little doubt 
but that one will surely take. 

The second preventive measure of importance is the absolute isolation of 
the patient, and the third the complete disinfection or destruction of all 
garments and bed-clothing which have been about the sick person, includ- 
ing those worn by his attendants. Finally, all individuals exposed to the 
contagion should be quarantined for a period of twenty-one days, in 
order that the physician may be sure ihat they are not going to be attacked 
and so spread the infection. 

Frequency. — Smallpox is so constantly present in the poorer part of large 
cities that it may be said to be almost endemic in all of them, but to a very 
moderate degree. Occasionally when a considerable number of unvac- 
cinated persons have accumulated in a city or country district, the disease 
bursts out in a small epidemic, and sometimes, without any such apparent 
cause, certain districts seem to be affected, many unvaccinated persons 
being attacked. During the winter of 1901 and 1902 smallpox appeared 
almost all over the United States in scattered localities. It can, however, 
always be stamped out by house-to-house vaccination, and its spread 
depends upon imperfect quarantine and inefficient vaccination. 



74 



DISEASES DUE TO A SPECIFIC INFECTION 



As an illustration of the extraordinary effect of vaccination and sanitation 
upon this malady it is interesting to note that during the eighteenth century 
fully two-thirds of all children born in Europe were sooner or later attacked 

Fig. 17 




Father and child suffering from smallpox. The child was vaccinated in the incubation period. 

(Allan Warner's cases.) 

by smallpox, and an average of one-twelfth died of the disease. On the 
other hand, the death rate from smallpox in the latter part of the nine- 
teenth century in London was 98.5 per cent, less than one hundred years 
before. To put it differently, the death rate from smallpox in 1838 was 



VARIOLA 75 

1064 per million, while in 18S9 it was 1 per million, and in 1890 nil per 
million. 

During 1904 the disease was totally eradicated from New York and 
Philadelphia by vaccination and quarantine. 

Pathology and Morbid Anatomy. — The most noteworthy lesion produced 
by smallpox takes place in the skin. The dermal papillae become hyper- 
rernic, the cells of the rete Malpighii swell and so raise the epiderm, and 
under this epiderm serum exudes and pushes the stratum still farther 
upward. The cells of the rete are more or less elongated, pigmented, and 
form fibrils extending from the epiderm to the base of the inflamed zone in 
the derma, constituting the vacuolar focal degeneration described by Coun- 
cilman, Magrath, and Brinckerhoff. In this reticulum still further serous 
exudation occurs, and so forms a vesicle which increases at its margin, 
where the exudation takes place very rapidly, while degenerative and 
necrotic changes progress in the epithelium of the area involved. As a 
result the area under and around the vesicle becomes indurated and we 
have the characteristic hard pock of variola. The persistence of this free 
exudation at the margin of the pock and the greater density of the centre 
lead to depression of the latter, giving rise to umbilication. Wright has 
shown that the central depression in the pock may be due to diphtheroid 
degeneration. It may also be due to retraction by a hair or small gland. 
Councilman, Magrath, and Brinckerhoff do not believe that the pock is 
always produced by the same cause, but that a number of factors enter 
into its formation. 

Following this stage, the serum in the pock is infiltrated with leuko- 
cytes, and these becoming great in number, the contents of the pock 
become opaque or turbid, and finally resemble pus. Sometimes if the 
inflammation in the adjoining pocks is very severe the deeper layers of 
the skin become involved, undergo necrosis, and so great local destruction 
of tissue takes place. After this stage epithelial regeneration progresses 
beneath the scab, which dries up and ultimately falls off, leaving a red or 
pink depression in the skin, which depends for its depth upon the degree 
of pustulation or necrosis present during the acute stage. Not only do 
vesicles form on the skin, but upon the mucous membrane of the mouth, 
pharynx, tongue, and even the rectum, anus, vagina, penis, and conjunctiva 
in some cases. 

The changes just noted probably arise from the minute organism recently 
studied by Councilman and his assistants, He has described its development 
in the following words: " In the lower layers of skin epithelia, before there is 
present any anatomical evidence of vesicle formation, there are found 
small, structureless bodies from one to four microns in diameter. The cells 
present, at this time, little or no evidence of degeneration. The bodies, 
one or more in number, lie in vacuoles in the cells. The vacuoles are, at 
first, but little larger than the enclosed bodies. The bodies increase in 
size, and evidence of structure, consisting of granules more distinctly 
stained, and lying in definite spaces, begin to appear. With the increase 
in size of the body, the vacuole of the cell enlarges until a large, central 
space around the nucleus is formed. At this time there is but little evi- 



76 DISEASES DUE TO A SPECIFIC INFECTION 

dence of degeneration of the nucleus. The body continues to increase 
and becomes granular, the granules lying in a reticular structure. The 
form of the larger bodies is irregular and suggests an amoeboid character. 
They may become as large as, or larger than, the nucleus of an epithelial 
cell. A definite nucleus has not been made out in them, unless the 
reticular structure which stains more intensely than the rest of the body 
be so considered. At this time segmentation takes place, leading to the 
formation of small, round bodies about one micron in diameter. All this 
is best seen in the acute hemorrhagic cases. It may also be seen in the 
advancing edge of a young vesicle, the bodies becoming larger and more 
definite in structure as the formation of the vesicle advances. The 
bodies in the cells we regard as living organisms, and the gradual 
growth and final segmentation as a cycle in its life history. Up to this 
time the nuclei, although showing such evidences of degeneration as the 
massing of chromatin in the periphery, are not greatly altered. 

"At the period of segmentation, and when most of the intracellular 
bodies have disappeared, small, round or oval, ring-like bodies appear in 
the nucleus. These increase in size and acquire a definite structure, con- 
sisting of a series of vacuoles around a large, central vacuole. The rim of 
the central vacuole stains more distinctly than do other parts of the body. 
One or more of these bodies may appear in a single nucleus. When several 
are present they are smaller, but have the same structure. The bodies 
become larger; the nuclear rim grows less distinct, and finally disappears, 
and the body lies in a completely degenerated cell, or this breaks down, 
setting free the body. With the growth and development of the intranuclear 
body the vacuolar structure becomes less evident, and finally a structure 
is formed which contains numerous fine vacuoles. At this time small, cir- 
cular bodies begin to appear in it, and groups of these are surrounded by 
a faint ring, which probably represents the remains of the body in which 
they were formed." 

Myocardial degeneration is present in most cases, and a variolous myo- 
carditis has been described. 

In general the cardiovascular changes of smallpox resemble similar 
alterations occurring in other infectious diseases. 

Proliferative changes occur in haematopoietic organs (spleen, lymph 
nodes, and marrow), associated with the production of basophilic mono- 
nuclear cells which enter the circulation and also phagocytic endothelial 
elements. The basophilic mononuclear cells infiltrate the testicle and usually 
the kidney, liver, and adrenals. 

Cloudy swelling occurs in the glandular viscera and a diffuse toxic 
degeneration takes place in the liver, kidneys, adrenals, and testicles. 

Pharyngitis and fatal bronchopneumonia occur; less commonly croupous 
pneumonia and pulmonary abscess or gangrene develop. 

Endocarditis, pleurisy, and empyema are infrequent. 

The kidneys are more or less altered in all cases; in milder degrees 
this may amount to little more than intense cloudy changes, but in other 
cases acute diffuse, glomerular, or, less commonly, suppurative nephritis 
occurs. 



VARIOLA 77 

Many of the lesions produced in the internal organs in smallpox are the 
result of the secondary infection from the skin and respiratory tract, and 
this usually depends upon the presence of the Streptococcus pyogenes. 

As in most of the acute infectious diseases, bronchitis is present in many 
cases of variola, and the secretion of the bronchial mucous membrane may 
be profuse and mucopurulent. 

Bronchopneumonia may also develop. 

When hemorrhagic smallpox takes place we have transudations of blood 
into the pocks and into the conjunctiva, the retina, the muscles, the sub- 
pleural tissues, into all the abdominal organs, and into the kidneys and 
the perirenal fat. 

Submucous extravasations also take place in all the organs of the body 
lined with mucous membrane. 

Symptoms. — After an incubation period of about twelve days the symp- 
toms develop. As in many acute infections, headache and backache are the 
predominant initial symptoms of smallpox, but they are peculiar in their 
severity in this disease, so that their very intensity possesses diagnostic 
significance. Sometimes the pain in the back extends down the posterior 
portions of the legs. Rigors also occur and pain in the epigastrium and 
vomiting may come on. Sometimes drowsiness and sleep with muscular 
twitching develops as a prominent initial sign in children. The urine is 
often scanty, loaded with urates, and usually contains some albumin. The 
temperature in smallpox is usually high from the onset, so that it may 
reach 104° as early as the latter part of the first day, and 105° or 106° by 
the end of the first forty-eight hours. It maintains this high degree with 
very slight remission until the eruption is developed. The pulse is rapid 
often as high as 120 per minute, in adults, and unless profound depression 
is very early manifested it is fairly strong. The abdominal organs present 
no signs of any importance, but constipation is more frequently present than 
is diarrhoea. 

The true variolous eruption makes its appearance, in the majority of 
cases, on the third day, although many writers state that it appears most 
commonly on the fourth day, while others insist that it appears on the 
second. The facts are that the time of the appearance of the rash varies 
materially in different cases, for it is delayed in mild attacks and develops 
early in severe ones. Sydenham said of the confluent form of this disease: 
''This kind usually comes out on the third day, sometimes earlier, but 
scarcely ever later; whereas the distinct (discrete) form appears on the 
fourth day or later, but rarely before." Boerhaave said: "The slower the 
small pocks come out, the milder they prove and the better they ripen. Those 
appearing on the first day of the illness are esteemed the worst kind; those 
on the second, milder; those on the third, still more gentle, and on the fourth 
the most favorable." Very rarely indeed the rash may be delayed till the 
fifth day, but this is an unfavorable sign. 

It must be borne in mind that the first signs of the eruption may be very 
scanty. But one or two papules may be present on the face or hand or 
forearm. In other instances the papules are very numerous on the face, 
the extensor surfaces of the forearms, and then on the trunk, these being 



7S 



DISEASES DUE TO A SPECIFIC INFECTION 



the parts which are particularly prone to present the first sign of the erup- 
tion. In still other cases the entire surface of the body is speedily covered 
and the mucous membrane of the mouth, pharynx, and vulva also are 
involved. The portion of the skin least affected in most cases is that 
of the anterior part of the thorax, the abdomen, and the flexor surfaces of 
the extremities. 

The eruption of smallpox proceeds through the following five stages of 
development with considerable rapidity: For the first few hours minute 
bright-red macules are present, which disappear on pressure. They soon 

Fig. 18 




Well-developed variola, 

become hard and elevated — that is, the macules become papules. By the 
end of the first twenty-four hours of the eruption the papule begins to show 
at its apex a tiny vesicle, which rapidly develops so that by the fourth or 
fifth day of the rash the vesicular stage has reached its full development. 
This vesicle is, as a rule, less than a sixth of an inch in diameter, contains 
fairly pearly looking fluid (lactescent), and is surrounded by a narrow 
areola of red. A peculiarity of the vesicle of smallpox is that though some 
serum may escape when it is pinched, it never empties itself or collapses 
because of the fibrilla which are present in the cavity of the vesicle, as already 



VARIOLA 79 

described. With the advent of the fifth or sixth day the centre of the vesicle 
is seen to be slightly depressed, showing the beginning of the stage of umbil- 
ical ion. 

The fluid in the vesicle now rapidly becomes cloudy and purulent, the 
surface of the pock gradually loses its umbilication, and by the seventh 
or eighth day of the eruption the eruption exists as a pustule, which by the 
tenth day is dome-like and surrounded by an areola. This pustule, when 
it is punctured and pressed upon, discharges pus and cloudy serum. If 
the pustule is not meddled with it ruptures in about twenty-four to forty- 
eight hours and the pus escapes, dries, and forms a dirty-looking scab, so 
that by the eleventh or twelfth day of the eruption the primary macule has 
advanced through its stages of maturation to the ruptured pustule. These 
scabs produce a disgusting odor. Sometimes the pustule does not rupture, 
but simply dries up; when the scab falls off it leaves under its former site a 
red or pink depression in the skin, the future pockmark. This stage of 
desiccation or drying, followed by exfoliation, may last in severe cases for 
several weeks, and it is followed by a period of desquamation of fine scales 
of epidermis, during which time the reddened pockmark gradually heals and 
cicatrizes. This desquamation rarely takes place earlier than the sixteenth 
and often about the eighteenth day. 

The eruption on the mucous membranes runs a much more rapid course 
than that on the skin, so that as early as the fifth day the pustule ruptures, 
leaving an ulcerated surface, which, if the eruption on the mucous mem- 
brane of the mouth has been confluent, may resemble the ragged, dirty- 
looking exudate of diphtheria. 

There are two additional facts of importance in connection with the 
eruption not yet named — viz., a peculiarity of the papule of smallpox is that 
when the finger is drawn over it it feels indurated as if a shot were under 
or in the skin. The second point is, that the rash does not all appear at once, 
but different parts of the body are affected, one after the other, so that one 
part may present vesicles while another is beginning to show pustules. 

Another point of interest from a diagnostic standpoint is the characteristic 
course of the fever. Primarily high till the eruption begins, it speedily falls 
to 99° in moderate cases, or to 100° in confluent ones, and remains low until 
pustulation begins, when the so-called secondary fever develops, which 
rises to 102° or even 104°. This fever, unlike the primary fever, has morn- 
ing remissions of 1° to 2°, and gradually ends by lysis, so that at about the 
twelfth day, which is the period at which the pustules rupture or become 
dry, the temperature reaches normal. 

As would be expected from the severity of the eruption the skin during 
the active stage of the disease is deeply inflamed and so greatly swollen 
that the features of the patient may be unrecognizable. (See Fig. 17.) 

In many cases the mind is clear throughout the illness, but in others it is 
clouded, and active delirium, which may be violent, is met with in severe 
cases. 

In the earliest stages of variola initial rashes may precede the true erup- 
tion and mislead the physician if he be not on his guard. In some instances 
an erythema, like that of early scarlet fever, is present, and in still others 



80 



DISEASES DUE TO A SPECIFIC INFECTION 



a rash appears which strongly resembles the early stages of the eruption 
of measles. These rashes may last from a few hours to a few days, and 
usually appear on the trunk and limbs and but slightly on the face. The 
scarlatiniform rash is to be separated from that of scarlet fever by the 
fact that it is not so punctate, nor so bright in hue, and is not associated 
with the presence of the sore throat of that disease. The rash which resem- 
bles measles is scarcely raised at all, as is the real rash of that disease; it 
develops much more rapidly, covering the entire body in a few hours, and 
disappears with a speed equal to that of its onset, rarely lasting over thirty- 
six hours. 

In some cases both the scarlatiniform and morbilliform rashes appear 
in very small patches on the wrists or about other joints. These initial 
rashes possess a considerable degree of prognostic importance, since they 
usually appear in mild cases. 



Fig. 19 




Variola in a child with scant eruption. (Schamberg.) 

Still another initial skin lesion, of some importance because of its prog- 
nostic features, is an intensely red rash, which appears on the second day 
of the illness and spreads over the entire body so that the surface may after 
a few hours look as if it were affected by a generalized erysipelas in its 
early stages. Such a rash is said to indicate the future development of the 
hemorrhagic or malignant type of the disease. 

Petechial rashes also occur as initial or preliminary lesions. They usually 
involve the suprapubic or inguinal regions, but sometimes they appear in 
the infraclavicular areas. The individual petechia? may be bright red, or 
dull red, or purple in appearance. In still other cases an eruption which 
closely resembles that of true purpura develops. In very malignant cases 
death may occur before any typical eruption of smallpox appears. 



VARIOLA 81 

Something more must be said in regard to the variations which occur in 
the eruption of smallpox. In the first place, it is possible for smallpox to 
occur without eruption, although, of course, such instances are exceedingly 
rare. In all probability, careful examination of such patients will reveal one 
or two papules which otherwise might be overlooked. Indeed, this type 
of smallpox may be considered as belonging to so-called varioloid, and 
to occur in those patients who have been imperfectly protected by early 
vaccination. 

Councilman, Magrath, and Brinckerhoff describe secondary vesicles 
usually formed on the surface of the primary vesicle, but occasionally 
seen in the base. 

Confluent smallpox, as its name implies, may be localized or general; 
that is to say, the confluence of the various pocks may occur only in certain 
portions of the body, while in other instances all portions of the body may 
be covered by a coalescence of the eruption. In these cases there is always 
an extensive dermatitis. There is usually great restlessness, delirium, 
marked circulatory disturbance, and death very frequently occurs from the 
ninth to the eleventh day. It is in this type of case, too, that the greatest 
degree of the oedema of the subcutaneous tissues appear, and the tempera- 
ture usually maintains a high degree. Sometimes, however, in confluent 
smallpox, the vesicles do not seem to reach as great a degree of fulness as in 
ordinary cases, and there is not the same degree of swelling of the subcu- 
taneous tissues, although the skin is apt to be harsh and thickened. Curiously 
enough, this form of confluent smallpox is considered by experts to be more 
frequently followed by death than that form in which the eruption seems to 
be more completely matured. 

Very rarely in the pustular stage, the epiderm at the base of a pustule 
may be displaced by the formation of a bulla, or bleb, which contains a 
clear, straw-colored serum, and which holds in its centre the pustule. 

Under the name of hemorrhagic or black smallpox, which is by no means 
rare, and which takes place both in sporadic and epidemic cases, a form of 
the disease occurs in which the initial symptoms are always very severe, and 
in which hemorrhages into the skin occur early. Not only do the spots 
become purpuric by extravasations of blood into the skin, particularly about 
the joints, but the hemorrhages also occur on the eyelids under the conjunc- 
tiva, and even on the tongue, the palate, the fauces, and the vagina. Bleed- 
ing also frequently takes place from the gums, and nose-bleed, bloody vomit, 
and bloody stools may occur. Sometimes hematuria also develops. In these 
instances the temperature usually does not rise above 100°, and the mind 
remains clear and unclouded, but they are distinctly typhoid in type, and 
death often occurs, sometimes as early as the third day, but more commonly 
between the third and sixth day, as the result of the profound toxaemia and 
associated cardiac failure. 

Under the name variola pustulosa hemorrhagica, a form of the disease is 
described in which the eruption does not become hemorrhagic until the 
stage of pustulation is reached. This type is not so severe as that just 
described. 

Under the name of variola fulminans, an exceedingly fatal form, with 
6 



82 DISEASES DUE TO A SPECIFIC INFECTION 

a high temperature of 105°, delirium, coma, and collapse occur. In these 
cases death comes on within a few hours after the onset of the disease, and, 
while no hemorrhages are manifest in the skin, since the eruption is as yet 
scarcely developed, internal hemorrhages are, nevertheless, found at autopsy. 
It is much more apt to occur in unvaccinated than in vaccinated persons. 

While the symptoms detailed up to this point may be considered 
as those of ordinary smallpox which runs a natural course, it is not to be 
forgotten that a modified form of the disease quite frequently occurs, in 
which by reason of vaccination many years before, or natural immunity, 
the manifestations of the affection are quite markedly modified. To this 
type of the disease the term varioloid is applied. 

The whole of the eruption may appear within half a day after the 
first papule is developed. The vesicles which in an ordinary case reach 
their maturity by the fourth or fifth day in these cases become fully 
developed in seventy-two hours, and they are often very small. Instead of 
the fluid in the pock becoming cloudy on the fifth day this change develops 
as early as the third or fourth day, and many of the vesicles never become 
pustules but dry up. Those that do develop into pustules reach this con- 
dition by the fifth or sixth day instead of as late as the seventh or eighth 
in the unmodified form of the disease. It is evident, therefore, that, as 
most persons have been vaccinated in all civilized countries, physicians 
will often meet with a modified type of smallpox rather than the severe 
form. 

The temperature in these cases runs a very mild course, often remain- 
ing at the normal point as soon as the rash develops, and never partaking of 
a secondary rise. Indeed, the entire symptom-complex of the illness may 
be of the mildest possible type as to objective symptoms, suffering, or 
discomfort. The appetite is good, the patient sleeps well, no complications 
develop, and convalescence is rapid. 

The important fact to be remembered concerning these mild or modified 
cases is that they are quite as competent to spread the disease as are the 
more severe types of variola, and they require as strict quarantine as any 
severe cases of the disease that may occur. There is therefore every reason 
why a case of varioloid should be quarantined most strictly. 

Even in some cases of modified smallpox, coalescence or confluence takes 
place with associated oedema. In these instances the confluence is not to 
be regarded as a very grave omen, since the pocks mature early, frequently 
do not rupture, and convalescence may begin as early as the eighth or ninth 
day of the illness. 

Smallpox almost never occurs a second time in the same individual. 
In nearly every instance where a second attack is stated to occur, there 
has been an error in diagnosis, either at the time of the first or second 
illness. 

Complications and Sequelae. — When the severity of variola as an infectious 
disease is considered, it is remarkable that it has so few severe complications, 
and, aside from the state of the skin, so few serious sequelae. In some 
instances where the infection of the skin seems to be very severe, multiple 
abscesses may develop, varying in size from a small bean to a large slough. 



VARIOLA 83 

They usually do not appear until after the eruption has passed on to the stage 
of desiccation, but they may persist for a long period of time and so prolong 
the illness. Moore speaks of a case in which a patient who suffered from this 
condition could not be discharged from the hospital until after a period of 
nine months and nine days, because he had forty-two large abscesses follow- 
ing confluent smallpox. The most common seat for these abscesses is upon 
the extremities and about the buttocks and shoulders, and occasionally on 
the scalp. Much more rarely abscesses which are more deeply situated 
form, as, for example, ischiorectal abscess. Such abscesses may produce 
marked systemic symptoms, but ordinarily evidences of septicaemia are not 
severe. 

Occasionally erysipelas occurs as a late complication of the disease, 
either upon the face and scalp or on the scrotum. Under these circum- 
stances it is a most serious malady, and frequently destroys the patient, 
since he has not the vital resistance to withstand the new infection. 

Bed-sores are rare if proper nursing has been carried out, but boils may 
occasionally occur, and are caused most frequently by the Staphylococcus 
pyogenes aureus. 

Gangrene of the skin complicating smallpox is almost unknown. But 
when it occurs it usually affects the scrotum. The eyelids sometimes become 
the seat of abscesses, or more rarely slough, as the result of the swelling and 
oedema, but actual disease of the eyeball complicating smallpox is not 
common. The ears, on the other hand, are not rarely affected, and deafness 
occurs in a certain proportion of cases. When earache is complained of, the 
possibility of an extension of the suppurative process to the mastoid should 
be borne in mind, as this sometimes occurs with serious results. 

So far as the respiratory organs are concerned, it is important to note 
that smallpox sometimes produces laryngitis, varying in severity from a 
catarrhal to an ulcerative type. As in typhoid fever, the development of 
aphonia, due to ulcerative laryngitis, is an exceedingly serious complication, 
since the cartilages of the larynx may become eroded. Bronchitis and 
bronchopneumonia may develop, and occasionally pleurisy results from an 
extension of the infection from the lung or by direct involvement of the 
pleura by pyogenic organisms. 

The circulatory system does not suffer with anything like the degree of 
severity which we would expect. 

Pericarditis and endocarditis are exceedingly rare complications. 

Myocarditis, on the other hand, is more frequently met w T ith as a 
result of the infection, as it is, indeed, in all of the acute infectious 
diseases. 

The kidneys, aside from the ordinary albuminuria of all acute infectious 
maladies, usually escape, as does also the nervous system. That there is 
irritation of the kidneys is evident from the fact that Arnaud, in 1898, found 
albuminuria in 95 per cent, of his cases. 

Septic arthritis occasionally occurs. 

The occurrence of smallpox in a pregnant woman very frequently results 
in abortion, but if the mother goes to term, the child is to some extent pro- 
tected from smallpox, although cases are on record in which children have 



84 DISEASES DUE TO A SPECIFIC INFECTION 

apparently had smallpox in utero, and, extraordinary to relate, there are 
instances reported in which the child bore the eruption at birth, although 
the mother seemingly did not have smallpox. MacCombie even states that 
one case is recorded in which the mother contracted smallpox from her 
newborn infant. 

Diagnosis. — In the later stages of well-developed smallpox there is little 
difficulty in making a positive diagnosis; but in the early stages, when the 
initial skin lesions which have been named are present, the diagnosis may 
be for a time impossible. Indeed, great difficulty may be experienced in 
expressing a positive opinion as to the presence of smallpox, even when the 
papular stage is in its early development. The unusually severe headache 
and backache, with chills, and pain in the epigastrium, are strongly in favor 
of smallpox, particularly if there is a history of exposure to this disease 
within the incubation period already named. The absence of throat symp- 
toms, of enlargement of the cervical and submaxillary glands, and of the 
peculiar coating of the tongue of scarlet jever may enable us to determine 
that the initial scarlatiniform rash sometimes seen is probably to be fol- 
lowed by smallpox, and, furthermore, as has already been pointed out, 
this scarlatiniform rash lacks the punctated appearance of true scarlet 
fever. 

On the other hand, it is to be borne in mind that in persons in whom the 
protective effect of an early vaccination is waning, it not rarely happens 
that true smallpox, or varioloid, develops in so mild a manner as to present 
but a few pocks and very mild systemic symptoms. A similar state may 
also be present in those who possess a natural immunity even if they have 
never been vaccinated. (See Symptoms.) 

When the measles-like rash is present, the absence of the characteristic 
catarrhal symptoms of that disease, with its cough, running at the nose, and 
puffiness of the face, should cause the physician to hesitate in making a diag- 
nosis until a sufficient time has elapsed for the eruption to be well developed. 
The papules which form in measles, while they are often confluent, do not 
possess the shot-like feeling so typical of the early papular stage of smallpox. 
Finally the measles-like rash preceding smallpox disappears in twelve to 
twenty-four hours, leaving no stain on the skin, while that of true measles 
pursues a course lasting several days. (See Measles.) 

Chickenpox is one of the diseases which is most frequently confused with 
smallpox. In this disease, however, the initial symptoms are always mild, 
and the temperature does not rise as rapidly as it does in variola. Then, too, 
in variola, the eruption occurs on the arms and face; whereas, in chickenpox 
it is most abundant on the trunk, and sometimes on the scalp. It is always 
discrete, and it appears in successive groups. The vesicles of varicella, when 
punctured, collapse, since they are unilocular; while, as has already been 
pointed out, those of smallpox are multilocular, and so do not completely dis- 
charge their contents when punctured. The vesicles in chickenpox also reach 
their full development in twenty-four hours, after the appearance of the 
papule; whereas, in smallpox they are not completely developed for five 
days. 

Next to varicella, syphilis may be considered as the disease which most 



VARIOLA 85 

• 

frequently produces confusion in diagnosis, for variola must be separated 
from that form of pustular syphiloderm which is sometimes called variola- 
form syphilide. In most instances pustular syphiloderm is preceded by 
macular or papular syphilitic eruptions, but in certain instances a history 
of these previous eruptions may not be present. Pustular syphiloderm is 
more frequently met with in negroes than in the white race, and occurs, as a 
rule, somewhere between the sixth month and the second year of the syphil- 
itic infection. Important points in the differentiation are that in pustular 
syphiloderm, the patient does not present the well-marked prodromal symp- 
toms of smallpox, such as intense backache, although there may be a 
moderate fever and some pain and aching. Again, in syphiloderm there 
is no marked remission of the temperature such as occurs when the erup- 
tion appears in smallpox, and syphilitic patients presenting such an eruption 
do not, as a rule, appear very ill or have to take to their beds. Further 
than this, the syphilitic eruption comes out in successive crops, is often 
profuse upon the trunk, and the individual pustules never become so large 
and deep seated as do those of variola. Again, they are practically always 
non-confluent. Many cases of syphilitic eruption have associated with the 
vesicles copper-colored papules, which should render the diagnosis easy. 

Drug eruptions, which are sometimes papular and pustular, are differ- 
entiated by the absence of fever and of constitutional symptoms. 

Prognosis. — The prognosis of smallpox differs greatly in different, epi- 
demics and in different individuals. The greatest difference, of course, 
exists between those who are vaccinated and those who are not vaccinated. 
The mortality present in the unvaccinated may be said to amount to nearly 
45 per cent., and in the vaccinated to about 8 per cent. If a patient has 
been vaccinated more than once, the mortality of the disease is wonder- 
fully decreased. Thus, while among those who have been vaccinated once 
the mortality may be 8 per cent., those who have been vaccinated twice have 
a mortality of less than 4 per cent. If the mark of both vaccinations is a 
satisfactory one, the prognosis is exceedingly favorable, for death very rarely 
occurs unless the patient is already suffering from some serious disease 
which has undermined his constitution and therefore aids materially in 
causing death. In most of the instances in which smallpox has occurred 
after even a single vaccination, the vaccination mark has been so unsatisfac- 
tory that there has been grave doubt as to whether the patient has been 
protected at all. 

The age of the patient influences the prognosis materially. It is much 
more grave in early infancy and after thirty years of age, and best at about 
the end of the second decade of life. 

Chronic alcoholism and the presence of any antecedent disease in the 
heart, lungs, or kidneys makes the prognosis more grave. 

Marked severity of onset is an evil prognostic sign, but a mild onset does 
not necessarily promise recovery, for in many instances cases which seem 
mild afterward become severe and fatal. Petechial rashes are always of evil 
import, whereas early maturation of the eruption or an aborted maturation, 
so that it does not go on to pustulation, is a favorable omen. Confluent 
smallpox, if it has not been modified by previous vaccination, is more dan- 



86 DISEASES DUE TO .1 SPECIFIC IXFECTION 

gerous than the discrete form, and varies in its mortality with the age of the 
patient. Young children almost invariably die from it. Older children and 
adults often recover, and it may be said that prognosis is favorable in con- 
fluent cases in direct proportion to the age of the patient until after the 
third decade. 

Great swelling of the hands and feet, associated with salivation and swell- 
ing of the face, in confluent smallpox has long been regarded by physicians, 
who have had a large experience, as possessing considerable prognostic value, 
since if the eruption fails to appear the patient very frequently dies. The 
swelling is, of course, due to non-maturation of the pustules. 

Hemorrhagic smallpox, if at all well developed, always ends in death. 

When death takes place from smallpox, it most commonly occurs about 
the twelfth or sixteenth day, as the result of pneumonia, hypostatic conges- 
tion of the lungs, or from the profound exhaustion and septicaemia. 

Treatment. — As in most infectious diseases, the treatment of smallpox 
consists chiefly in good nursing and the maintenance of vitality by the use 
of proper nourishment and care. The air of the room should be fresh and 
cool, and frequently changed. Draughts should be avoided, and food should 
be given frequently in small quantities. Water should be given freely for 
the purpose of allaying thirst and flushing the kidneys, and there is no 
objection to the patient receiving a small quantity of ice to relieve the 
dry condition of the mouth. If the urine is scanty 5 grain doses of 
citrate of potassium or citrate of lithium should be given every six hours. 
Stimulants are not needed, unless there are evidences of circulatory feeble- 
ness, when alcohol is considered by most practitioners of experience to be 
valuable. Good brandy and whiskey are the best forms of alcohol to 
employ. For the relief of intense nervous irritation, opium or morphine 
may be administered in small doses, particularly if the condition of the 
skin seems to be the chief cause of the patient's suffering. These drugs 
are also, perhaps, the best for the purpose of allaying excessive delirium, 
since they do not irritate the kidneys as do some of the newer hypnotics. 
Where the delirium is active and threatens to exhaust the patient, a hypo- 
dermic injection of J to J grain of morphine will often produce several hours 
of restful sleep, with benefit. 

For the relief of the intense irritation of the skin all over the body, a very 
useful dressing is ordinary carron oil — that is, lime-water and olive oil mixed 
in equal parts. To this may be added 1 per cent, of carbolic acid for its 
local antiseptic and anaesthetic properties, and where great pain is expe- 
rienced, because of the occurrence of the eruption in the thick skin of the 
hands and feet, prolonged hand-baths and foot-baths of lukewarm water 
may be employed, or hot poultices used. An ointment of aristol of the 
strength of one drachm to the ounce may also be used. 

It seems to be generally considered that local applications to the eruption 
are of little value in the sense of modifying its severity, although certain 
parts of the skin which seem to suffer from an excessive degree of irritation 
may be relieved by cool compresses or by the application of antiseptic 
poultices. MacCombie states that the best dressing for the face is a mask 
with holes cut for the eyes, nose, and mouth. Upon this mask is smeared on 



VARIOLA 87 

its inner surface a small linseed poultice, over which is placed some vaselin 
which contains iodoform. This poultice should be changed every two 
hours. It aids materially in separating the crusts, and so leaves the skin 
free for the application of the dressings, which tend to prevent ulceration 
and the formation of scars. The local use of antiseptic drugs to the 
surface of the entire body has not met with favor. 

The mucous membrane of the mouth should be kept cleansed by mouth- 
washes of boric acid or chlorate of potassium and myrrh. When the mouth 
is exceedingly dry, flaxseed-tea, sweetened with a little white sugar and 
acidulated with lemon-juice, may be used. 

The primary fever of smallpox does not last long enough to require treat- 
ment, but the secondary fever may be sufficiently high to demand relief. 
Cold compresses may be applied to the head, and sponging the body 
with cool or tepid water may be employed, but the cold-bath treatment, 
so successfully employed in typhoid fever, has not apparently given good 
results in smallpox, and it is practically never employed. 

Should any irritation or inflammation of the eyes appear, they should be 
carefully washed every few hours with boric acid solution, and, if necessary, 
cold wet compresses should be applied, great care being taken that the 
warmth of the body does not speedily change the cool compress into a hot 
poultice. 

During the suppurative stage, it is exceedingly important that the nutri- 
tion and vitality of the patient be preserved by the frequent administra- 
tion of easily digested and predigested food. 

In considering the general condition of a patient who is suffering from 
smallpox, it must be borne in mind that the disease is essentially one which 
is prone to produce profound toxaemia, since it is incredible that such wide- 
spread infection can take place all over the body without simultaneously 
resulting in septic absorption on the one hand, or profound exhaustion on the 
other. For this reason the degree of suppuration should be controlled as 
far as possible, measures should be introduced to aid in the escape of pus, 
and the treatment should be stimulating and supporting. 

Finally, mention should be made of the so-called red-light treatment of 
smallpox, in which patients are kept in rooms to which no light is allowed 
to enter save through red glass, it being claimed by advocates of this method 
that the severity of the eruption, and so indirectly the severity of the disease, 
is greatly modified,' and, further, that scarring of the skin is diminished. 
Suffice it to state, that while certain European clinicians have claimed to 
have obtained excellent results from this method, Welch and Schamberg in 
Philadelphia, and others, have found it entirely useless. 

There are several points in the treatment of variola which should be care- 
fully avoided. For the relief of the severe backache and headache, counter- 
irritation is sometimes employed in the early stages of the disease. Such 
treatment frequently results in severe ulceration or sloughing of the part 
to which the irritation is applied. Again, the application of powders, anti- 
septic or otherwise, is, as a rule, disadvantageous. The opening of individual 
pocks by means of a needle or the fine blade of a knife is not advisable. 



8«S DISEASES DUE TO A SPECIFIC INFECTION 



VACCINIA AND VACCINATION. 

History. — Little is known of the history of vaccinia, save that it has been 
recognized for many years as a disease which affects heifers and cows, and 
that it causes an eruption to appear on the teats and udder or neighboring 
parts. Although it was known among those persons who milked these 
animals, or otherwise handled them, that the disease could be transmitted 
from the cow to the human being, and although many of these persons also 
knew that this transmission protected the human being from smallpox, it 
was not until Jenner, on May 14, 1796, first inoculated a patient with the 
contents of a cow-pock that the preventive influence of vaccination was first 
tried in a scientific manner. Two years before this an English farmer, by 
the name of Benjamin Jesty, inoculated his wife and two children in a similar 
manner, but at the time no report of the procedure was made. From this 
small beginning so-called vaccination, or the inoculation of human beings 
with vaccine virus, has spread all over the world, and is a well-recognized 
procedure, by which millions of lives have been saved. There are a few 
persons, not medical men as a rule, who still express doubt as to its efficacy, 
but they are not worthy of credence, and the statistics of every civilized land 
prove that vaccination is one of the greatest blessings yet discovered for 
mankind. It is only necessary here to state that vaccination is now ob- 
ligatory in most civilized lands, and that the frequency of smallpox is in 
direct ratio to the laxity with which vaccination laws are enforced. Im- 
mense statistics as to its protective value are to be found in all works on 
public health. 

Vaccination, when properly performed, and when an active vaccine is used, 
may be said to be a sure preventive of smallpox for a very considerable space 
of time, if not for the lifetime of the individual; but it is safer to be vaccinated 
every few years, and every year if exposed during an epidemic. Not only 
does vaccination protect the individual for a long period of time, but it also 
modifies the severity of smallpox if the patient contracts this disease before 
the vaccinia can completely protect him. This has been proved by practical 
experience so often that it is a fact beyond all doubt, and it bears this impor- 
tant truth with it, namely, that when a person who has not been recently 
vaccinated is exposed to smallpox he should be revaccinated at once, since 
if the vaccine fails to confer complete immunity it will modify the disease 
if it develops. The degree of immunity, or the degree of modification, if 
smallpox develops, depends upon the space of time elapsing between ex- 
posure to the smallpox and the vaccination. Further than this, if the patient 
contracts smallpox many years after a vaccination, the severity of the disease 
is usually modified. Thus in 58,278 cases of variola collected from various 
sources, occurring in individuals who had been vaccinated, but in whom 
the "takes" were not known to be good, there were 4872 deaths, a percentage 
of 8.35; whereas in 23,360 cases of variola, occurring in individuals who had 
not been vaccinated, there were 8682 deaths, a percentage of 32.88. 

Method of Vaccination. — The skin on the arm or calf of the leg, having been 
cleansed by washing it with soap and water, is scarified or scratched by a 




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VACCINIA AND VACCINATION 89 

noodle or knife-blade in such a manner as to remove the epiderm and expose 
the true skin over an area of about an eighth of an inch in all directions. Care 
should be taken that the spot is not so deeply scratched as to cause free 
bleeding. Upon this area is now deposited the vaccine, which is then gently 
rubbed into the part and allowed to dry before any clothing comes in contact 
with it. Several forms of vaccine are used, but that most commonly employed 
at present is known as " glycerinated vaccine lymph," prepared from the 
contents of the vaccine vesicles as they have developed on the belly of a heifer. 
This glycerinated lymph is put up in small glass tubes, which are her- 
metically sealed at the ends, so that it may not be contaminated before it 
is used. 

Primary Vaccinia in Man. — Three or four days after vaccination has been 
performed the infected area begins to be slightly reddened, and this red- 
dening increases while at the same time a reddish papule develops which 
by the fifth day begins to look like a vesicle, particularly if the margin of 
the area inoculated be examined. This vesicle increases in size, becomes 
filled with thin, clear lymph, and by the eighth day reaches its greatest 
development. At this time the contained fluid begins to be more opaque 
and yellow and the top of the vesicle is seen to be slightly sunken — that is, 
the early stage of its umbilication has been reached. The skin surrounding 
the vesicle is now surrounded by a zone or areola of red which by the ninth 
or tenth day becomes very well developed, so that it extends for a consider- 
able distance in all directions; the spot inoculated is painful and the neigh- 
boring lymphatic glands may be swollen and tender. At this time, too — that 
is, about the tenth day — constitutional symptoms may come on and the 
patient suffer from moderate chills, a slight rise of temperature, and malaise. 
Sometimes roseola (roseola vaccinosa) may develop over the body. By the 
eleventh or twelfth day these symptoms are modified, the vesicle begins 
to desiccate, and by the end of the fifteenth day it is completely dried up, 
although the scab may not fall off till the twenty-first or twenty-fifth day. 
The crust or scab is dark red in color and thin at its centre and at its edges, 
but there is a thickened area, or ridge, between the centre and the periphery. 
After the crust falls off it leaves a pink spot which gradually fades and 
leaves, after some months, a foveated or pitted mark from which small scars 
may radiate. It is to be borne in mind that in some cases the constitutional 
symptoms are so mild as not to be worthy of note, while in others they may 
be quite severe. To be a true ''take," the full development of the pock by 
the stages named is essential, but it is possible for the "take" not to ensue 
for a month after inoculation. (See Plate II.) 

Secondary Vaccinia in Man. — Very few persons who have once been 
successfully vaccinated present the conditions just described when inocu- 
lated a second time. It is this variation from the appearance of true primary 
vaccination that has led to much misunderstanding in secondary cases. 
In other words, the secondary vaccination of a person who has lost the pro- 
tective effect of the primary attempt may in its effects be very like primary 
vaccination, but usually it is so greatly modified as to be very different in 
its appearance. The difference, however, is one of degree, not one of kind, 
and vesiculation and umbilication should appear in all cases. 



90 DISEASES DUE TO A SPECIFIC INFECTION 

It is a point worthy of note that the so-called " raspberry excrescence " 
which sometimes follows vaccination on the fourth or fifth day, looking 
like a small mevus, is not a vaccine pock and confers no immunity to small- 
pox upon the patient — that is, it is not to be considered as a "take." Care 
must be taken, too, that the sore or mark produced by the injury of the 
operation be not taken for the specific lesion of vaccinia. 

Children should always be vaccinated during the first year of life, or 
immediately after birth, if exposed to smallpox. Vaccination should be 
repeated through life every five years and oftener if smallpox is prevalent. 
If one inoculation fails it should be repeated at least three times, since 
sometimes primary failure is due to poor vaccine or to an error in technique. 
If after three attempts no "take" is produced the patient may be considered 
as immune, at least for a time. 



VARICELLA. 

Definition. — Varicella is usually called chickenpox. It is an acute infec- 
tious disease which usually occurs in children under ten years of age, and 
rarely attacks individuals after puberty. In adults it is still more uncom- 
mon, although Tyzzer reports 38 cases occurring in adult male Filipinos 
and states that at the time of the last observation 300 cases had been re- 
corded. The men were prisoners, and this, together with race and climate, 
are considered possible factors in increasing susceptibility. In all proba- 
bility one of the reasons for its rarity in those of mature years is that it 
affects so large a proportion of all children that most adults are rendered 
immune by an attack in childhood. The most marked characteristic of the 
disease is the appearance within the first twenty-four or forty-eight hours of 
fever and malaise and of papules, followed by vesicles, upon the skin of 
the forehead and face or upon the chest and back. (See Fig. 20.) 

Etiology. — Like all acute infectious diseases, chickenpox is produced by 
a micro-organism, but as yet it has not been isolated. Tyzzer found 
specific nuclear and cytoplasmic inclusions in all the lesions, but obtained 
no evidence favoring the hypothesis that they are parasites. It also resembles 
the other acute infectious eruptive diseases in that it occurs in epidemics, 
although at times isolated cases take place that cannot be traced to any 
source of contagion. While the eruption in its peculiarities resembles to 
some extent that caused by smallpox, chickenpox bears absolutely no rela- 
tion to that malady and in no way protects a patient from developing a 
typical attack of variola. (See Variola.) 

Symptoms. — At a time varying from ten to fifteen days after exposure 
to varicella the child usually manifests some evidence of a beginning illness. 
If very young it may be unusually restless and fretful, there may be some 
disorder of the digestive apparatus, and vomiting may occur. Fever is an 
early symptom and it may be moderately high — that is, about 103° or even 
104°. Often, however, it fails to reach such a height. If the child is old 
enough to describe its sensations, some aching in the back or in the limbs 
may be complained of. 



VARICELLA 



91 



After about twenty-four hours the eruption appears in the form of red 
papules, which speedily become vesicles containing clear or turbid serum. 
The vesicle is superficial, it is not surrounded by a zone of induration, as 
it is in smallpox, and it does not become umbilicated, although the top of 
the vesicle, when it is ripe, may be flattened. By the end of thirty-six to 
forty-eight hours the vesicle becomes a true pock, the previously clear serum 



Fig. 20 




Chickenpox. (Schamberg.) 

becoming opaque but not purulent unless it is denuded by scratching, and 
then infected. These pocks speedily shrivel and by the fourth day form 
crusts, which readily fall off and rarely leave a scar unless the skin be 
scratched by the child so that the deeper layers become infected. Many 
individuals bear scars of this sort upon the face, and they are particularly 
well marked in women with a fair skin. 



92 DISEASES DUE TO A SPECIFIC INFECTION 

The eruption of chickenpox develops in a series of crops, or, to speak 
more accurately, it continues to develop in new areas as those which were 
affected first begin to pass into the stage of crusts. An examination of the 
patient on the third day may therefore reveal the eruption in all stages of 
development. 

It is a noteworthy fact that the eruption of varicella is always discrete 
and never confluent. It is never profuse as in smallpox. Rarely the vesicles 
appear on the mucous membranes. 

The severity of the fever and of the signs of general illness vary greatly 
in children affected by varicella. In some cases the disease runs so mild 
a course that the child is not kept in bed, in others it causes a considerable 
degree of illness; but in the majority of instances it is a very mild malady. 
In children who are weakened by previous disease it sometimes develops 
into a dangerous malady in that the associated digestive disturbance still 
further impairs vitality, or because the lesions of the skin become infected 
and sloughing or gangrene appears. Sometimes erysipelas is developed 
in this manner in poorly nourished children. Rarely, if the child is exposed 
to cold, nephritis develops. Allaire reports peripheral neuritis cf the left 
arm following an attack of varicella in a child aged eight years, the pocks 
having suppurated. 

Diagnosis. — The eruption of chickenpox must be separated from that 
of modified or mild smallpox. The most important factors in this separa- 
tion are the superficial character of the pock, the lack of the sense of indura- 
tion when it is taken between the thumb and finger, the early appearance 
of the rash on the chest rather than on the forearms, as in smallpox, and 
the mild character of the general symptoms, combined with the brief course 
of the disease and the speedy completion of the illness. 

Additional diagnostic factors are the presence of a good vaccination 
mark which largely excludes variola. Again, the onset of varicella is usually 
devoid of prodromes, whereas smallpox presents for some days backache, 
vertigo, fever, nausea, and chills. The mere fact that the eruption is scanty 
does not, however, exclude smallpox. The vesicles of varicella do not become 
umbilicated as do those of variola, but they rapidly dry up and make a 
dark-colored scab. The eruption of smallpox comes out in one crop, that 
of varicella in several crops ; that of smallpox lasts from ten to twelve days 
in typical cases, never less than six days, whereas chickenpox lasts but 
from two to four days. 

Prognosis. — The prognosis is always favorable unless the unfavorable 
preliminary states just noted are present. 

Treatment. — Medicinal treatment of varicella is usually unnecessary. 
Careful nursing that prevents exposure to cold and wet, regulation of the 
diet, and the use of a few drops of sweet spirit of nitre in a teaspoonful of 
liquor potassii citratis every four hours, to keep the kidneys active, are all 
that is needed in most cases. The fever runs so brief a course that anti- 
pyretic measures are not necessary. 



SCARLET FEVER Q;> 

SCARLET FEVER. 

Definition. — Scarlet fever is an acute infectious disease which chiefly 
affects children under fifteen years of age. It is characterized by the devel- 
opment of an intensely scarlet, punctated rash on the second day of the ill- 
ness, accompanied by a marked febrile movement. It is sometimes called 
" scarlatina,'' and it is to be clearly understood that this word is synonymous 
with scarlet fever and that it does not describe a modified or diminutive 
form of the malady, although the laity often employ the term in this 
manner. 

History. — Hirsch states that the oldest reference to an epidemic of scarlet 
fever dates from Sicily in 1543, but Sydenham, of London, first differen- 
tiated it from measles. Prior to his time it had been considered a form of 
measles. 

Distribution. — Like almost all of the acute infectious maladies, scarlet fever 
occurs in all parts of the world, although it seems to be much more prevalent 
in the temperate zone than elsewhere. In the United States it occurs less 
frequently in the Southern States than in the Northern States. It did not 
develop in the United States until 1735, nor in South America until 1830. 
In Australia and in Polynesia the disease first appeared in 1848, assuming a 
mild type but a severe epidemic occurred in Melbourne in 1876. It is said 
that only imported cases are met in India, and only one case has been reported 
in Greenland. It does not occur nearly so frequently as does measles, and 
very many persons reach adult life without having suffered from it. This 
is in part due to the fact that it is not so readily transmitted as some of the 
other acute infectious fevers, and also because a large number of persons 
seem to be resistant to the disease. Johannessen states that of 185 children 
exposed only 28 per cent, developed scarlet fever, and out of 314 adults 
exposed only 5 suffered from the malady. If the same number of cases 
had been exposed to the infection of measles, very few of the children 
would have escaped. 

Scarlet fever is more apt to occur in the winter months than at any other 
time, but statistics differ as to the winter months' frequency. Thus, White- 
legge from his statistics based upon cases occurring in nine English towns, 
found in the first quarter 219 cases; second quarter, 194; third quarter, 327; 
fourth quarter, 460; and Reece has supported his conclusions by the accom- 
panying chart. (See Fig. 21.) 

On the other hand, Seibjrt, of New York, gives a statistical table which 
shows that the last winter months are those of greatest frequencv. (See 
Fig. 22.) 

August Hirsch gives the following statistics based on an analysis of 435 
epidemics occurring in all parts of Europe and North America: 178 epi- 
demics occurred in winter; 157 in spring; 173 in summer; 213 in autumn. 

The frequency and mortality of scarlet fever have greatly decreased in the 
last sixty years. (See Fig. 23.) 

Etiology. — Scarlet fever does not disseminate itself through the air as does 
measles; direct contact or near association with the infected person, or with 



94 



DISEASES DUE TO A SPECIFIC INFECTION 



the desquamated scales from his skin, being needful for the transmission of 
the disease. The disease can be transmitted by the nasal mucus, clothing, 
and other articles which have been in contact with the patient. Thus books, 
cards, letters, and pets, such as dogs and cats, and other means of convey- 



Fig. 21 

Per cent 
+ 70 
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+ 50 
+ 40 
+ 30 
+ 20 
+ 10 
Mean 

- 10 

- 20 

- 30 

- 40 

- 50 
Showing seasonal mortality of scarlet fever in all ages and both sexes in England 

and Wales. (Reece.) 

ance may assist in spreading the infection. The clothing of the nurse and 
physician may convey the disease, and cases are very numerous in which 
physicians have so communicated scarlet fever to their own children after 
visiting patients ill with this malady. 

Fig. 22 



Jan. 


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The persistence of the infection in articles of clothing is very remarkable. 
No other acute disease renders the surroundings of the patient a source of 
danger for so long a period. Instances in which clothing or upholstered 



SCARLET FEVER 



95 



goods have transmitted the disease to healthy children two years after 
recovery of the first patient are recorded. 

The breath of the patient and the air of the bed-room are probably incap- 
able of transmitting the infection, unless the latter is laden with the dust 
containing the micro-organism. It is noteworthy that nurslings are not 
as susceptible as children of from two to five years, at which period of 
life the disease most often occurs. The age incidence is well shown in 
Fig. 24. 

A patient who is a sufferer from the infection of scarlet fever is not capable 
of transmitting the disease until the rash develops. At the fourth or fifth 
day of the disease the infectiousness of the case is perhaps at its height, 
and the ability to transmit the malady exists as long as the skin of the 
patient continues to desquamate, which is often for as long a period as 
six weeks. It is important to remember that not only the desquamating 
skin, but the nasal mucus, the discharge from a purulent otitis media or 



Fig. 23 



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Showing the decreasing mortality of scarlet fever in England and Wales. Deaths per 100,000 
population. (Modified from Wilson and Reece.) 

from a chronic consecutive scarlatinal pharyngitis are also active sources 
of infection, and until all these parts are entirely healthy the danger of 
spreading the disease exists. Indeed, numerous instances are recorded 
in which children with such mild consecutive pharyngitis as to escape 
notice have conveyed the disease several weeks after apparent complete 
recovery from scarlet fever. 

Articles of food may also convey the infection. Thus Ekholm has 
recently reported an instance in which six families who partook of milk 
from a dairy in which there was a milkmaid who had a phlegmonous 
pharyngitis, suffered from scarlet fever. 

Many investigators have endeavored to isolate the specific micro- 
organisms of scarlet fever, but without success. Loeffler, Fraenkel, and 
other German physicians first demonstrated the presence of streptococci 
in cultures prepared from secretions taken from the throats of scarlet fever 



90 



DISEASES DUE TO A SPECIFIC INFECTION 



patients, but their observations were limited to a small number of cases 
and are of interest from an historical rather than a practical standpoint. 
The same statement may be made concerning the researches of Klein in 
connection with an epidemic of scarlet fever (1885) caused by contaminated 
milk from a farm at Hendon, in England, for although Klein cultivated a 
micro-organism from lesions on the udders and teats of cows on this farm, 
which apparently was identical with one he found in the blood of scarlet fever 
patients, and although this latter organism when injected into calves pro- 
duced a lesion resembling the one with which the Hendon cows were affected, 
the inquiry instituted by the Medical Society of Edinburgh and the investiga- 

Fig. 24 



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Showing- age incidence of scarlet fever based on 7470 cases, and representing the combined 
statistics of Whitelegge, Ballard, and Keen. 



tion of Dr. Crookshank, of London, proved that the disease from which the 
cows suffered was a modified form of cowpox, and, moreover, that the persons 
who milked the cows did not contract scarlet fever. A similar history as 
to cows and patients has recently been recorded in Lincoln, England. In 
1891 Kurth found in the throats of scarlet fever patients, in pus from the 
cervical abscesses and in the viscera of persons who had died from scarlet 
fever, a streptococcus which formed a twisted, gelatinous mass when grown 
in broth. This organism, called by Kurth Streptococcus co?iglomeratus, was 
subsequently studied by Mervyn Gordon, who found it present in the 



SCARLET FEVER 97 

throats of twenty out of twenty-seven scarlet fever patients, in the internal 
organs of most patients who died from the disease, and in the fluid of a 
scarlatinal pleural effusion. Baginsky and Sommerfield, who published 
the results of their investigations at about the same time as Gordon, found 
a streptococcus, having virulent properties and generating a toxin, in all 
cases of scarlatinal angina, and in cultures made from the viscera, bone- 
marrow, and blood of one hundred and forty-two children in whom the 
disease terminated fatally. This streptococcus they considered to be the 
specific organism of scarlet fever. 

Of the work done by American bacteriologists that of Class, of Chicago, 
should be mentioned. In 1899 Class noticed the frequent presence of a 
diplococcus in cultures made from the throats of patients having different 
forms of angina, and upon further investigation he found that the organism 
invariably occurred in cases of scarlatinal angina. He then made cultures 
from the blood of scarlet fever patients and from desquamated epidermal 
scales, and found the same diplococcus. Gradwohl, of St. Louis, and 
Calvin Page, of Boston, have also found an organism identical with the 
one described by Class, but their observations w r ere confined to a small 
number of cases. 

From this brief resume of the bacteriology of scarlet fever, it is apparent 
that streptococci are generally present in the throat of scarlet fever patients, 
and that they are often found in the blood and internal organs; but when 
we come to consider that streptococci have been found in healthy throats, 
that cases of streptococcic angina exist independent of scarlet fever, and 
that streptococci are found in the blood in other diseases, it is not justifiable 
to assume that any one of the forms thus far described is the specific organism 
of scarlet fever. Closely associated with the specific germ of scarlet fever, 
whatever it may be, we alw T ays find a variety of the streptococcus, and it 
has been claimed by some that this is the cause of the disease. There can 
be no doubt that it is responsible for a large number of the symptoms and 
complications of the disease. 

Mallory has recently described a parasite of the animal group — a pro- 
tozoon — which he suggests may be the cause of the disease. He suggests 
the name Cyclasterion Scarlatinalis for it. 

Prevention or Prophylaxis. — Every case of scarlet fever should be promptly 
isolated and every attendant of the patient should also be prevented from 
mingling freely with the inmates of the house. The food should if possible 
be placed in an outer room and from there obtained by the nurse for the 
patient. If the nurse is to leave the room her clothes should be changed. 
Before she leaves the convalescent patient to take care of other cases she 
should take a hot bath and have her hair shampooed. The clothing she 
has worn in the sick-room should be sterilized by boiling. The physician 
should always change his clothes on entering and leaving the room, or at 
least wear over his street dress a long operating gown to protect him from 
the infection. If he is attending, or about to attend, a case of confinement 
he should refuse to take charge of a case of scarlet fever. The same rule 
holds true as to operative cases. 

All clothing and bed-clothing should be immersed in boiling water, or in 
7 



98 DISEASES DUE TO A SPECIFIC INFECTION 

a disinfectant solution, before they are taken from the sick-room, and books 
and cards which have been in the patient's room should be burned. If 
possible it is better to burn the pillows and mattress than to attempt to 
disinfect them. If they are disinfected, steam should be used for this 
purpose. The hanging of sheets saturated with disinfectant fluids over 
doorways and the placing of pans of disinfectants about the house are 
utterly useless except that their presence constantly reminds the inmates 
or visitors that an infectious disease is present and so aids in the main- 
tenance of caution. An amount of disinfectant in the air sufficient to 
destroy the contagium will destroy the patient and nurse. After the illness 
is over and the patient has left the room, it should be carefully disinfected 
by an adequate formaldehyde generator, the floors and walls being first 
moistened with water to aid in the efficiency of this gas. Afterward the 
floors and walls should be scrubbed with 1 : 2000 bichloride solution or one 
of chlorinated lime. 

No case should be isolated less than four weeks, and no case should be 
allowed to mingle with other persons as long as desquamation or nasal, 
aural, or pharyngeal discharges exist. Before the patient is discharged he 
should receive at least three hot baths, after each of which he should be 
scrubbed with carbolic acid and water (1 : 100) or with bichloride solution 
(1 : 4000). Particular attention should be paid to the scalp and hair. Sleeping 
with other children is to be prohibited for several months. 

After exposure a child should be placed in quarantine for at least a week 
to discover if the disease is to develop. When an epidemic is present all 
schools should be closed. 

There can be no doubt that the use of inunctions of carbolized oil or 
vaselin is an active agent in diminishing the spread of the disease, particu- 
larly during desquamation, but great care must be taken that the acid is 
not too freely used, lest it be absorbed and increase or produce renal irrita- 
tion. In many instances ordinary olive oil is equally useful. 

Pathology and Morbid Anatomy. — A point of primary importance to be 
borne in mind in considering the pathology of scarlet fever is that the organs 
of the body suffer from a multiple not a single infection. Whether a special 
form of streptococcus is the cause of the disease, or whether an entirely 
distinct organism is the cause, the fact is that the disease is accompanied 
by streptococcus infection in all cases and not rarely by other forms of 
infection as well. 

The organic changes produced in the body by an attack of scarlet fever 
are marked, but none of them can be said to be characteristic of the disease. 
Alterations in the skin and inflammation of the mucous membrane of the 
mouth and pharynx are the most constant changes, but even these may 
escape notice. The skin is the seat of a very acute inflammatory process 
involving to a varying degree all its layers and terminating, even in mild cases, 
in exfoliation of the superficial cells, often in large flakes. The pharyngeal 
mucosa is inflamed, the inflammation varying in degree from a mild acute 
attack to extensive necrosis involving the deeper strata of the uvula and 
tonsils. This inflammation in a modified form extends at times all the 
way down the oesophagus and by way of the Eustachian tube into the 



SCARLET FEVER 99 

middle ear, where it not infrequently causes so destructive a change as to 
produce permanent deafness; or if the infection be severe and no vent for 
the pus is afforded the mastoid cells become involved and, finally, a second- 
ary meningitis, or abscess of the brain, is produced. This is a rare sequel. 
In still other instances the inflammatory process extends into the nasal 
cavities and from them proceeds to an infection of the antrum of High- 
more or even the frontal sinus. Extension of the pharyngeal lesions to 
the lymphatics of the submucosa may cause infection of the cervical 
and submaxillary lymph nodes, so that there is developed great swelling 
under the jaw, and in some instances suppuration, the so-called "collar 
of brawn." 

Equal in frequency with these changes, and of more importance, are those 
which take place in the kidneys. These changes not only endanger the life 
of the patient during the illness, but occasionally leave him with kidneys 
structurally so impaired that complete restoration to health may never take 
place. The renal changes are primarily those of an acute diffuse nephritis 
involving the whole texture of the kidney, particularly the cortex, and accom- 
panied by marked albuminuria, intertubular cellular infiltration and necrosis, 
and desquamation of the epithelium lining the tubes. Areas of necrosis 
and infarction and even acute suppurative nephritis occur, although infre- 
quently. 

When the infection with the streptococcus is particularly severe and the 
evidences of toxaemia are profound the autopsy reveals degenerative changes 
in the heart muscle, areas of necrosis in the liver, and bronchopneumonia 
with swelling and softening of the bronchial glands. Degenerative or 
necrotic changes in the myocardium and endocarditis, vegetative or ulcerative, 
may be present. Pericarditis may be marked. As in all septic infections 
arthritis may be found in numerous joints. Pleurisy, if present, often 
results in empyema. 

With the onset of scarlet fever there develops a hyperleukocytosis 
amounting according to Tileston and Locke to from 18,000 to 40,000. 
After the eighth day, if there are no complications of an inflammatory 
nature, there is a gradual decline to the normal, somewhere about 6000 
to 8000. The increase is chiefly in the polymorphonuclear cells. 

Incubation. — The period of incubation of scarlet fever is about two to 
six days, but cases are recorded in which it has been as brief as twenty-four 
hours and as long as twenty-one days. Reimer gives the following figures: 
1 day, 379 cases; 2 days, 928 cases; 3 days, 751 cases. The period of 
incubation is, therefore, the shortest of all the acute exanthematous fevers. 

Symptoms. — The symptoms of an ordinary case of scarlet fever chiefly 
consist in sore throat, a moderately high jever, a scarlet rash first appearing 
on the chest, albuminuria of moderate degree, and a tendency to middle-ear 
inflammation. 

The onset of the symptoms in scarlet fever is usually abrupt and the 
severity and abruptness of these symptoms is often indicative of the 
severity of the attack which is to follow. A child apparently in good health 
in the evening passes a restless night, and in the morning suddenly, 
without apparent cause and perhaps without preliminary nausea, vomits 



1()0 DISEASES DUE TO A SPECIFIC INFECTION. 

actively as soon as its breakfast is swallowed. If the temperature is taken, 
it will usually be found to be 101° or 103°, the skin feels hot and dry, the 
pulse is quick, the eyes bright, the expression listless, and the tongue and 
mucous membrane of the mouth distinctly reddened. Sometimes the first 
complaint on the part of the patient is one of sore throat, in other cases 
no such discomfort is mentioned; but if the mouth be opened the pharyn- 
geal mucous membrane is seen to be angry and inflamed, and perhaps 
unduly dry. The child is manifestly ailing, is peevish, and is anxious to 
lie down. In from twelve to twenty-four hours from the manifestation 
of the preliminary symptoms just detailed, and in some cases in even 
less time than this, the eruption, or rash, develops, beginning on the neck 
and upper part of the chest, as a rule. 

No one of the eruptive diseases is so characteristic in its appearance 
as is scarlet fever, the skin of the patient being, as the name of the 
disease indicates, actually scarlet or as bright a red as is the shell of a 
boiled lobster. Again, in no other one of the eruptive diseases does the 
rash appear over so wide a surface in the first hours of its appearance as in 
scarlet fever. Not rarely the entire body and extremities are involved in 
four or five hours. 

There are four peculiarities about this rash which are worthy of note : 
first, it is punctate — that is, about each hair follicle in the skin the color 
is slightly deeper than elsewhere; second, the rash is often most marked 
in the folds of the joints, as about the groins; third, the skin of the face 
about the mouth or in the nasolabial line is pallid, forming a marked 
contrast to the scarlet hue elsewhere; and fourth, the rash on the upper 
part of the thorax is often very profuse. 

When the rash is developed, the sense of heat conveyed to the hand and 
complained of by the child is notable. The eruption persists from three to 
seven days in the majority of cases, and ends in desquamation of the epi- 
derm, which comes away in large flakes, rather than in fine bran-like scales. 
The skin may literally peel off the hands and feet. In rare instances it may 
be shed from the hand in the shape of an old glove. This desquamation lasts 
from a week to three weeks, beginning about the neck and continuing longest 
on the palmar and plantar surfaces, where the skin is thick. Indeed, I have 
seen it continue between the toes for six or eight weeks. The period of 
desquamation is, however, greatly shortened, as a rule, if during the illness 
the child has been anointed by some oily substance to allay dermal irritation, 
or if during convalescence it is frequently bathed. As long as desquamation 
lasts there is danger of the spread of the disease from the patient. 

The stage of invasion, already described, varies in certain cases to a consid- 
erable degree. It may be so mild as to lead to a belief that the rash is due to 
indigestion, and it may be so severe that the patient is first convulsed, and 
then speedily overwhelmed by toxsemia. The eruption may not be widely 
diffused, but appear for a short time on the chest and abdomen, in the groin, 
or about the buttocks before it spreads elsewhere. It may not spread farther 
than these areas, and may last only one day. Such cases are often given 
the unfortunate name of "scarlet rash." They are just as capable of giving 
scarlet fever to another child as a more severe attack. In other cases, of a 



SCARLET FEVER 



101 



malignant type, the rash seems to be suppressed, the skin is mottled, but the 
true rash fails to appear, or it may appear in blotches, which may seem to 
be macular, as in measles. When doubt exists in such cases, the patient will 
be benefited and the diagnosis cleared by a hot bath or hot pack to stimulate 
the peripheral circulation and bring out the rash. 

The temperature in scarlet fever runs its course side by side with the 
severity of the disease. It reaches its acme within a few hours from the 
onset, and is often as high as 105° within twelve hours. As a rule, this 
height is not maintained, but after twenty-four hours to three days it falls 
gradually to about 103°, and then gradually decreases daily by lysis, reaching 
normal, as desquamation begins, about the eighth or ninth day (Fig. 25). If 
it remains high or if a recrudescence occurs, some secondary trouble, such as 
middle-ear disease or bronchopneumonia, is to be sought for. 















Fig. 


25 
















DAY OF 
DISEASE 


1 


o 


3 


4 


5 


6 


7 


8 


9 


10 


11 


12 


18 


14 


15 


io5 c 
io4 c 
io3° 

I02° 
IOI° 
IOO c 

99 c 

NORM'L 
TEMP.. 

^8- 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 




/ 


A 


























/ 


\/ 


V\ 


A 






























V 




n 




























1/ 


J 






























1/ 


/ 






























V 


\A 


/ 


A 


A 










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.... 




— 






V- 


Y- 


/ 


Y- 


'/■ 















Chart of scarlet fever. 



In the stage in which the disease is fully developed the clinical picture 
presents very great variations in different cases. In some children with a 
well-developed rash, the systemic symptoms are so mild that it is difficult to 
keep the patient in bed, and all the manifestations seem of little moment. 
In others the general symptoms are sufficient to show that the child is seri- 
ously ill, and in still others of a severe type the systemic state may be one 
of deep toxaemia, so that the child seems overwhelmed by the infection. The 
cases in which toxsemia is marked are not necessarily those in which great 
glandular involvement is present, although both sets of symptoms may 
occur simultaneously. 

Sometimes the throat symptoms by their severity mask all others. Not only 
may the pharyngeal and tonsillar surfaces be ulcerated, but they may be cov- 
ered by a false membrane, which, in some cases, is due to a concurrent diph- 
theria, but which may also be due to the streptococcus, and is always poly- 
microbic in nature. Such cases often present a horrid type of the disease, 
for the lips and teeth are covered with sordes, the tissues of the neck are 
infiltrated and swollen, and the head thrown far back to diminish pressure 
on the air-passages produced by the swelling. In such cases the general 
infection extends rapidly into the chest, and bronchial or pulmonary symp- 
toms develop with great rapidity, thereby causing a fatal issue, although 
even with these grave complications recovery sometimes takes place. 

If to these malignant manifestations are added a tendency to suppression 



102 DISEASES DUE TO A SPECIFIC INFECTION 

of urine, because of the Intense nephritis which has been produced, the signs 
of toxaemia deepen into stupor and death ensues. Cases of this type rarely 
die before the sixth or twelfth day, since this time is required to develop the 
condition described. There is, however, a fulminant form of the disease 
in which the malady, after being ushered in by severe convulsions, 
speedily develops into deep stupor, with hyperpyrexia and death. In 
some of these cases, however, the infection is so profound that a high 
temperature does not occur, the temperature never rising above 101°. 
These cases are very rare and are described more frequently by French 
clinicians than they are seen by Anglo-Saxon practitioners. 

A few cases are on record in which no fever has developed, and others 
in which no rash has been seen. 

Under the name "surgical scarlet fever" is described a febrile affection 
which attacks persons, usually children, after surgical operations or injuries. 
The term is an unfortunate one, for no such malady exists as a distinct 
disease. The condition is an erythema due to sepsis or else it is an attack 
of scarlet fever coming on during convalescence from the operation. 

Complications and Sequelae. — Scarlet fever depends very largely for its gravity 
upon its complications and sequelae, which are not rarely met with. The 
most constant of these is a certain degree of renal irritation or inflammation. 
The condition of the kidneys from a time very early in the attack is such that 
slight albuminuria may be considered a fairly constant symptom. In some 
instances this febrile albuminuria is the only evidence that the kidneys are 
affected, but in others the character of the urine and the general systemic con- 
dition render it very plain that a true nephritis is present. Not only does the 
urine of such patients show considerable quantities of albumin and casts, 
but there is distinct puffiness of the eyelids and oedema of the ankles, or even 
a generalized anasarca. In such patients, if this state persists, transudation 
may take place into the serous cavities of the body,and the patient suffers from 
the pressure produced by the fluid upon the heart and lungs. He may develop 
uraemic symptoms, and these in turn may cause death. In many of these 
cases, however, the acute nephritis, responsible for these manifestations, 
speedily diminishes with the subsidence of the disease itself, and recovery 
follows with a rapidity which is extraordinary. I have seen recovery take 
place, even after the anasarca was so marked as to almost close the eyes and 
after repeated severe ursemic convulsions. 

Suppression of urine may be the first symptom. 

There is still another type of renal disorder met with in a few cases of 
scarlet fever in which the infection seems so intense that the kidneys are 
completely suppressed in their functional power very early in the attack, and 
in which we find great diminution of urinary flow, hematuria, and copious 
amounts of albumin and casts. In these cases the toxaemia of the disease 
and that resulting from the renal lesions produces death in a very short time. 

The renal changes of scarlet fever are, therefore, to be carefully watched, 
and the greatest care must be taken that the kidneys are not permitted to be 
additionally congested by the patient being chilled. Exposure during and 
soon after scarlet fever may change a mild renal state into a most desperate 
condition. 



SCARLET FEVER 103 

As a sequel, rather than a complication of scarlet fever, inflammations of 
the joints sometimes occur. This is not acute rheumatism, but of the nature 
of a septic arthritis. Rarely the joint suppurates. The swelling does not 
persist, as a rule, if the effusion be simply serous. Another very rare sequel of 
scarlet fever is dislocation of the hip-joint. In 1804 J. Franck reported a case 
of dislocation of the hip occurring in an attack of scarlet fever. In 1894 
Champenois published anaccount of three other cases, which were all he could 
collect from the literature. Since 1894 H. Stanfield Collier has reported two 
cases. Robert Jones, of Liverpool, states that one such case has come under 
his observation. 

Much more common than arthritic changes during or after scarlet fever 
are those which are met with in the ears, due to an extension of the septic 
inflammation from the throat through the Eustachian tube to the middle ear. 
These have already been referred to when considering the pathology of the 
disease. The physician should always be on his guard for aural inflamma- 
tion in the course of this malady and after it has run its course. Permanent 
deafness not rarely results from the otitis media due to this cause. 

Parotitis sometimes occurs as a complication. 

Next to acute articular rheumatism, scarlet fever stands as the most 
common of all the acute infections in producing valvular disease of the heart. 
These changes are in the endocardium and myocardium, and may be 
acute and transient or become permanent. Very rarely does the endo- 
carditis become severe enough to be called ulcerative. Great responsibility 
rests upon the physician in regard to the cardiac- changes in this disease, 
because, while it is true that he cannot prevent them, he can, by insisting on 
rest during the attack and during convalescence, to a large extent, limit their 
severity, both as to their temporary and permanent character. This is the 
more important, since, as in all acute infections, the heart is often the seat 
of a myocardial change. 

Bronchopneumonia develops in a small proportion of cases. Empyema 
may be a sequel of scarlet fever, and is usually insidious in onset. 

The induration of the cervical glands, which may suppurate, has already 
been referred to. 

Nervous complications of scarlet fever, aside from delirium and convul- 
sions due to the toxaemia, are rare. As a sequel, chorea may develop, or hemi- 
plegia arise, caused by an embolus lodging in a cerebral vessel. Very rarely 
an acute ascending paralysis, which is the result of neuritis, may develop in 
the lower limbs. 

An exceedingly rare complication of scarlet fever is peritonitis, due in all 
probability to a streptococcus infection of the peritoneum. McCollom and 
Blake, of Boston, have reported two such cases in the Boston City Hospital 
Reports. 

Diagnosis. — While scarlet fever in its typical development is not difficult 
of diagnosis, it not infrequently happens that mild attacks render a decision 
as to the exact nature of the illness most difficult to determine. The chief 
reason for this is that children very commonly, and adults more rarely, 
develop a roseola or rose rash as a result of many different causes, and if 
the manifestation of scarlet fever be mild, or the rose rash be severe, the skin 



104 DISEASES DUE TO A SPECIFIC INFECTION 

lesions may not only not aid in diagnosis, but greatly impede the physician in 
reaching a decision. The most common of these rose rashes is that pro- 
duced by certain types of indigestion, and particularly that which follows 
eating fish, shell-fish seeming especially prone to cause it. As active vomiting 
and diarrhoea and even fever may be present in such cases, the patient at 
first sight quite markedly resembles one suffering from scarlet fever; but the 
absence of sore throat, of enlarged tonsils, of enlarged cervical glands, and 
of a history of no exposure to the specific fever, all aid in excluding scarlatina, 
particularly if it can be discovered that indigestible food has been ingested. 
Then, too, the rose rash of indigestion does not, as a rule, appear first on the 
chest. In some persons, with a very sensitive skin, contact with nettles or 
other irritants may cause a roseola. In all such cases the physician should 
not be hasty in making a diagnosis, but insist that enough time be given to 
permit him to make a careful study of the case for several days before express- 
ing an opinion. In such instances the patient should be isolated until 
the diagnosis is decided. 

The rose rash sometimes met with in German measles is never as scarlet 
as it is in true scarlet fever and is distinctly maculated. Further, it appears 
on the face before it is seen on the chest, the punctation of the rash of scarlet 
fever is absent, the fever is slight and lasts but two or three days, and flaky 
desquamation does not occur. 

Roseola due to vaccination and that due to the use of diphtheria antitoxin 
are easily diagnosticated by the history of the patient. 

Should a rose rash with fever develop in an adult there is much more like- 
lihood of its being due to early secondary syphilis than to scarlet fever. The 
rose rash of syphilis is not, however, so bright a red as that of scarlatina. Such 
a rash, when due to syphilis, disappears and reappears, becomes dusky, and, 
finally, it is apt to be circinate. 

Sometimes in acute and chronic nephritis not due to scarlet fever a rose 
rash develops. The absence of throat symptoms and the signs of nephritis 
revealed by the urine aid in the differentiation. 

A condition called " erythema scarlatiniform" has a sudden onset with 
fever, and is characterized by a rash which develops rapidly over the 
whole body, lasts for several days, and ends in desquamation. The absence 
of throat symptoms in these cases is once more an important differential 
point. Further, the other symptoms are by no means so severe as the 
rash would lead one to expect. Such patients, too, usually have a history 
of repeated attacks. 

A factor of very great value in diagnosis is the peculiar appearance of 
the tongue in many cases of scarlet fever. At the time of onset it may 
have a white coating, which soon diminishes in degree and becomes dotted 
with red and enlarged papillae. This has been called the "strawberry 
tongue" of scarlet fever. 

Another point of some importance is the time at which desquamation 
appears, for the mere occurrence of desquamation is by no means peculiar 
to scarlet fever. In this disease this symptom usually develops about the 
fourth to the sixth day on the face and about the sixth day on the chest and 
neck. The hands do not begin to desquamate until as late as the twelfth 



SCARLET FEVER 105 

day, and the feet some days later than this. Other eruptions which resemble 
scarlet fever and desquamate usually begin to shed the skin in these areas 
earlier than the days just named. 

In the cases of scarlet rash due to sepsis it is noteworthy that the 
progress of the malady is always aberrant or irregular, for the throat 
symptoms are often absent, the temperature is rather that of sepsis than 
scarlatina, and the septic symptoms may be severe. These cases are par- 
ticularly interesting and worthy of the most careful study, because anti- 
septics, when absorbed, sometimes produce a scarlatiniform rash, and 
because if the case be one of true scarlet fever it is a menace to all other 
children, sick or well. 

As the differential diagnosis of such cases cannot be made in some instances 
till the disease has lasted for some days or until desquamation has begun, 
all patients w T ith such symptoms should be promptly isolated. A focus of 
septic infection is to be carefully sought for. 

Prognosis. — This varies greatly in different epidemics and depends 
largely upon the severity of the symptoms in a given case. The malady 
is always to be considered a grave one. The actual mortality is shown in 
the following statistics. Of 26,921 cases of scarlet fever, 3216, or 11.9 per 
cent., were fatal. Holt states that the average mortality is from 10 to 14 per 
cent., but that for children under five years of age the mortality varies 
from 20 to 30 per cent. (See Fig. 26.) The diminution of mortality after 
the first decade of life is noteworthy. 

Treatment. — In the treatment of scarlet fever the fact must never be lost 
sight of that the disease is self -limited, that it is bound to run its course, and 
the most the physician can do is to guide his patient through the illness with 
the hope that complications may be avoided and that severe symptoms may 
be modified. 

First and foremost in the treatment of this malady, it is essential that 
the patient have hygienic surroundings, with plenty of fresh air and careful 
avoidance of draughts and exposure to sudden changes of temperature, 
since such exposures by chilling the surface of the body are almost certain 
to exaggerate the renal congestion or inflammation which is practically 
always present during the acute stages of this disease. Indeed, it may be 
said that the prime object of the physician and nurse, from the beginning 
to the end of the attack, is to use every effort to avoid sources of 
irritation to the kidneys, for it cannot be doubted that many cases of serious 
renal difficulty which arise in connection with scarlet fever depend upon 
carelessness in this respect. It is also important to remember that these 
precautions in regard to exposure are not only necessary during the acute 
attack, but until convalescence has been thoroughly completed and until 
the urine no longer shows any evidence whatever of renal irritation. As 
these lines are written I have seen in consultation a boy, aged fourteen years, 
who apparently had recovered entirely from an attack of scarlet fever, except 
that there was still some desquamation in the palms of his hands. He was 
allowed to play ball out-of-doors, became overheated and then chilled, and 
within forty-eight hours suffered from violent ursemic convulsions, which 
nearly cost him his life. 



10(i 



DISEASES DUE TO A SPECIFIC INFECTION 



Showin 
ing to 



Medicinally, it is usually well in cases 
of scarlet fever to prescribe from the 
first a mild alkaline diuretic, of which, 
perhaps, the best is 5 grains of citrate 
of potassium with 20 drops of sweet 
spirit of nitre in water three or four 
times a day to a child of eight years, 
giving at the same time copious quan- 
tities of such pure water as the non- 
sparkling water from Poland Springs, 
or any other spring water which con- 
tains a very small amount of organic and 
inorganic matter. By these means we 
flush the kidneys of toxic substances 
which in a concentrated form might 
produce serious renal irritation. 

The second point of therapeutic im- 
portance is the condition of the throat. 
If the child is old enough to gargle its 
throat with a weak solution of chlorate 
of potash (3 or 5 grains to the ounce) 
four or five times a day, such a gargle 
is useful from the very beginning to the 
end of the attack. When the inflam- 
matory changes in the pharynx are 
severe, the part may be cleansed with a 
spray of peroxide of hydrogen, or this 
drug may be applied by means of a 
cotton applicator, the throat being after- 
ward cleansed by a spray of Dobell's 
solution. For the pseudomembranous 
pharyngitis which sometimes develops 
a similar local treatment is advisable, 
and, combined with this, both diph- 
theria antitoxin and antistreptococcic 
serum should be given. If the false 
membrane be due to the Klebs-Loeffler 
bacillus, diphtheria antitoxin is cer- 
tainly indicated, and, as the strepto- 
coccus is always present in scarlet fever, 
and is probably responsible for the 
formation of false membranes in some 
cases, the use of serums designed to 
antagonize both of these poisons is 
manifestly rational. 

For the relief of the intense burn- 
a inff and itching of the skin which is 

g the mortality of scarlet fever accord- lll 5 ailu / o imj 

age, based on johannessen's 9855 cases, present in some cases, the child may 











Fig 


. 26 


















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SCARLET FEVER 107 

be anointed with olive oil containing 0.5 to 1 per cent, of carbolic acid, or 
weak carbolized vaselin may be used. Sometimes a very distinct fall in tem- 
perature can be produced by allaying irritation of the skin in this manner. 

Should the fever become high enough to deserve attention — that is, if it 
persistently remains above 103° or if it occasionally rises as high as 105° — 
the patient should be sponged with tepid water and alcohol, a small ice-bag 
being simultaneously applied to the head. Such a sponging, given early in 
the evening, will, by diminishing the irritation of the skin and quieting 
the peripheral sensory nerves, often cause the child to pass a comfortable 
night. The antipyretic coal-tar drugs are contraindicated in these cases, 
except under extraordinary circumstances. 

If intense nervous irritation is present, 5 or 10 grains of the bromide of 
strontium or sodium may be given several times a day. Full doses of chloral 
have been highly recommended, but they are often contraindicated because 
of the irritant effects upon the kidneys and the depressant influence upon 
the heart. Should evidence of circulatory failure develop, small doses of an 
old brandy poured over shaved ice, or given in cool water, may be admin- 
istered every two or three hours with advantage. Or, small doses, frequently 
repeated, of aromatic spirit of ammonia may be used in the same manner. 
If the circulatory failure is acute or sudden, either the aromatic spirit of 
ammonia or Hoffmann's anodyne should be used as rapidly acting diffusible 
stimulants. 

Pain in the ear should be relieved by irrigating the external auditory canal 
with normal salt solution as hot as the child can bear it. In all these cases a 
careful examination of the ear-drum should be made twice a day to see whether 
there is any bulging due to accumulated secretion or suppuration in the 
middle ear, and if this is present paracentesis of the tympanum should be 
performed at once to relieve the pain and avoid danger of infection of the 
mastoid cells. 

If evidences of septicaemia are present and the patient seems anaemic, 
either during the later stages of the attack or during convalescence, the 
tincture of the chloride of iron, in the dose of 5 drops three or four times a 
day, is advantageous, since it tends to combat the anaemia and the infection 
and also exercises a slight stimulant influence upon the kidneys. For the relief 
of persistent albuminuria after the attack is passed, the child should be 
prevented from taking excessive exercise, but, nevertheless, should live in 
the sunshine as much as possible, and may take either small doses of the 
tincture of chloride of iron or a very minute dose of the tincture of cantharides 
— say, J to 1 drop twice or thrice a day, well diluted ; but the cantharides is 
contraindicated if the microscope shows in the urine the presence of red 
blood cells, indicating that the kidneys are still acutely inflamed. 

In those cases of scarlet fever in which the rash fails to develop its full 
efflorescence promptly, and particularly in those cases in which the skin is 
mottled and marbled, indicating poor capillary circulation, it is exceedingly 
useful to immerse the child in a hot bath. In other cases the cool-warm pack 
may be used. This consists in stripping the child of its night-clothing and 
rolling it in a sheet which has been dipped in warm water, which, by the time 
it is wrapped around the child, has become considerably cooled by evapora- 



108 DISEASES DUE TO A SPECIFIC INFECTION 

tion. As soon as the sheet is wrapped about the child, an ice-bag being in 
the mean time applied to the head, it is wrapped in a blanket, and in a few 
moments the heat of the child's body transforms the cool sheet into a warm 
pack. The primary effect of the cool sheet is to drive the stagnant blood out 
of the peripheral capillaries, and the effect of the warm sheet is to bring new 
blood into these vessels. By these means we are very frequently enabled 
not only to improve the circulation and develop the rash, but to diminish 
the toxic symptoms and relieve nervous stress. It is hardly necessary to add 
that exposure for any length of time to the cool sheet is to be avoided. The 
blanket is to be placed tightly about the child at the earliest possible moment 
after the cool sheet comes in contact with its body, so that the chilling of the 
surface will be only instantaneous. French therapeutists, and some other 
practitioners, have advised that in those cases in which cerebral symptoms are 
very marked and toxsemia is evidently profound, the child should be placed 
in a warm bath, and that cool water should be poured over its head, neck, 
and chest for a moment, in order to produce a certain amount of shock and 
rouse the flagging powers of the body. This method has been so highly 
endorsed by excellent practitioners that it cannot be condemned for theoret- 
ical reasons, but the author has never been brave enough to employ it. 

Within the last few years several attempts have been made to produce an 
antiscarlatinal serum without very satisfactory therapeutic results. In the 
cases in which the author has directed its use, it has seemed to modify 
the throat symptoms, but otherwise it has not affected the progress of the 
disease. 

MEASLES 

Definition. — Measles is an acute infectious disease, usually epidemic, which 
most commonly attacks children and rarely occurs after the second decade 
of life. The skin during an attack is covered more or less profusely by a 
dusky red eruption of a maculopapular type. The eyes are congested and 
lachrymose, and the nasal and pharyngeal mucous membranes swollen and 
red. One attack usually confers immunity. Measles is sometimes called 
"Morbilli." 

Distribution. — Measles is met with in all parts of the civilized world. If 
by chance it is carried to a people who, by reason of isolation, have not been 
exposed in previous generations to its effects, it often develops in a malignant 
form and causes a great mortality. Perhaps the most noteworthy example 
of this is the case of the inhabitants of certain of the Fiji Islands, who, being 
exposed to the infection, fell ill and died by thousands, so that it is estimated 
that 20,000 deaths occurred in four months. The epidemic ceased only after 
every person on the islands had been infected. 

The susceptibility of children in the first ten years of life to the infection 
is quite remarkable. If a large number who have not been rendered immune 
by a previous attack are exposed to the infection, nearly all fall sick. Smith 
and Dabney report an instance in which 110 children between eight and 
eighteen years of age were exposed, and only 2 were not taken ill. 

Measles is much more prevalent in the spring and winter months than in 



MEASLES 109 

the summer months, probably because the open-air life and free ventilation 
of the warmer season aids in preventing the exposure of susceptible persons 
to a concentrated form of the contagion. 

Etiology. — Measles is in all probability due to a distinct micro-organism 
but so far it has not been isolated. Bacilli have been found in the blood and 
in the pharyngeal and nasal secretions of persons affected with the disease 
but no evidence has been adduced to show that they are its causative agents. 
The bacillus isolated and cultivated by Canon and Pielicke in 1892 pro- 
duced no ill effects when injected into animals. Czajkowski and Borini 
have also obtained bacilli from the blood. A micrococcus which Lesage 
found in 1900, although highly virulent for rabbits, did not reproduce the 
disease. Protozoa have been found by Doehle and Pfeiffer (1892) in the 
blood of patients suffering from measles. Rosenberger and Wilson (1906) 
found in the blister fluid of 39 out of 41 cases a small hyaline body, 
containing a motile granule. Its relation to the disease is not yet clear. 

The disease spreads with great readiness through the air and contact with 
the patient or his garments is not necessary for its transmission, although 
such contact, of course, provides the infection in more concentrated form. 
There is no doubt that the breath of a patient suffering from measles carries 
the infection, and so does the nasal and pharyngeal mucus, so that the 
expulsion of these secretions by coughing or sneezing may result in nurses 
or visitors becoming a means of transmitting the disease by their garments 
being contaminated in this manner. 

Very short exposure to infected air is sufficient for infection, and even 
when careful precautions are taken to prevent the spread of the disease it 
not infrequently happens that all the other children in a house develop the 
malady, partly because it is infectious from the earliest period of invasion 
before its presence is recognized, but largely because of the ease with which 
it is conveyed by the air. This great diffusibility of the virus of measles 
is quite in contrast with the limited diffusibility of the poison of scarlet 
fever. 

Although it is true that the diffusibility and activity of the infection of 
measles is exceedingly active while the disease lasts, it is also a fact that it 
speedily disappears after convalescence is established. Three weeks after 
the attack begins, the patient rarely transmits the disease, and by this time, 
with ordinary ventilation, the room and surroundings of the patient are 
usually innocuous. Any condition of ill-health which diminishes vital resist- 
ance very distinctly increases the susceptibility of an individual to infection, 
and in these instances the disease is prone to be severe. 

The period of incubation of measles is usually from eleven to fifteen days, 
but cases are recorded in which the disease began one week afetr exposure. 

Prevention. — Measles is to be prevented by complete isolation of the 
patient, by the disinfection of all garments of the patient and nurse before 
they leave the sick-room, and by free ventilation, so arranged that the other 
rooms in the house are not exposed to a draught from the sick-room. After 
the attack has passed the patient should be given several hot baths to rid 
the body of all desquamating skin, and the scalp should be cleansed with 
special care. 



110 



DISEASES DUE TO A SPECIFIC INFECTION 



Frequency. — Measles is one of the most common of the acute exanthemata 
and affects nearly all persons living in cities before they reach adult life. 
Indeed, it may be said to be the most common of all diseases in childhood. 

Pathology and Morbid Anatomy. — There are no noteworthy changes pro- 
duced in the various viscera by measles, if we exclude those ordinarily con- 
sidered as complications and the changes in the mucous membranes of the 
respiratory and digestive tract, consisting of acute irritation and catarrh. 
With the onset of the disease these membranes become hypersemic, and, it 
may be, dotted with an eruption much like that which is seen on the skin. 

The pathological changes due to complications are chiefly those of bron- 
chitis and bronchopneumonia, conditions which are exceedingly common in 
young children, and in patients who are poorly nursed and badly nourished, 
when suffering from acute infectious diseases. 



Fig. 27 




Showing initial fever with the subsequent fall and then a rise when the rash is well developed 
in a case of measles. Also shows an ending of the fever by crisis. 



Symptoms. — Measles is usually ushered in by the symptoms of an ordinary 
cold or attack of coryzi. There may be an initial chill, but this is often 
absent, the fever being the first additional symptom which becomes mani- 
fest. The patient's face looks flushed and, it may be, slightly swollen about 
the eyes and nose, and the conjunctivae are injected, the general expression 
of the face being tearful. At this time, and later, in the disease photophobia 
may be marked. Sneezing may be noticeably constant, and an examination 
of the pharynx will reveal the fact that its mucous membrane is reddened 
and the hard palate dotted with a measles-like rash, which often appears 
here before it develops on the skin. Some cough may be present in the stage 
of onset as the result of the pharyngeal and laryngeal irritation, and 
headache may be complained of. 

There is present in many cases upon the buccal mucous membrane a 
number of small, white-tipped, reddish spots first described by Filaton, but 



PLATE III. 



Fig. l 



Fig. 2. 





Fig. 3. 



Fig. 4.. 





The Pathognomonic Sign of Measles (Koplik's Spots' 



Fig. 1. — The discrete measles spots on the buccal or labial mucous membrane, showing the isolated 
rose-red spot, with the minute bluish- white centre, on the normally colored mucous membrane. 

Fig. 2. — Shows the partially diffuse eruption on the mucous membrane of the cheeks and lips; patches 
of pale pink interspersed among rose-red patches, the latter showing numerous pale bluish-white spots. 

Fig. 3. — The appearance of the buccal or labial mucous membrane when the measles spots completely 
coalesce and give a diffuse redness, with the myriads of bluish-white specks. The exanthema on the skin 
is at this time generally fully developed. 

Fig. 4. — Aphthous stomatitis apt to be mistaken for measles spots. Mucous membrane normal in hue. 
Minute yellow points are surrounded by a red area. Always discrete. 



MEASLES 111 

more commonly called "Koplik's spots." (See Plate III.) When present 
they are pathognomonic of measles, but their absence does not negative the 
diagnosis of the presence of this disease. 

The fever usually begins to rise with the onset of the catarrhal symp- 
toms, increasing day by day till it reaches its acme of 103° to 105° on 
the fourth or fifth day from invasion, and remains fairly constant at about 
this level until the rash begins to fade, on the fifth to the seventh day, 
when the fever ceases abruptly or by lysis, reaching normal in a few hours 
or by the end of two or three days (Fig. 27) . 

The eruption of measles develops on the third or fourth day of the 
disease, and at first is most marked back of the ears and about the roots of 
the hair or on the forehead. The individual spots look like a flea-bite 
and are rather dusky red in appearance. By the end of twenty-four hours 
or at the expiration of the fifth day this rash is usually pretty well diffused 
all over the body, and the macular appearance of the eruption begins to 
become papular, so that it can be distinctly felt by the finger-tip of the physi- 
cian. This rash varies greatly in its degree. Sometimes it is so profuse that 
every part of the body is covered ; in other instances very considerable spaces 
of unaffected skin can be found between the groups of papules. It has been 
generally stated that the crescentic arrangement or grouping of the rash is 
diagnostic of measles. That this is erroneous the author is convinced, as 
he has frequently seen it occur in other morbilliform eruptions. When the 
disease is in its fully developed stage the skin of the face may be quite swollen 
and that of the neck and chest well covered by the eruption ; but as the lower 
part of the trunk and the low T er limbs become involved the rash on the face 
usually begins to diminish and slowly fades, leaving, for several days after it 
has entirely disappeared, a faint mottling of the skin with the desquamation 
of branny scales, which is scanty in some cases, but profuse in those who have 
had an intense eruption. The entire duration of the rash is from five days to 
one week, and the period of desquamation lasts for about the same length of 
time. 

During the well-developed stage of the disease the patient nearly always 
presents some symptoms of bronchitis. This may be so mild as to be unde- 
monstrable, or so severe as to threaten life. The thorax should be frequently 
examined, in order that the development of this complication may be recog- 
nized and its severe effects, as far as possible, avoided. 

Variations. — It must not be thought, however, that measles always follows 
the course just described. All the acute infections present widely different 
symptoms in different epidemics and in different persons, and measles is no 
exception to this rule, for in some cases the systemic or constitutional dis- 
turbance is so slight as to be of no importance, whereas in others it is 
exceedingly severe. In strong, hearty children the course of measles is 
rarely grave if they are protected from cold and exposure, whereas in puny, 
badly nourished infants it is one of the most fatal maladies. 

The following variations from the ordinary course of measles are met with : 

A mild type, with a scanty rash and almost no constitutional disturbance, 
which runs its course without complications if ordinary care is exercised. 

A severe type, in which nervous and constitutional symptoms predominate, 



112 DISEASES DUE TO A SPECIFIC INFECTION 

in which the eruption may be exceedingly profuse, but is more commonly 
indistinct or poorly developed, perhaps because of poor circulation in the 
skin by reason of toxaemia. 

Another severe type is known as hemorrhagic or " black" measles, 
because of the tendency to the occurrence of hemorrhages in the skin. Still 
another form is a respiratory type, in which the patient may suffer from 
great laryngeal and tracheal distress or from a serious bronchopneumonia. 
It is often said of these cases by the laity that the rash has been driven in by 
exposure to cold and is exerting its deleterious influence on the lungs. This 
is not exactly true, but it is, nevertheless, a fact that when we can, by means 
of a hot pack, restore the peripheral circulation and so indirectly cause the 
rash to be manifest, the symptoms of toxaemia and respiratory disorder often 
become decidedly less. 

Rare cases are met with in which, after vomiting, purging, convulsions, 
and coma, death speedily occurs, even before the rash has had time to 
become well marked. 

Complications and Sequelae. — It has already been intimated that measles 
in itself is a disease which, in most individuals, with ordinary care, pursues 
a safe course and ends in recovery. While this is undoubtedly true, it is 
also a fact that it takes high rank among the acute infectious diseases which 
produce death, by reason of the complications which are prone to occur. 

Of all these by far the most frequent and deadly is bronchopneumonia, a 
complication which is often severe in its course and which causes a great 
number of deaths when measles attacks young infants. The physical signs 
and symptoms are described in full in the article on that disease, but it 
is important to remember that in measles the disease is insidious and speedy 
in its onset, so that a pneumonia may be developed before the physician dis- 
covers it, unless he be on his guard and resorts to frequent examinations 
of the chest. Bronchopneumonia during an attack of measles in a child 
under one year of age is an exceedingly common and very grave complication 
of the disease. In children of five years or more this complication usually 
does not occur if the primary state of the health is fairly good and if careful 
nursing prevents exposure to " catching cold." 

A second complication of far less importance than bronchopneumonia, 
both as to frequency and results, is diarrhoea and vomiting due to a catarrhal 
state of the bowels and stomach. It also is a complication which is due 
in a considerable proportion of cases to bad nursing and can generally be 
avoided by proper feeding and the avoidance of draughts. It not infre- 
quently happens that these digestive disturbances are mild during the acute 
illness, while the patient is required to be prudent and quiet, and become 
pronounced when the acute illness is past and the attendants become care- 
less as to exposure and feeding. This gastrointestinal disorder varies from 
a mild catarrh to a severe enterocolitis. 

Another complication seen in many cases is a mild degree of stomatitis, 
which in poorly nourished children may become ulcerative. Even so severe 
and fatal a lesion as noma may develop in cases with very low vitality. 
Very rarely gangrenous ulceration of the ear, the labia?, or the prepuce takes 
place. 



MEASLES 113 

So far as the nervous system is concerned, it may be said that it is rarely 
affected. In the stage of onset in very young children with poor resistance 
and an unstable nervous system there may be convulsions, but they are 
exceedingly rare. Meningitis as a sequel to measles is also very rare. Even 
meningitis due to middle-ear disease is rarely met with, for the otitis of 
measles, while not uncommon, is usually mild and rarely causes secondary 
lesions. 

The eyes are usually inflamed and there may be a mucopurulent con- 
junctivitis, or, if the general health be poor, keratitis may prove troublesome. 

So rarely are the heart and kidneys affected to any serious degree that 
these organs may be considered almost immune. A feebleness of the heart 
due to the infection and fever may be present for a time, and a tran- 
sient albuminuria is often manifested, but both of these symptoms usually 
rapidly disappear if the patient is kept at rest. 

Measles is an infection which is not rarely complicated by other acute 
infections. Diphtheria may develop during its course, and whooping- 
cough is so exceedingly frequent that some relation between the two dis- 
eases has been thought to exist. When whooping-cough does occur as a 
complication the danger of bronchopneumonia is greatly increased. Still 
another sequel of measles is tuberculosis, probably because the catarrhal state 
of the mucous membranes offers a path for infection by the tubercle bacillus 
or because the devitalizing influence of measles permits an old focus of 
tuberculous infection to become active. 

The persistence of a febrile movement in a case of measles after seven 
days should always arouse the suspicion of some inflammatory complication 
which should be most carefully searched for. 

Diagnosis. — Measles must be carefully separated from a large number of 
conditions which somewhat resemble it. Many kinds of food, particularly 
shell-fish, produce a rash which looks remarkably like measles, but which 
usually lasts only a few hours. Antipyretic or other coal-tar products do like- 
wise in some persons, and the physician should always enquire as to the 
use of these foods or drugs before stating that measles is present. Some- 
times a morbilliform rash follows vaccination or precedes smallpox. The 
use of antidiphtheritic serum may also cause such an eruption. The con- 
tact of a caterpillar with the skin in some persons may cause a measles-like 
eruption which lasts only a few hours. None of these states, however, are 
accompanied by the appearance of Koplik's spots, by marked coryza, nor 
by the appearance of the rash on the mucous membrane of the soft palate. 
Fever, too, is usually absent. (For the diagnosis from Rotheln, see Rubella.) 

Prognosis. — From what has already been said it is evident that the prog- 
nosis in a case of measles is dependent not on the fact that measles has 
developed, but rather upon the age of the patient, the vital resistance or 
the general condition of the system, and the surroundings as to sanitation 
and nursing. Given a poorly nourished infant in bad surroundings and 
with inefficient care, measles becomes one of the most fatal diseases to be 
met with, whereas in a case where these conditions are good the prognosis 
is fairly favorable. We find, too, that the danger of the disease decreases 
greatly with each year of life; so that children near puberty rarely die from 
8 



114 



DISEASES DUE TO A SPECIFIC INFECTION 



this malady unless poorly nourished or badly neglected (Fig. 28). If broncho- 
pneumonia develops, the prognosis must be guarded in direct proportion to the 
youth of the child. Thus, out of a series of 40S cases of measles complicated 
in this manner, 290, or 71 per cent., died. This, however, is an exceedingly 

high figure and by no means represents 
the death rate in a general run of cases 
in which all ages and conditions of 
patients are considered. Under these 
conditions the death rate for all cases 
is probably about 35 per cent. Thus, 
Holt speaks of an epidemic in the 
Nursery and Child's Hospital in New 
York in 1892, in which the mortality 
was 35 per cent., and in 9239 cases of 
measles occurring in France, prin- 
cipally in the hospitals of Paris, there 
were 3096 deaths, or a mortality of 
33.5 per cent. It is, moreover, to be 
carefully borne in mind that hospital 
or asylum statistics are utterly worth- 
less in determining the death rate 
for ordinary private practice, be- 
cause most of these hospital cases 
are primarily in bad health or are 
brought to the hospital desperately ill 
from neglect. Including all cases in 
private practice, the mortality should 
not be over 5 to 10 per cent., and in 
many epidemics it is much lower, even 
in institutions and where good nursing 
is not to be had. Thus, in an epi- 
demic in the Faroe Islands only 8 cases 
out of 1123 cases died, and at the 
Boston City Hospital only 5 were fatal 
out of 366. 

Treatment. — When measles runs a 
natural course, little or no medication 
is required ; for, as it is a self-limited 
disease, it cannot be jugulated. The 
therapeutics of an attack of measles, 
therefore, consists in the prevention of 
complications and the relief of symptoms which are so prominent as to be 
distressing or perhaps even dangerous. In order to avoid irritation of the 
eyes and to lessen the suffering due to photophobia the sick-room should 
be kept dark. Light bed-covering should be employed, and heavy quilts 
which cause the child to perspire unnecessarily are to be tabooed. As a 
mild gastrointestinal catarrh is often present with the fever, food should 
be light, given at frequent intervals, and should consist chiefly in nutritious 



Fig. 28 


PERCENTAGE 

UNDER 
1 YEAR 

BETWEEN 

1 AND 2 

BETWEEN 

2 AND 3 

BETWEEN 

3 AND4 

BETWEEN 

4 AND 5 


40 


39 J T 


38 !\ 


37 ::1t ::::::: ::_ 


36 7_I ___] 


35 M 


34 _t__L 


33 _ __!__[ 


32 7 \ 


31 / 1 


30 h \ 


29 1 V 


28 __ _7T___i 


27 it.! - 


26 ____[_____[ 


25 1 \ 


24 7 ] T 


23 t 1_ 


22 T _t _ 


21 f \ 


20 1 K 


19__I \ 


18 V 


17 \ 


16 -------- ------.----- - 


15 3 


14 ___ C 


13 j 


12 V 


11 T 


10 \ 


9± J_ \ 


8 T 


7 !__ 


6 


5 


4 


3 



Showing the mortality of measles according 
to age, based on 29,464 cases collected by H. 
Courtenay Fox. 



RUBELLA 115 

fluids, such as the various broths, milk, an Qgg boiled only one minute, and 
similar substances. 

If the irritation of the conjunctivae is marked, eye drops, composed of 4 
grains of common salt and 4 grains of boric acid to an ounce of water, may 
be used several times a day; and if the cough is sufficiently constant to pre- 
vent sleep, it may be controlled by small doses of codeine, ^ of a grain 
once, twice, or thrice in twenty-four hours, to a child of two years, or 
heroin may be used. Should the fever reach 105° there is usually no 
necessity of reducing it owing to its short duration, but the child's comfort 
can be much increased by sponging it with tepid water and alcohol, 
or even with water at 70°, using active friction at the same time. These 
cases do not need an immersion bath and it is not wise to give it to them. 
If the circulation has a tendency to fail, carbonate of ammonium in the 
dose of 2 grains four or five times a day may be given in syrup of acacia. 
For the relief of headache a small ice-bag may be applied to the head, pro- 
vided that a nurse is at hand to prevent it from slipping down upon the neck, 
or about the ears, and also to prevent it from wetting the pillow. It should 
usually be wrapped in a towel to prevent the accumulation of moisture, 
and also to protect the head from too great cold. 

In cases in which the rash is not well developed and the skin is dusky in 
hue, the brief use of a hot pack is very useful. 

Should diphtheria arise as a complication antitoxin should be given. 

After the disease has run its course, convalescence should be aided by 
the use of simple bitter tonics, the hypophosphites, iron, and arsenic, and, 
if malnutrition is present, cod-liver oil proves itself an exceedingly valuable 
remedy, since it improves the nutrition of the patient and exercises a most 
beneficial effect upon the mucous membranes. If the bronchitis is per- 
sistent and a considerable quantity of mucus is in the bronchial tubes, 3 
grains of chloride of ammonium may be given in a teaspoonful of fluid 
extract of liquorice and a teaspoonful of water three or four times a day, 
and gentle counterirritation in the form of chloroform liniment or ammonia 
liniment may be applied to the chest. After the eruption has disappeared 
and desquamation has begun, the child should be bathed daily in order 
that its skin may be thoroughly rid of dead epithelium; and before the 
patient plays with other children the scalp should be shampooed several 
times, since not infrequently desquamation continues upon the head long 
after it has ceased upon the trunk. 

For a long time after the rash of measles has disappeared the greatest 
care should be exercised that the patient is protected from exposure, as 
acute and chronic catarrhs of any or all the mucous membranes are very 
prone to develop under very slight provocation. 



RUBELLA. 

Definition. — Rubella is sometimes called " rothebi "or " German measles," 
" rubeola noiha" " epidemic roseola," and " hybrid scarlet fever." It is 
a disease distinct from measles and scarlet fever, and is one of the mild 



116 DISEASES DUE TO A SPECIFIC INFECTION 

acute infectious eruptive diseases of childhood. It rarely affects adults. 
Johann Seitz studied an epidemic involving 21 families and comprising 111 
cases, and found that 4 per cent, of all adults were attacked. The ratio 
for children was much higher, being 64 per cent. Rubella occurs as a rule 
in epidemics, but sporadic cases are met with. 

Etiology. — The micro-organism of this affection has not been isolated, 
but the disease is distinctly infectious and is contracted by one patient 
from another, not only by contact, but also by clothing and through the air. 

Symptoms. — After a period of incubation lasting from ten to twelve 
days the stage of onset manifests itself by chilliness, general malaise, some 
running of the eyes and nose, and headache. As early as the first day of 
the illness the rash appears as a macular eruption which is red in hue, but 
is not scarlet. This is a so-called "rose rash." In some cases, however, 
this rash does not develop till the third day. The rash shows itself first on 
the face, then on the anterior surface of the thorax, and speedily covers the 
entire body. It can often be seen on the soft palate before it appears on 
the skin, in the form of bright rosy-red spots (Forchheimer's spots). The 
individual macules may remain separate or coalesce. In some instances, 
however, the skin has a diffuse redness like that of scarlet fever, but it is 
less scarlet. The macules last about three days and then fade gradually, 
being usually, but not always, followed by slight scaly desquamation. The 
skin is rarely as much stained after the rash disappears as it is after 
measles. 

A noteworthy sign to be sought for is the enlargement of the lymph glands 
below the ears, in the lateral cervical region, and at the back of the neck. 
Sometimes the inguinal glands are also affected. 

The febrile movement is usually very moderate, the temperature often 
not rising above 100°. The general symptoms may be so mild that the 
attention of the nurse is first called to the illness by the rash. 

If the child is carefully nursed and clothed and properly fed, the malady 
pursues a rapid course to recovery. If, on the other hand, the child be feeble 
and exhausted, this disease may be more severe in its manifestation and be 
accompanied by otitis media, catarrhal pneumonia, or even albuminuria 
and jaundice. 

Diagnosis. — Rubella is to be separated from true measles by the moderate 
character of the coryza, by the absence of Koplik's spots, the early swelling 
of the glands in the neck, and by the absence of bronchial irritation. From 
scarlet fever it is separated by the absence of high fever and of the well- 
diffused scarlet rash, which is not macular, and by the absence of the sore 
throat of that affection. While these differential points are of value in 
many cases, it is a fact that in some instances a diagnosis is most difficult 
until the case has been studied for some days, when the mildness of the 
symptoms and the brevity of the attack aid in deciding that neither measles 
nor scarlatina are present. 

Treatment. — The treatment of rotheln consists in rest in bed and the use 
of spirit of nitrous ether and citrate of potash as diuretics and diaphor- 
etics, and in attention to the bowels and kidneys. Exposure to cold should, 
of course, be avoided. 



MUMPS 117 



MUMPS. 



Definition. — Mumps, or epidemic parotitis, is an acute infectious disease 
affecting the parotid gland and accompanied by mild systemic symptoms 
which may not be severe enough to demand notice. It occurs in the great 
majority of instances during childhood, between the fourth year and puberty, 
and one attack protects the patient from a second. 

Etiology. — Mumps is usually conveyed by contact from one patient to 
another, but it may be carried by a third person or by garments to a sus- 
ceptible individual. It is contagious from the beginning to the end of the 
attack, and it is probable that persons who have so far recovered as to 
have no visible swelling of the parotids can still transmit the disease. For 
this reason the patient should be kept separate from other children for a 
period of ten days after the swelling disappears. It is, however, a note- 
worthy fact that mumps is by no means so infectious as are the eruptive 
fevers, and many children escape the disease even when thoroughly exposed 
to it. 

The period of incubation is uncertain. Sometimes it is brief, in other 
cases surprisingly prolonged. Holt, in 42 cases collected from literature, 
found it varied from three to twenty-five days. In all probability it is about 
fifteen days in the average case. 

Pathology. — The chief change in mumps, and, indeed, the only one which 
is characteristic, is the swelling of one or both parotid glands. The swelling 
is due to a primary parenchymatous inflammation, followed by involvement 
of the connective tissue of the gland as well. Rarely the other salivary 
glands become swollen, and still more rarely the parotids suppurate. This 
result occurs only in children w T ho are impoverished by other diseases, and 
is due to an invasion of the gland, through the duct of Steno, by pyogenic 
organisms. 

Symptoms. — The chief symptoms of mumps, aside from the swelling of 
the glands, is pain in the parotid region, which is greatly increased by moving 
the jaw or by taking any sour material into the mouth. In susceptible 
persons there may be some feeling of malaise or wretchedness and the fever 
may reach 103° or 104° on the first day, although a temperature of 102° is 
more commonly met with. 

The swelling of the gland is usually at its height by the third day and 
remains at this stage for tw T o or three days more, when it begins to decrease 
and then gradually disappears. In some cases the degree of swelling is so 
marked that the tissues of the face and neck share in it to such an extent 
that the patient is unrecognizable. The swelling is bilateral in the vast 
majority of instances, but it often begins in a single gland. 

Complications and Sequelae. — While mumps is a very mild disease in 
many cases, it at times becomes severe, chiefly because of the complications 
which arise. These are more frequently met with in adults than in chil- 
dren. The most common of them is orchitis, which may be bilateral and 
severe enough to cause the patient intense suffering and force him to 
remain in bed. 



118 DISEASES DUE TO A SPECIFIC INFECTION 

Before the age of puberty the testicles are rarely involved, but after 
puberty orchitis is a frequent complication. Bich collected statistics on 
862 cases of mumps occurring in young men between the ages of eighteen 
and twenty-five years, and found that 29 per cent, of the number were 
affected with orchitis. Granvier's record of cases occurring in the French 
army gives a percentage of 23. Usually only one testicle is involved. Thus, 
of 159 cases collected from various sources 152 were unilateral. The com- 
bined statistics of Grangier and Bich, based on 309 cases of orchitis, showed 
that atrophy of the testicle resulted in 176 cases, or 57 per cent. Active 
exercise seems to predispose to this complication, and it seems much more 
frequent in some epidemics than in others. Some years ago mumps appeared 
in an epidemic among the students of the Jefferson Medical College, and 
a very large proportion of those attacked developed metastasis to a testi- 
cle. The development of the orchitis is usually associated with a second 
rise of temperature and a general sense of illness which is in excess of that 
present at the onset of the primary illness. The swelling of the testicle 
lasts about a week, and after the acute inflammation has passed the gland 
may be enlarged for a long period of time. 

Cases have been recorded in which convulsions, meningitis, and arthritis 
have developed as complications of mumps. 

In young girls who have mumps, secondary swelling of the mammary 
glands, of the ovaries, or of the labise may develop, but secondary changes 
are far more rare among females than are those detailed as occurring in 
males. 

Simonin, a French surgeon, has reported 10 cases of pancreatitis which 
occurred among 652 cases of mumps. The symptoms of pancreatitis 
appeared from the first to the twelfth day of the disease, but usually from 
the third to the sixth day, and lasted from two to seven days. The chief 
symptoms were epigastric pain and vomiting, but no glycosuria. Cuche 
has stated that he found epigastric tenderness present in 20 out of 26 cases 
of mumps. 

Treatment. — The treatment of mumps consists in the use of mild alkaline 
diuretics and rest, for if the patient can be persuaded to avoid exercise and 
to use a light diet active medication is never needed. Sour foods and acid 
drinks are to be avoided, for when they are taken into the mouth they cause 
severe pain. If the febrile movement is marked and the pulse is quick 1 
minim of tincture of aconite every two hours is useful for the first twenty- 
four hours of the malady. By decreasing the congestion in the gland the 
aconite not only moderates the inflammation, but also diminishes the pain. 
Local applications to the swollen parotids are usually not needful, but if 
any are employed they should be hot rather than cold. Should metastasis 
to the testicle occur, rest in bed is imperative, since taking exercise at such 
a time causes great increase in the swelling and pain. The scrotum should 
be supported by a bandage. Aconite in full doses and citrate of potassium 
are useful remedies when the swelling of the scrotal contents is severe. 



]YIIOOPIXG-COUGH 119 



WHOOPING-COUGH. 

Definition. — Whooping-cough is sometimes called Pertussis, and is an 
infectious disease chiefly met with in childhood. It consists, as its name 
implies, in a respiratory disorder which is peculiar in two particulars. The 
patient in the well-developed stage of the disease is seized at varying inter- 
vals by a paroxysm of coughing which is so constant and violent that in a 
few seconds the quantity of residual air in the thorax is greatly decreased 
below the normal amount, producing in this way a sense of suffocation and 
flushing of the face or cyanosis. Immediately after the cough ceases the 
patient endeavors to take a deep inspiration to compensate for the excessive 
expiratory effort, when there is developed a narrowing of the glottic open- 
ing so that it is very difficult for the air to enter the larynx. This violent effort 
to draw air through a narrow opening produces a peculiar "whoop," which 
gives the disease its name. The name "whooping-cough" does not signify 
that the cough is whooping in character, but that there is a cough followed 
by a whooping sound. 

Distribution and Frequency. — Whooping-cough is a disease which is found 
in all parts of the world, and is apt to occur in epidemic form, particularly 
during the months of March and April. It is least prevalent in September 
and October. As already stated, it is particularly prone to attack children; 
so that few persons reach adult years without suffering from an attack. If 
they do escape during childhood, they may suffer from it even in advanced 
old age. Even sucklings are attacked by it, and in this class of cases it is 
an exceedingly fatal malady. It is also a grave disease in old age. 

Whooping-cough attacks both sexes with about equal frequency. Rosen 
collected 43,393 cases, of which 21,850 occurred in boys and 21,543 in 
girls. If the statistics of Goodhart, Comly, and Rilliet and Barthez are 
combined, it is found that in 4157 cases 1868 occurred in boys and 2289 in 
girls. 

Etiology. — The cause of whooping-cough is certainly a micro-organism, 
and several investigators claim to have isolated it. Unfortunately no uni- 
formity of opinion exists as to the specific organism of this disease. In 
1887 Afanassjew, of St. Petersburg, isolated from the sputum of children 
affected with whooping-cough a short, slender, motile, anaerobic bacillus, 
cultures from which, wdien injected into dogs and rabbits, produced a dis- 
ease similar to pertussis. This organism was found afterward by Szemte- 
schenko, of St. Petersburg, and Koplik, of New York. In 1892 Ritter, of 
Berlin, described a diplococcus which he thought was specific, and more 
recently a bipolar bacillus resembling the Bacillus influenza? has been con- 
sidered the pathogenic agent by Czaplewski and Hensel (1897) and by 
Arnheim (1900). Jochmann,Krause,and Moltrecht, of Hamburg (1903), also 
have isolated an organism resembling the bacillus of influenza, but differing 
from the one described by Czaplewski and Hensel, which they have named 
Bacillus pertussis Eppendorf, and which they believe plays an important 
role in the production of whooping-cough, and also the bronchopneumonia 
which complicates it. Davis (1906), found this organism in the sputum 



120 DISEASES DUE TO A SPECIFIC INFECTION 

of almost all of a large number of pertussis patients. Morphologically 
and culturally it is identical with the influenza bacillus which he believes 
it should be called. The evidence at hand does not prove it specific for 
whooping-cough. Leuriaux, of Brussels (1902), ascribes the disease to an 
aerobic bacillus ovoid in form and having rounded ends. This organism 
grows on all ordinary culture media and stains with aniline dyes and by 
Gram's method. 

Whooping-cough so often occurs in close connection with an attack of 
measles that the two diseases must be regarded as nearly related. 

The exact period of incubation is unknown. It probably varies greatly 
in different persons and in different epidemics. Sometimes it seems to be 
as short as two days; in others it apparently takes ten days, or even longer 
than this. The infection is perhaps conveyed by the air and certainly is 
transmitted by the sputum, either by the direct expulsion of particles of it 
into the face and air-passages of the child not as yet affected, or upon 
clothing or the food, so that it gains access to the respiratory tract. 
The infection is most marked during the acme of the malady, but is active 
at all times during the attack, and probably for a week or more after the 
cough has lost all characteristics of the disease. Children who have suf- 
fered from this disease should not come in contact with those who have not 
had it for three or four weeks after the last whoop is heard. 

Pathology and Morbid Anatomy. — Primarily the only noteworthy change 
present in the thoracic organs during whooping-cough is a mild catarrhal 
state of the mucous membranes of the whole respiratory tract. Secondarily, 
the pathological results are far more serious in that the bronchitis and the 
great strain thrown upon the heart by asphyxia result in conditions which 
may destroy the patient, death usually ensuing in fatal cases from exhaustion 
due to excessive cough, lack of food, and lack of rest combined with broncho- 
pneumonia, which in turn is also due to several causes of which lowered 
vital resistance and a feeble heart are important factors. Then, too, in the 
violent inspiratory efforts of the patient small particles of food or infected 
mucus may be drawn into the smaller bronchi and so produce local infec- 
tion. As stated in the article on Bronchiectasis, this condition in its cylin- 
drical form may be caused by pertussis. (For further pathological changes 
see Complications.) 

Symptoms. — The symptoms of whooping-cough have already been 
described to some extent. Usually the patient develops what is apparently 
a slight cold in the head and thorax, followed by a cough which may be 
described as nervous or spasmodic. Perhaps the word " sudden " can best be 
applied to it in the sense that each coughing spell is sudden in onset. At first 
there may be only one or two coughs, but soon they come in series, which 
day by day increase in frequency and violence. Sometimes the whoop, which 
occurs at the end of the series of short, sharp coughs, does not appear for 
several days. It may never appear in the mild type of case, the patient suf- 
fering only from the paroxysms of cough which exhaust the chest of air to 
a considerable degree. When the whoop does come on it appears at the end 
of the repeated coughs, and is caused by the attempt to inspire air suddenly 
and forcibly through the narrowed glottis. The whole paroxysm, there- 



W'HOOPIXG-COUGH 121 

fore, consists, first, of a series of coughs which increase in rapidity as one 
would count 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12 with increasing speed, and, 
secondly, in the long-drawn inspiratory whoop. Owing to the violence of 
the cough the face becomes suffused, the tears run, and the patient may 
even seem more or less convulsed. The frequency of the paroxysms varies 
very greatly in different cases and at different times in the twenty-four 
hours. Some patients cough but once or twice a day, while others are 
seized every few minutes. Usually the child is greatly frightened if the 
attack is severe, and often it soon learns to recognize the early signs of an 
approaching seizure and runs to its mother or nurse for help. The attacks 
are provoked by crying, laughing, eating or drinking, and by inhalation 
of dust-laden air. Between the paroxysms perfect quiet and respiratory 
comfort may be present unless complications arise. In the severe cases 
nose-bleed and ecchymoses of the conjunctiva may occur and blood may 
come from the ears and mouth. The convulsive efforts during the cough 
very frequently cause vomiting, and at times the urine or feces may be 
forcibly expelled, or they escape after an attack because of profound exhaus- 
tion and the relaxation produced by the asphyxia. A nodular infiltration, 
or an ulcer, at the freenum of the tongue is often produced by irritation of the 
projecting organ upon the lower incisor teeth. The circulation is usually 
not much affected save during the paroxysm, when it is labored, owing to 
the asphyxia. Between the paroxysms it may be rapid and feeble if the 
attacks are frequent and severe enough to strain and dilate the heart. Some 
clinicians assert that permanent cardiac feebleness and dilatation may 
result from this disease. 

In severe cases in young children and in feeble individuals great asthenia 
may be produced by the violence of the spasm, the loss of sleep, and the 
loss of food from vomiting, which may occur at every paroxysm. 

Inspection of the bared chest during the inspiratory part of each attack 
reveals in the stage of inspiration deep retraction of the intercostal spaces, 
of the episternal notch, and of the epiclavicular areas. The epigastrium is 
also retracted, for all the auxiliary muscles of respiration endeavor to aid 
in the drawing in of air. Auscultation of the chest, particularly over the 
posterior surface, almost always reveals bronchial rales, due to the bron- 
chitis which is present in all cases, even if they be mild. Care should always 
be exercised that this bronchitis is not increased by exposure to cold and 
dampness, since it is exceedingly prone to develop into bronchopneumonia, 
particularly in young children and old persons. Indeed, it may be said that 
the high mortality of the disease is due almost entirely to this complica- 
tion. 

A number of clinicians, particularly Cima and Meunier, have shown that 
even in the very early stages of pertussis there is present a very extraordinary 
degree of leukocytosis. This leukocytosis is largely composed of lympho- 
cytes, the polymorphonuclear cells being relatively decreased. As in most 
infectious diseases, a small amount of albumin is found in the urine in 
the majority of cases. 

The duration of whooping-cough varies from six to eight weeks, more 
commonlv the latter than the former. 



122 DISEASES DUE TO A SPECIFIC INFECTION 

Complications. — The complications of whooping-cough are chiefly con- 
nected with the respiratory tract. Bronchopneumonia, as just stated, is 
very common, and follows the bronchitis which usually is developed in the 
earlier stages of the disease. It is particularly apt to attack young children 
and to occur in the winter months. Sometimes a true lobar pneumonia 
develops. 

In nearly all cases of whooping-cough a moderate degree of compensatory 
emphysema comes on because of the violent respiratory efforts of the patient, 
and rarely this strain on the tissues of the lungs results in the rupture of 
an air vesicle and the development of interstitial or interlobular emphy- 
sema. In other instances the quantity of air which escapes in this way is 
very large and infiltrates the tissues of the mediastinum, the subcutaneous 
tissues of the chest, and in extreme cases those of the entire body. Instances 
of this condition have been reported by Gelmo, Ferrell, and Bierbaum, 
and have usually proved fatal. Cases are also recorded in which pneumo- 
thorax has been produced. It is by no means uncommon, particularly 
among the children of the poorer classes, for whooping-cough to be followed 
by pulmonary tuberculosis, probably because of the lowered vital resistance 
of the patient. Another complication of importance, although it has been de- 
scribed as a symptom, is vomiting, which if it becomes constant is a serious 
condition, particularly in infants, since it may cause death from asthenia. 

The bronchial glands are nearly always enlarged and may be so much 
increased in size as to cause dulness on percussion over the sternum. The 
area of cardiac dulness is increased by reason of the dilatation of the heart 
due to the strain thrown upon it in the attack of coughing. 

Measles and whooping-cough are, as already stated, very commonly 
associated, but the whooping-cough complicates the measles more fre- 
quently than the measles complicates the pertussis. Sometimes in very 
young children the disease becomes so severe that the spasm of the cough 
seems to spread to all the muscles of the body and produce general convul- 
sions. These cases are nearly always fatal. 

Paralysis complicating whooping-cough is not common. It is usually 
in the form of a hemiplegia, and occurs either during the acute period of 
the disease or as a sequel. When it takes place during the paroxysmal 
period it is due in the majority of instances to meningeal or cerebral hemor- 
rhage in all probability, although statistics as to this question are scanty. 
Twelve cases of cerebral hemorrhage due to whooping-cough have been 
collected by Townsend of which seven recovered, and Brown has reported 
a case in which he operated for the relief of cerebral compression due to 
this cause with excellent results to the patient. The literature of this subject 
has recently been analyzed by W. G. A. Robertson. Sometimes paraplegia 
or monoplegia has occurred during the stage of convalescence. The 
prognosis seems to be fairly favorable, indicating that the lesion producing 
these conditions cannot be permanent. Small conjunctival hemorrhages 
are not infrequent, and more rarely large extravasations of blood into the 
conjunctival tissues take place, amounting to ecchymoses. Still more rarely 
temporary amblyopia develops as a result of disordered circulation in the 
retina or possibly of an actual retinal hemorrhage. 



WHOOPING-COUGH 123 

Diagnosis. — The important points in the diagnosis of whooping-cough 
are the repeated and rapid coughs in series until the chest is almost emptied 
of air, followed by a sudden inspiration through the narrowed glottic open- 
ing. Some cases develop only the series of short coughs, and present no 
whoop afterward. 

Prognosis and Mortality. — The prognosis in whooping-cough as in most 
infectious diseases, depends upon the age of the child, its general nutrition 
and vital resistance, and upon the care the child can receive. In general 
terms it may also be stated that the prognosis is not so good in winter as in 
summer, as fresh air is not so readily obtained and there is greater danger 
of exposure to cold in the winter months. In itself whooping-cough is not 
a fatal disease. Death is due to the complications which ensue, and if 
these can be prevented the patient always gets well. In very young children, 
however, it is almost impossible to prevent the development of broncho- 
pneumonia, and this is a dangerous condition in proportion to the youth 
of the child. In London whooping-cough stands second as a cause of death 
from the infectious diseases in children under two years of age. 

Hagenbach, of Basle, gives the following mortality statistics, which are 
based on the cases that came under his observation during a period of 
eleven years: under one year, 26.8 per cent.; between one and two years, 
13.8 per cent.; between two and five years, 3 per cent.; between five and 
fifteen years, 1.8 per cent. 

Holt states that the mortality for children under one year of age is 25 
per cent. 

Treatment. — It is vitally important that children who have whooping- 
cough should be put under the most favorable hygienic conditions as to 
sunlight, fresh air, and equable temperature. In the summer they do best 
out-of-doors when the weather is not too cool, if they are prevented from 
acting imprudently, as, for example, getting the feet wet. In winter they 
should be kept in a warm room, the temperature of which should be 70° 
night and day. The air of this room should also be moistened by liberating 
in it small quantities of steam obtained from a kettle of boiling water, 
from a croup kettle, or by dropping pieces of unslaked lime in a bucket 
of water. This is an exceedingly important measure if the room is heated 
by a furnace, since the air from the ordinary furnace is exceptionally dry 
and often laden with dust, and these two causes act as an irritant to the 
already irritated respiratory tract. When it is not possible to confine the 
child to a room which is heated evenly, a most excellent method of treat- 
ment, particularly in those cases where the paroxysms are frequent at 
night, is to place the child in a bronchitis tent. A bronchitis tent consists in 
throwing over a bed a large sheet which is supported several feet above the 
head of the child by means of broomsticks or poles, which are tied at each 
corner of the bed. This tent can be made quite attractive for children by 
decorating it. Into this tent, at the foot of the bed, may be discharged a 
small quantity of steam such as is given off from an ordinary kettle of water 
when it is kept constantly boiling. In this way the child's mucous mem- 
branes are not irritated by dry or cold air, but on the contrary are greatly 
soothed, and I have frequently diminished the number of paroxysms per 



124 DISEASES DUE TO A SPECIFIC INFECTION 

day at least one-half by the institution of this plan of treatment, which 
has the additional advantage that it is prophylactic, and prevents the 
development of those serious complications like vomiting and broncho- 
pneumonia, which are much aided in their development by repeated 
and violent paroxysms of cough. With a little attention a child may 
be kept in such a bronchitis tent night and day through the entire 
attack. 

In the way of drugs there is no remedy so efficacious in diminishing the 
severity of the attack as small doses of antipyrin; that is to say, i to 1 grain 
of antipyrin every three or four hours to a child of one or two years, or 
2 grains every three or four hours to a child of five or six years, care being 
taken that the drug does not too greatly relax the skin or depress the cir- 
culation. There is a widespread belief among the laity that quinine in 
small doses is not only a prophylactic against whooping-cough for other 
children in the family who have not as yet contracted the disease, but that 
it is also of curative value. Some physicians have used a spray of a weak 
solution of quinine in the throat with asserted advantageous results, but 
its value is doubtful, and its bitter taste makes its use impossible in a large 
proportion of cases. 

The development of complications, such as bronchopneumonia, neces- 
sitates the institution of those lines of treatment which will be found 
suggested for that disease. For the relief of the individual paroxysms of 
cough several remedies may be employed, of which the best is probably 
chloroform. It is needless to say that this drug should be used with 
great caution, and the patient's parents and the nurse should be instructed 
never to use it on a cloth, but, when the paroxysm is threatened, to pour 
the remedy over the back of the hand and place the hand under the 
child's nose. Under these circumstances a sufficient quantity of the chloro- 
form is often inhaled to relax the spasm, without producing any of the 
marked physiological effects which would certainly be obtained to an un- 
desirable degree if the drug were poured on to a napkin. This method 
also prevents an overdose of chloroform being given, since the excess of 
the drug rapidly runs off the hand or evaporates. As the hurry of an 
approaching paroxysm often makes the attendant careless as to the quantity 
which is poured out of the bottle, the physician should insist that the chloro- 
form be used in no other way than that which has just been described. If 
the paroxysms are too severe to be controlled in this way, nitrite of amyl 
may be occasionally employed. 

An innumerable array of drugs have been recommended for the palliation 
and cure of whooping-cough. Suffice it to say that most of them are entirely 
useless. Even such powerful nervous sedatives as the bromides cannot act ad- 
vantageously in many of these cases, and the use of more powerful ones such 
as chloral and opium are contraindicated for evident reasons. The physician 
should always remember that whooping-cough is a disease which is bound 
to run its course, uninfluenced in its duration by any treatment which he 
can employ. The most that the physician can do is to prevent complica- 
tions, treat them if they arise, and endeavor to modify the frequency and 
severity of the individual paroxysms, being careful in so doing that the 



INFLUENZA 125 

remedy is not worse than the disease, in the sense that it produces digestive 
or circulatory disorders which are distinctly disadvantageous. 



INFLUENZA. 

Definition. — Influenza is sometimes called la Grippe. It is a pandemic 
disease; that is, one which appears in widely separated parts of the world 
simultaneously. It is also highly infectious, and the infection is produced 
by the bacillus of Pfeiffer. Influenza of this type is to be separated, theo- 
retically at least, from that condition sometimes called "common cold" or 
"coryza, " which often causes somewhat similar symptoms in a milder form, 
although during the presence of an epidemic of la Grippe the differential 
diagnosis may be impossible. At the present time the term "influenza" is 
often employed when the physician is unable to reach a diagnosis, and as a 
consequence is greatly abused, particularly in the early stages of typhoid 
fever and tuberculosis. 

Leichtenstern has divided the disease into two varieties, namely, true 
epidemic influenza (influenza vera) due to the bacillus of Pfeiffer, and 
endemic influenza due to the same cause and occurring for some 
years after an epidemic has been present. Both of these forms are to be 
separated from ordinary pseudo-epidemic influenza or an attack of ordinary 
cold in the head. A peculiarity of true influenza in its epidemic form is 
the large percentage of persons which it attacks within a short space of 
time, more than any other epidemic disease except dengue. 

History. — At various times in the past great epidemics have broken out 
and raged over the entire world, and have been followed by long periods of 
immunity. Thus, when the great epidemic of 1889 occurred, only a few 
physicians, and they of advanced years, had ever seen a case, for the previous 
epidemic had occurred in 1847 and 1848. 

Pandemics have occurred during the last century in 1830-33, 1836-37, 
1847-48, and 1889-90. In 1889 the disease began in remote parts of Russia 
in October, reached Moscow in November, ten weeks later it got to Berlin, 
a month later to London, and soon after to New York and Philadelphia, 
and thence it spread all over the continent of North America. Within the next 
few months nearly the whole civilized world was affected by it. Since the 
last outbreak the disease has been endemic, but it is an attenuated form of 
the infection. An individual locality is rarely subject to an epidemic for 
more than two months, but sporadic outbreaks occur for a long period 
afterward. 

Etiology. — It is interesting to note that the word influenza is derived from 
the Latin sentence ab coeli occultes quadam influentia — from some hidden 
influence in the sky. Influenza, if entirely dependent upon a micro-organism 
for its infectious character, must also be dependent upon certain telluric 
influences, at present unknown, which render the human race more suscep- 
tible to the effects of the germ at certain times or which render the germ 
more capable of producing infection at certain periods. 

There are two chief factors involved in the production of an attack of 



126 DISEASES DUE TO A SPECIFIC INFECTION 

influenza, namely, the presence of the bacillus, usually received directly 
from another patient by contact, or through the air; and, second, atmos- 
pheric states which are favorable to the growth of the germ or to the 
production of individual susceptibility. A third factor, always of importance 
in connection with infectious diseases, is the presence of pre-existing 
disease which decreases the general vital resistance of the patient. 

The bacillus of Pfeiffer was first isolated by that investigator in 1892. 
The organism is small and non-motile, and can be well stained bv Loeffler's 
methylene blue or by well-diluted watery solutions of carbol-fuchsin. It 
develops in myriads on the nasal and bronchial mucous membranes and in 
the secretions of those parts. A number of observers, and more particularly 
Ricciardi, have shown that the bacillus is readily distributed and spreads 
most actively by droplets of mucus. Even after the patient has recovered 
from an attack his nasal secretions may reinfect himself or other persons 
for a period of weeks, and therefore all handkerchiefs, towels, and pillow- 
cases used by him should be boiled before being used by others. The 
room occupied by the patient should be fumigated with formaldehyde 
after his recovery occurs and before anyone else occupies it. 

It is a noteworthy fact that during an epidemic of influenza other infec- 
tious diseases seem to be less common. This is particularly true of malarial 
fevers, if the statistics collected by Anders, of Philadelphia, are correctly 
interpreted. 

Incubation. — The period of incubation is probably from twenty-four to 
seventy-two hours, but in some cases it seems to be longer than this. 

Symptoms. — The onset of symptoms of epidemic influenza is nearly 
always sudden. A person feeling perfectly well may suddenly be seized by 
a sense of chilliness or a severe rigor, followed by severe aching pains in the 
back and in the legs. There is usually congestion of the nasal mucous 
membrane, so that the patient seems to have a severe cold in the head. 
The chill is quickly followed by fever which may rapidly rise to a point as 
high as 105°, although as a rule 103° is the more common acme. Associated 
with these early symptoms there is usually a sense of severe illness and a 
feeling of great wretchedness, so that the patient not only expresses himself 
as feeling very ill, but seems so to the physician. 

About this time the symptoms are wont to be associated with additional 
ones indicating involvement of certain viscera. Most frequently the respi- 
ratory system is affected, and, in addition to more or less intense conges- 
tion of the nasal mucous membrane, an acute bronchitis develops; the 
physical signs in the chest being typically those of acute bronchitis w T ith 
excessive, unproductive cough and a sense of thoracic soreness. When the 
nasal mucus is examined it is seen to be unusually thin, and if any bron- 
chial mucus is expelled it is also of this character. As the disease pro- 
gresses the sputum becomes greenish-yellow and thick. 

The general state of the patient at this time is often one of profound 
depression, far in excess of that which usually accompanies such signs of 
bronchitis. The action of the heart may be feeble and the skin is relaxed 
and clammy, or it may be very hot and dry. 

If convalescence is not soon established the disease often develops into a 



INFLUENZA ]27 

peculiar form of pulmonary congestion or pneumonia, in which the sputum 
may be blood-tinged and frothy or in which no sputum may appear. A 
peculiarity of this pulmonary involvement, in one of its forms, is the fact 
that it moves from place to place with remarkable rapidity. An area of 
impaired resonance which existed yesterday is clear to-day, and still another 
area of congestion develops elsewhere — a form of wandering congestion. 
AVhen true pneumonia develops it may be croupous in type and be due to 
mixed infection by the bacillus of Pfeiffer and by that of true pneumonia, or 
it may be in the form of bronchopneumonia. The latter type is the more 
common, but both forms are apt to be serious and particularly so in the 
feeble, the aged, the very young, and in alcoholic or renal cases. Pneu- 
monia and heart-failure due to an action of the toxin of the disease on the 
heart muscle are the chief causes of death in all epidemics. 

Pleurisy followed by empyema is not very rare. 

In studying a case of influenza accompanied by pulmonary signs the 
physician must always bear in mind the possibility of the presence of asso- 
ciated tuberculous infection, because an attack of influenza not only often 
predisposes to this disease, but in addition permits unrecognized foci of early 
tuberculous infection to become active. 

In some cases of influenza the Heart seems to bear the chief brunt of the 
attack, so that repeated attacks of syncope ensue. These instances are met 
with chiefly among patients who have persisted in remaining at work during 
the early stages of the disease, or who have had, previous to the attack, an 
impaired heart muscle. Thus, a heart dilated as the result of excessive 
exercise may succumb readily, or one in which early but hitherto unrecog- 
nized degenerative changes were developing may suddenly fail. Often 
the symptoms of influenza are chiefly gastrointestinal or nervous. 

The gastrointestinal form of the disease may ha\e its onset in severe 
diarrhoea and vomiting, with collapse and violent abdominal pain. In some 
cases the pain is entirely absent, and profuse watery stools are present. 
Jaundice may be present, due to an extension of the gastrointestinal catarrh 
to the common biliary duct. 

In the nervous form the symptoms consist of profound nervous and 
mental depression, or in severe neuralgic pain which may or may not be due 
to neuritis. Mental disturbances in the course of an attack of influenza 
are by no means rare. Indeed, it may be said that no other acute infectious 
disease is commonly so complicated, or followed, by such a condition. Leich- 
tenstern states that he met with fewer psychoses among 2000 cases of typhoid 
fever and 3000 cases of pneumonia than he found among 439 cases of influ- 
enza. These psychoses may be of the exhaustion type, but usually are due 
to a toxic state induced by the malady. The mental disturbance may 
develop during the stage of onset, the febrile stage, or the stage of decline 
or convalescence- The latter cases are usually of the exhaustion type. 
The prognosis in these cases as to the state of the mind is usually good 
unless there is a bad history as to heredity. 

Very rarely meningitis develops, and still more rarely true encephalitis. 
Cases of cerebral abscess have also been ascribed to this disease. In 
rare cases a toxic neuritis develops, and this may be single or multiple. 



128 DISEASES DUE TO A SPECIFIC INFECTION 

Even paraplegia due to this cause may arise. Not only may this type of 
influenza affect the nerves of sensation and motion, but specialized nerves 
such as the vagus, thereby causing disturbances of the circulation such as 
paroxysms of tachycardia and bradycardia. In an analysis of 29,000 cases 
Lee found that 7000 were of the nervous type. In some instances the dis- 
turbance of circulation is due more to an influence exercised upon the 
vasomotor nervous system than to any direct effect upon the nerve supply 
of the heart, so that attacks of syncope come on from acute vascular relaxa- 
tion. 

Complications and Sequelae. — It is difficult to separate the complications 
of influenza from the ordinary symptoms of the disease because the natural 
course of the disease presents such diverse manifestations in different 
organs. Without doubt pulmonary, cardiac, and renal disorders are the 
most common complications. In many cases death is due to an attack of 
pneumonia, which rapidly carries off the patient whose vitality is already 
sapped by the onset of la Grippe. In other instances the kidneys, which 
have been impaired before the attack, suffer from an acute congestion or 
true nephritis superimposed upon the subacute or chronic state, and so 
urremia speedily comes on, with its helpmate, pulmonary oedema. 

Patients with influenza develop cardiac complications in three chief classes : 
either they already have mild cardiovascular degeneration which enables the 
influenzal toxin to work havoc with the cardiac muscle, or they have dilated 
feeble hearts, or, again, as already stated, they persist in remaining at work 
after the attack begins and refuse to go to bed. These patients not only 
have serious cardiac difficulty during the attack, but very frequently suffer 
from cardiac weakness and distress for manv weeks after convalescence 
should be well established. The man who persists in remaining out of bed 
when attacked by this disease literally " takes his life in his hand." 

The German collective investigation of the epidemic of 1889-90, based 
on an analysis of 3185 cases, gave the following results as to the relative fre- 
quency of complications, which results, however, differ materially from 
clinical experience in America so far as the cardiac complications are con- 
cerned : 

1. Diseases of the respiratory organs, exclusive of pneumonia, 48.76 per 
cent. 

Of these complications pleurisy was the most frequent, being present in 
27 per cent, of the entire number of cases. Pneumonia was present in from 
6 to 8 per cent, of all cases. 

2. Diseases of the nervous system, 45.77 per cent. 

3. Diseases of the ear, 37.95 per cent. 

4. Hemorrhages, 25.33 per cento 

5. Diseases of the heart and vascular system, 14.09 per cent. 

6. Diseases of the digestive organs, 10.36 per cent. 

7. Polyarthritis, 7.28 per cent. 

8. Diseases of the eye, 7.03 per cent. 

9. Albuminuria and nephritis, 4.52 per cent. 

Diagnosis. — It is so easy to make a diagnosis of influenza during the 
presence of an epidemic that physicians are wont to be careless in exam- 



INFLUENZA 129 

ining the patient thoroughly, and so may overlook complications of 
importance or decide that the case is one of influenza when in reality the 
chills, the fever, the aching, and the prostration are due to an oncoming 
typhoid fever or an acute tuberculosis or malaria. All of these diseases, 
and also ulcerative endocarditis and sepsis, should be carefully excluded 
before a diagnosis of influenza is made. 

Treatment. — Above all other things in the treatment of influenza is rest 
in bed. This is as true of mild as of severe cases and of the patient who 
is stalwart as of the patient who is feeble. A robust man who fails to rest 
almost always suffers from a severe attack or from sequelae, such as cardiac 
disorder and giddiness, which may invalid him for weeks. Aside from rest 
in bed little medicine is needed except for the purpose of relieving symp- 
toms which are troublesome. For the relief of the excessive pain in the back 
and limbs the coal-tar products have been employed by the ton. Although 
they give ease they are harmful if the doses are large, and often fail if they 
are used in moderate amounts. They tend to increase nervous and circula- 
tory depression, and to decrease the ability of the patient to resist the infec- 
tion from which he is suffering and the possible secondary infections which 
may occur. If the patient will rest they may be used moderately; if he will 
not rest they should not be used, for they not only do harm directly, but by 
diminishing discomfort they also enable and encourage him to remain out 
of bed. 

A very useful drug for the relief of the aching and pains in the back and 
limbs is salicin in 5 grain doses every five hours in capsules. Many prac- 
titioners believe that this drug alone, or when combined with 2 grains of 
quinine, acts as a specific in the cure of the affection. Should the pain in 
the back be intense it may be relieved by the application of hot stupes or 
compresses or by rubbing with soothing liniments. A more ancient but 
nevertheless very useful remedy for this condition, particularly in the early 
stage of the malady, is Dover's powder in the dose of from 2 to 10 grains 
once or twice a day. At one time used as a matter of routine in all infec- 
tions, it has fallen into an undeserved disuse. 

Headache, if it be due to congestion, may be modified by the use of an 
ice-bag, or by the administration of 1 to 2 grains of caffeine with 5 grains of 
bromide of sodium or potassium every few hours. This formula can be 
given in the form of an effervescent granular salt without the use of the 
coal-tar products often added by manufacturers of headache cures. Hot 
foot-baths also decrease headache. Menthol pencils may be used locally 
for neuralgia or a spray of chloride of ethyl may be used locally for the same 
purpose. 

As in all infectious maladies, it is of the greatest importance that the 
organs of elimination be kept active. The bowels may be first moved by a 
grain or two of calomel, followed in twelve hours by a Seidlitz powder, or, 
if constipation has been marked, they may be opened at once by citrate 
of magnesium. For the purpose of keeping the kidneys active 5 grains of 
citrate of potassium or of bicarbonate of potassium may be given every four 
hours in copious draughts of water if the urine is acid, or the same amount 
of benzoate of ammonium if the urine is alkaline. The latter drug is best 



130 DISEASES DUE TO A SPECIFIC INFECTION 

given in capsules, and possesses the additional advantage of acting favorably 
upon the respiratory mucous membrane and upon the muscular pains. A 
hot compress or poultice applied over the loins will often establish renal 
secretion when it seems scanty. 

Dryness and soreness of the mucous membrane of the respiratory tract, 
in the stage of onset, may be much relieved by telling the patient to inhale 
steam which may be medicated by the addition to the water from which it 
arises of a few grains of menthol or of equal parts of menthol, oil of eucalyp- 
tus, and oil of pine. In other instances the patient may add to the boil- 
ing water a tablespoonful of compound tincture of benzoin. The medi- 
cated steam may be taken directly from an inhaler or the vapor may be 
set free in the air of the room by the use of a bronchitis kettle. When the 
nasal mucous membrane is so congested and occluded that breathing is 
difficult and oppression is marked, adrenalin chloride, 1 : 5000, with chloretone 
may be sprayed into the nostrils or applied on pledgets of cotton. It loses its 
effect if applied too often, but it does not do so as rapidly as does cocaine, 
nor is it dangerous in its systemic effects. 

For the relief of the congestion of the respiratory mucous membrane, 
when the illness has lasted for several days and the secretion is thick and 
tenacious, chloride of ammonium in 5 grain doses four times a day may be 
administered combined with codeine or heroin to relieve cough, or terpin 
hydrate may be used with the same sedatives in the form of the well-known 
elixir of terpin hydrate with heroin. For the persistent cough of convales- 
cence, oil of sandal- wood in 5 minim doses four times a day is very useful. 

Circulatory and nervous stimulants are not to be used unless there is 
distinct evidence of their need. Alcoholic drinks are as a rule to be ex- 
cluded, unless the patient uses them habitually when well, when they have 
to be given, preferably in the form of an old brandy or good w T hiskey. Great 
care must be taken that the patient does not overuse them in his endeavor 
to make himself feel stronger. For acute circulatory failure aromatic spirit 
of ammonia or Hoffmann's anodyne are the remedies of choice. When the 
failure of the circulation is associated with nervous depression the use of 
strychnine is indicated, but it is greatly abused and should not be given 
day after day except as a tonic in convalescence, as it loses its power, is not 
a true stimulant but a nervous irritant, and often causes great irritability 
if not employed skilfully. 

As influenza is a disease which produces great prostration, a diet which 
is easily digested and nutritious is essential for the maintenance of strength, 
particularly in the very young, very feeble, and very old. Animal broths, 
oysters, and predigested foods are useful, and they may be fortified with 
advantage by barley-gruel, the digestion of which may be aided by the use 
of taka-diastase. Indeed, the various vegetable gruels with taka-diastase 
are in many cases better than the animal broths. Arrowroot and milk- 
toast and eggs are also useful. 

Prophylaxis. — There can be no doubt that much can be done to prevent 
the spread of la Grippe from one person to another by isolating the ill and 
by forbidding healthy persons to occupy the sick-room after it is vacated, 
until it is thoroughly disinfected. This is particularly advisable when the 



DENGUE 131 

old and feeble are about the house and when persons who are still weak 
from one attack are exposed. Every effort should be made to keep the 
malady out of the non-medical wards of hospitals, insane asylums, and 
almshouses. Patients in these institutions when taken ill should be iso- 
lated. 

All rooms, clothes, and books used by patients suffering from influenza 
should be disinfected as carefully as if the patient had suffered from some 
more fatal malady. 

DENGUE. 

Definition. — Dengue is an acute infectious, but non-contagious, usually 
epidemic fever, which is probably dependent for its development upon the 
presence of some specific organism the exact nature of which is still obscure, 
although McLaughlin and Graham believe that they have succeeded in 
isolating it. The disease is characterized by two febrile attacks with severe 
pains in the muscles and joints. Because of these latter symptoms it is 
often called "breakbone fever," and from the peculiar gait caused by this 
condition "dandy fever." A large number of other popular names have 
been given it, such as "three-day fever," "bouquet fever," or sometimes, as 
a corruption of the last name, "bucket fever." 

History and Distribution. — The earliest accurate description of dengue 
that we possess is that of Brylon, who described the outbreak of 1779; later 
the celebrated epidemic in Philadelphia, in 1780, was described by Hush. 
Since then it has occurred in a considerable number of epidemics in various 
parts of the world, such as Batavia, Spain, India, Bermuda, Brazil, the 
West Indies, and in various parts of the Southern United States. Within 
twenty years it has also visited Turkey, Greece, Fiji, and Tripoli. It is, 
however, distinctly a disease of warm climates, and, so far as I know, has 
never been met with north of Philadelphia. The disease spreads from 
point to point along lines of travel, being carried by infected individuals 
and perhaps by clothing. 

A peculiarity of dengue is the rapidity of its spread and the few people 
in a community who escape its attack. In this respect it surpasses epidemic 
influenza. No age sex, or race escapes, and in an incredibly short time 
after the first case is seen a multitude may be down with it. As Manson 
well says, it "bursts" upon a place. The spread of an epidemic is always 
arrested by the appearance of cold weather. High altitudes are also unfav- 
orable to its spread. 

Pathology and Mode of Propagation of Dengue. — H. Graham, of Beyrouth, 
has observed in the blood of dengue patients an unpigmented, oval-shaped 
protozoon, having amoeboid movements, and frequently showing a sharply 
pointed extremity such as is seen in the parasite of the so-called Texas 
fever. This parasite is of lighter color than the red blood corpuscles in 
which it constantly changes its position. Dr. Graham also conducted 
experiments for the purpose of determining whether the disease is propa- 
gated by mosquitoes, as a result of which he came to the conclusion that 
the Culex jastigans carries the parasite from the sick to the well. 



132 DISEASES DUE TO A SPECIFIC INFECTION 

In several instances Graham placed persons suffering from dengue in 
apartments in which all mosquitoes had been destroyed by chlorine gas, and 
allowed healthy individuals to associate with the sick. In no case of this 
kind was the disease contracted. In addition to this negative evidence 
Graham offers positive evidence which he obtained by allowing mosquitoes 
which had bitten affected persons to bite two healthy individuals who 
resided in a district where no cases of dengue were present. Both of these 
men developed the disease, one on the fourth and the other on the fifth day 
after they were bitten. They were kept under mosquito nettings until they 
had completely recovered and the infected mosquitoes were all killed. No 
other cases of dengue occurred in the village where these experiments were 
made. The same organism which was found in the blood of dengue patients 
was also found in the blood and the stomach of Culex jastigans, even up 
to the fifth day after the insect had bitten an infected individual. 

The organism multiplies by sporulation in the stomach walls and veno- 
salivary glands of the mosquito. Inoculation of a human subject with a 
solution of the salivary glands of an infected mosquito produced, on the 
third day, a chill and high fever followed by a typical attack of dengue. 
As yet Graham's observations have not been confirmed. 

Symptoms. — Dengue is characterized by a train of symptoms which is 
quite remarkable. In the first place, the suddenness of its onset is note- 
worthy. A patient may be in perfect health at one hour and sick in bed 
with well-developed symptoms the next. In any event the onset is sudden, 
and sometimes it is ushered in by a chill or by pains in the limbs. Fever 
rapidly develops and may reach as high as 106° or 107°, but usually the 
acme is 103° to 105°. There is intense headache and the pains in the limbs 
are so excruciating that the term "breakbone fever" is well applied. The 
discomfort of the patient is increased by the pain caused by moving the 
body. The tongue is usually heavily coated, and nausea and vomiting 
may be distressing symptoms. 

With the onset of the fever there develops a rash which is of the nature 
of erythema. In from one to three days, usually two days, the fever 
suddenly ends by crisis and simultaneously the patient not only sweats 
freely, but also has free diuresis, diarrh&a, and nose-bleed. This nose- 
bleed, by relieving the cerebral congestion, greatly decreases the headache, 
and the rash rapidly fades. 

In other instances the fever gradually falls by lysis, but this is less 
common than crisis. The fever having fallen to normal the patient, still 
feeling weak, is able to be about, although he suffers from twinges of pain 
in the joints and muscles, which impress upon his mind the fact that he is 
as yet ill. After a remission of several days, usually from two to four, the 
fever returns with some violence, but it is rarely as severe as in the primary 
paroxysm, and it usually lasts only a few hours. With the appearance of 
this secondary fever a roseolous rash develops, and with its development 
the patient may have a return of his bone and joint pains to a very severe 
degree. Although the fever soon disappears the rash lasts for several days 
and may end in a slight desquamation. Taking it all in all, the secondary 
attack is usually much milder than the first. 



DENGUE 133 

The rash of the second attack is roseolous, and is peculiar in that it is 
usually first seen on the hands, both the palmar and extensor surfaces, 
and thence rapidly spreads to the entire body. The spots are as large as a 
pea, circular in appearance, dusky red, and perhaps elevated. As the dis- 
ease progresses they may coalesce, leaving patches of healthy skin between. 
This rash is more apt to be profuse and to coalesce around the joints than 
elsewhere. The roseola fades as it begins, first on the hands, then on the 
arms and body, and lastly on the legs. The desquamation may last for 
weeks, but it is so fine that it may be overlooked. The skin never peels 
as after scarlet fever. In some instances the patient passes on to rapid 
convalescence after the terminal or roseolous rash fades, but in others he 
remains miserable for a long time from wandering pains in his joints or in 
the soles of his feet. The muscles are sore on pressure and stiff on moving 
after a long rest, and debility may be persistent. In some instances insomnia 
or furunculosis delays complete recovery. 

In certain epidemics there is sufficient degree of swelling and redness 
about the joints to suggest the presence of acute rheumatism. 

Relapses of dengue occur not infrequently. 

Diagnosis. — Dengue may be separated from rotheln, which it resembles 
during the period of its secondary rash by the lymphatic swellings of the 
latter disease. The differentiation is also accomplished by the sudden severe 
onset and the pain in the joints. It is distinguished from scarlet fever by 
the lack of sore throat and the peculiar scarlet hue of that disease, and from 
syphilitic roseola by the absence of a history of venereal infection, and the 
fact that associated symptoms of the early secondary stage of syphilis are 
absent. On the other hand, it is to be recalled that many syphilitics, with the 
onset of the roseola of that disease, suffer from a chill and general wretch- 
edness with pains in the bones. Influenza is separated by the absence of 
catarrhal symptoms and by the presence of the rash in dengue. Acute 
articular rheumatism and malarial infection are two other diseases which 
must be borne in mind when the diagnosis of an individual case is in 
question. 

Prognosis. — The prognosis in a case of dengue is always favorable if the 
patient, prior to the attack, is in good health, and not debilitated by some 
other malady or old age. Death may be said not to be known as a result 
of this malady in ordinarily healthy persons. Convalescence, after a severe 
attack, is, however, very often quite slow, and if the patient is living in a 
hot climate recovery may not be complete until a change of residence is 
made. 

When dengue attacks the aged and feeble, or very young children, it 
sometimes indirectly causes severe illness and death by predisposing the 
patient to other infections so that there develops a severe bronchitis or 
bronchopneumonia, or some other evidence of acute infection. In such 
cases the prognosis depends chiefly upon the character of the secondary 
ailment. 

Treatment. — In discussing the treatment of this disease it is to be recalled 
that it presents very different degrees of severity in different cases. In 
many persons the symptoms are so mild that the patient seems scarcely 



134 DISEASES DUE TO A SPECIFIC INFECTION 

at all ill, and in others the manifestations are so severe that convulsions 
and unconsciousness may be present. In the mild cases no drugs are needed, 
but in the severe cases active treatment may be essential. In general terms 
it may be stated that the treatment of the patient suffering from dengue 
consists in absolute rest in bed from the earliest stage of onset till the con- 
clusion of the second stage of fever. Indeed, the longer he will consent to 
rest in bed after the fever develops, the more rapidly will complete convales- 
cence be established. 

So far as drugs are concerned, there are no specifics for this disease, 
which, if permitted, will usually run its own self-limited course to recovery. 
When the pains are intolerable they may be controlled by moderate doses 
of morphine given hypodermically or by the use of acetanilid or phenacetin. 
A gentle antipyretic and sedative mixture, containing 5 grains of potassium 
citrate and 30 minims of sweet spirit of nitre in a dessertspoonful of water, 
is useful to keep the kidneys active. An ice-bag may be applied to the head 
to relieve the cephalalgia, and if the face is very much flushed and the head 
throbs a hot foot-bath is advisable. Sometimes a hot bath is useful to 
develop the rash and relieve the pains in the body and limbs. In these cases 
the salicylates may also be used for the same purposes, 20 grains of sodium 
or strontium salicylate, or of aspirin, being given every three or four hours. 

When the circulation is strong and full McLaughlin asserts that large 
doses of tincture of gelsemium serve to quiet the excited pulse and to 
relieve the neuromuscular pains. The dose he recommends, namely, 20 
to 30 minims every three or four hours, seems to the writer much too large 
and capable of causing serious depressions; but as McLaughlin has had 
large experience with the disease, his views demand respectful attention. 
The fever is rarely sufficiently high or prolonged to require treatment. 
Should it require attention tepid spongings are usually sufficient to control it 
within safe limits; but should it reach as high as 105° or more, then it must 
be reduced by cold spongings, or even by the use of the cold bath, with active 
frictions. Should nervous symptoms be very manifest and convulsions be 
threatened, chloral should be given in the dose of 5 grains by the mouth, or 
10 grains by the rectum, if the patient is a child, and bromide of sodium used 
to aid it in its sedative action. 

The patient should be urged to drink freely, if his stomach will retain 
liquids, in order to keep his kidneys active in eliminating the poisons of the 
disease. When the stomach is not retentive a pint of cold water may be 
given by the rectum every eight hours. Should diarrhoea be troublesome 
it can be best controlled by giving castor oil to cleanse the bowels, and 
following it by opium. 

CEREBROSPINAL FEVER. 

Definition. — Cerebrospinal fever, sometimes called " cerebrospinal menin- 
gitis," " spotted fever," or " petechial fever," is an acute, often malignant, 
infectious, but rarely contagious disease, due to the diplococcus of Weich- 
selbaum, which is sometimes called the meningococcus or the Diplococcus 
intracelhdaris meningitidis. It is characterized by a rapid course, rigidity 



CEREBROSPINAL FEVER 135 

of the neck, retraction of the head and the formation of inflammatory exu- 
dates under the membranes which cover the brain and spinal cord. 
It is to be clearly understood that a number of pathogenic micro-organisms 
are capable of producing inflammation of the pia arachnoid, and conse- 
quently all the symptoms of true epidemic cerebrospinal meningitis. Such 
cases are not instances of this disease, but rather are to be considered as 
sporadic cases of meningeal infection. Indeed, it is a noteworthy fact 
that the sporadic cases of cerebrospinal meningitis which are due to the 
pneumococcus, are prone to be more virulent than those due to the specific 
organism just named. While the epidemic form has been proved to be 
always due to the Diplococcus intracellular is meningitidis, it is not cor- 
rect to call all cases of cerebrospinal meningitis instances of cerebro- 
spinal fever. 

History. — No definite description of this disease is to be found in medical 
literature prior to the nineteenth century. In 1805 the first case was described 
by Vieusseux, in Geneva, Switzerland, where several deaths took place 
from the disease. In America it first appeared in Medfield, Massachusetts, 
in 1806. During the next ten years the malady broke out in different parts of 
Europe and America, but disappeared after 1816 till 1822, when it reap- 
peared in France. In 1828 it broke out in Ohio. It was not, however, till 
1839 that it became sufficiently prevalent in any one place to cause a very 
large number of deaths. In that year, at Versailles, it ravaged the town 
and garrison and produced a mortality of nearly 75 per cent. Scattered 
epidemics have since occurred in the United States at intervals of every 
few years, and it is constantly present in scattered cases in the central 
part of the State of New York. (Eisner.) A noteworthy point in con- 
nection with the disease is the fact that it suddenly appears simultaneously 
in widely separated areas, and without any dependence upon lines of 
travel. Thus during a recent period of twelve months many cases occurred 
in New York, but none in Philadelphia, which is only ninety miles away. 
Certain atmospheric influences may make this possible, but its cause is 
not definitely understood. 

Etiology. — There can be no doubt that cerebrospinal fever is due to 
the diplococcus already named, but the same anatomical conditions and 
a similar clinical picture may be produced by other bacteria, for example, 
the pneumococcus and other pyogenic cocci. In cases of cerebrospinal 
meningitis which have appeared sporadically and presented all the signs 
of the epidemic disease the streptococcus, the staphylococcus pyogenes, 
the pneumococcus, the gonococcus(?), and even the bacilli of influenza 
and typhoid fever have been found as apparently the only cause of the 
affection. A similar acute serofibrinous meningitis may accompany pyaemia 
or septicaemia, or may be due to injury, with infection or extension of infec- 
tive processes from the frontal, ethmoidal, sphenoidal, or mastoid sinuses, 
middle or internal ear, or other parts of the envelope of the brain and 
cord. Such forms of meningitis are often called consecutive, incidental, or 
secondary, and are to be distinguished from the epidemic malady. 

Infection probably takes place through the respiratory passages, partic- 
ularly in the nose. 



136 DISEASES DUE TO A SPECIFIC INFECTION 

Climatic conditions undoubtedly exercise some influences, for the disease 
confines itself almost entirely to the colder parts of the temperate zone, but 
this is not to be taken as indicating that it is a disease of the winter months. 
On the contrary, it appears about equally frequently in winter and summer. 
While it is true that unhealthy surroundings favor all diseases, it is also true 
that they do not seem to greatly influence this malady, for it occurs on high 
and on low land, when it is dry and when it is wet, on hill and in marsh, 
with equal frequency. As Stille says, "It has passed by large cities reeking 
with all the corruptions of a soil saturated with ordure and populations 
begrimed with filth, to devastate clean and salubrious villages and the 
families of substantial farmers inhabiting isolated spots." 

The disease affects children and young adults far more frequently than 
persons in advanced life. It is slightly contagious, but cases of undoubted 
transference from one patient to another occur. The occurrence of the 
malady in a number of persons living in the same district is usually due to 
the fact that they have all been exposed to the same cause. 

Prevention. — We know of no method of preventing epidemic cerebro- 
spinal meningitis, but physicians and others who are attending cases, 
should wash the nasal mucous membrane with normal salt solution to aid 
in preventing infection. Cases should be isolated. 

Frequency. — From what has already been said, it is evident that this dis- 
ease is met in epidemic form, but is comparatively rare. Many practitioners 
never meet with a single or sporadic case in a long career; whereas, others 
may be so unfortunate as to meet several outbreaks. 

Pathology and Morbid Anatomy. — In fulminating cases death may occur 
before the meningeal exudate forms; in these the meninges may exhibit no 
exudate, showing only intense hyperemia and oedema, but the membranes 
and cerebrospinal fluid are usually rich in the specific organism. Death 
in such cases seems to depend on the toxic action of the serous bacteria- 
laden exudate. 

The characteristic lesion of this disease is an acute inflammatory exudate 
of the pia-arachnoid enveloping the brain and spinal cord. These mem- 
branes become infiltrated, and the surface appears to be covered by a white 
or creamy-white exudate, which is most conspicuous in the sulci. The ven- 
tricles may contain a cloudy, opaque, or even distinctly purulent fluid. The 
inflammatory exudate is most copious at the base of the brain and on the 
dorsal surface of the spinal cord, particularly in the lower thoracic and 
lumbar regions. When the disease affects children the lateral ventricles are 
often found at autopsy to be distended with purulent fluid, but in adults this 
condition is not likely to be marked. In the early stages of the disease the 
diplococcus is found in large numbers in the leukocytes contained in the 
exudates, but when death occurs late in the course of the malady the germ 
may be demonstrated with difficulty, if at all. 

In addition to the lesions in the meninges the nerves and ganglia exposed 
to the toxic action of the exudate undergo inflammatory and degenerative 
changes. The involvement of these nerves may leave irreparable damage, 
manifested by blindness, deafness, or other phenomena dependent upon the 
structures involved. Secondary alterations in other parts of the body may 



CEREBROSPINAL FEVER 137 

be present. These are due to the toxins of the disease or to the presence 
of the micro-organisms in the affected areas. Thus, we find petechias in 
the skin and mucous membranes and somewhat similar punctate extrava- 
sations of the blood in the endocardium. Not rarely multiple abscesses are 
found scattered through the body and multiple suppurative arthritis may be 
present. Hyaline and granular degeneration of the voluntary muscles is 
also demonstrable, and the heart muscle, kidneys, and liver may manifest 
necrotic, degenerative, or inflammatory changes. Occasionally there is 
found, associated with the meningitis, croupous pneumonia, ulcerative endo- 
carditis, and otitis media. These pathological conditions are characteristic 
of the severe forms of the disease. 

In some cases the lesions are much more moderate in that hypersemia, or 
intense congestion, of the pia mater only is seen, although the sulci between 
the convolutions of the brain may contain fibrin or pus. 

Incubation. — The period of incubation is from one to four days. 

Symptoms. — The symptoms of epidemic cerebrospinal meningitis may be 
grouped into five classes — viz., the moderate, the malignant, the intermit- 
tent, the typhoid, and the chronic form. 

In the moderate form, after an unknown period of incubation, the patient 
suffers from a sudden chill, which may be preceded by headache and dizzi- 
ness. The headache rapidly becomes very severe and is accompanied by 
severe pain in the back and down the back of the thighs, the muscles of 
which are often tense or fixed. The fever which follows the chill is usually 
moderate, rarely exceeding 102°, and it presents no characteristic curves. 
On the contrary, it is exceedingly irregular and does not show any con- 
stant morning and evening variations. Very rarely hyperpyrexia may 
develop. 

As the disease develops the tenseness of the muscles of the legs extends 
to those of the back, neck, and arms, and, finally, they may become almost 
rigid, and contracted to such a degree that the patient develops opisthotonos. 
The abdomen is rigid and scaphoid. Not rarely spasmodic movements 
of the muscles of the face develop as the result of irritation of the roots 
of the cranial nerves, and by reason of this same cause strabismus, ptosis, 
amaurosis, and diplopia may be present. The conjunctivae are usually 
reddened. 

Delirium is a very frequent symptom, and is sometimes so severe as to be 
maniacal. From this state the patient may pass into coma. 

The pulse and respiration are not greatly affected, except that as the disease 
progresses they may become feeble. Toward the end of the attack, if it be 
fatal in its nature, Cheyne-Stokes breathing may develop and the pulse 
become rapid and small. 

An eruption develops on the skin in about one-half of the cases. When 
it appears about the mouth it is herpetic, but on other parts of the body it is 
usually petechial, although herpes of the skin of the trunk and about the 
genitals may appear. At times a general erythema may be present or in its 
place an urticaria is developed. 

The presence of arthritis has already been referred to. It appears in 
about 20 per cent, of the cases. and ; as it is septic in nature, it may cause 



138 



DISEASES DUE TO A SPECIFIC INFECTION 



serious changes in the joints and result in permanent deformity if the 
patient survives. 

The blood shows no marked changes, save that the inflammation of the 
meninges results in a leukocytosis of the polymorphonuclear cells. 

As an almost constant symptom, mention should be made of " Kernig's 
sign,'' which consists in the fact that in inflammatory processes in the mem- 
branes of the cord it is not possible to extend the leg on the thigh when the 
thigh is at right angles to the plane of the body. Rarely this sign is 
unilateral (Fig. 29). 

In the malignant type of the disease the onset is remarkably sudden. The 
patient is seized by a chill, followed by headache, unconsciousness, and 
death. Convulsions occur more commonly in children than in adnlts. 
The fever may be absent, the pulse slow, the breathing labored, the urine 



Fig. 29 




Kernig's sign, showing the strong contraction of the flexors on attempting to extend the leg. 

(After Osier's case.) 



greatly decreased in amount and loaded with albumin, and the stupor pro- 
found. The patient in such an instance is probably overwhelmed by 
toxaemia, so that death may ensue in a few hours. 

In the intermittent form, which is probably due to the Streptococcus pyogenes, 
or Staphylococcus pyogenes alone, or to association of those organisms with 
the specific coccus of Weichselbaum, the fever intermits, as in malarial fever, 
but the intermittence is irregular, as in sepsis, and is not distinctly periodic, 
as in malaria. The typhoid form is characterized by symptoms of apathy, 
feebleness, and abdominal disorders. 

The chronic form consists in the prolongation of the ordinary type, with 
special symptoms, such as headache, pains in the nerves, vomiting, and 
progressive emaciation, with secondary arthritic changes and increasing 
inability to move the limbs. Here, again, it is probable that the main- 



CEREBROSPINAL FEVER 139 

tenance of the illness is due to septic organisms rather than to Weichsel- 
baum's coccus. 

While for the sake of description these several types of the disease have 
been named, it is, of course, true that it may manifest various degrees of 
severity in the same case at different periods. Some cases which seem quite 
severe at the onset gradually ameliorate and pass into the chronic or sub- 
acute form. The fact that the malady presents widely different types is well 
illustrated by the seemingly exaggerated, but nevertheless correct, state- 
ment of Hirsch that the duration of epidemic cerebrospinal meningitis may 
be between several hours and several months. N. S. Davis has stated 
that its duration in his experience varied from twenty-four hours to twenty- 
eight days. I have seen death occur in eighteen hours. 

Complications and Sequelae. — The complications and sequelse of epidemic 
cerebrospinal meningitis are very numerous. During the attack croupous 
pneumonia not only often develops and aids materially in producing a fatal 
issue, but acute pleurisy also is not uncommon. So, too, inflammation of other 
serous membranes, such as the pericardium and the endocardium and the 
synovial membranes, is often met with, because the coccus has an affinity 
for these membranes in all parts of the body. In the nervous system the 
most common sequela? are blindness or impaired vision due to optic nerve 
atrophy, ptosis due to oculomotor paralysis following neuritis or to changes 
arising from the inflammatory exudate at the point where the nerves leave 
the membranes, and deafness arising from the effects of the acute inflam- 
mation or infection upon the auditory nerves. Sometimes the deafness arises 
from an otitis media due to the specific coccus. Aside from chronic naso- 
pharyngeal disease and scarlet fever, this disease is responsible for deafness 
in larger proportion of cases than any other malady. 

Diagnosis. — While it is true that in a majority of cases the diagnosis of 
this disease is readily made, it is also a fact that many other diseases may 
produce symptoms which so nearly resemble those of epidemic cerebro- 
spinal meningitis that it may be absolutely impossible to make a differentia- 
tion. In the first place, it must not be forgotten that cerebrospinal menin- 
gitis is, as its name implies, an inflammation of the cerebrospinal mem- 
branes, and this change may be produced by a host of causes, none of which 
have any true relationship with the true epidemic form of the disease. As 
already pointed out in this article, and in that on typhoid fever, the bacillus 
of Eberth may cause a train of symptoms and morbid changes which is 
identical with that due to the diplococcus of Weichselbaum, yet such a case 
would not be one of epidemic cerebrospinal meningitis. It is evident, 
therefore, that cases of retraction of the head, rigidity of the limbs, and 
twitchings of the face should not be called true cerebrospinal fever unless 
the specific diplococcus can be demonstrated, or unless the disease can be 
found to be present in other patients in the vicinity. In the midst of an epi- 
demic of typhoid fever the development of cerebrospinal symptoms should 
be credited to this infection rather than to the specific fever now under discus- 
sion. If any doubt exists as to the true nature of the affection, it should not 
be forgotten that herpes is very rare in typhoid fever and in typhus fever, 
but is common in true cerebrospinal fever. Both these fevers run a course 



140 DISEASES DUE TO A SPECIFIC INFECTION 

which is marked by a natural limit; whereas, epidemic cerebrospinal men- 
ingitis does not begin to decline after the lapse of a definite course, but is 
exceedingly irregular in its duration. 

Croupous pneumonia is the infection, above all others, which is capable 
of misleading the physician in his diagnosis of cerebrospinal fever. It has 
already been stated that pneumococcus is often found to be the cause of 
inflammation of the meninges, and in children in particular the cerebro- 
spinal symptoms may be so well developed that unless the physician 
examines the lungs very carefully, he may diagnosticate cerebrospinal 
meningitis when in reality the true cause lies in the lung. It would seem 
that two types of cerebrospinal symptoms develop in pneumonia, namely, 
those due to the secondary meningeal infection with the pneumococcus and 
those in which there is no true infection, but simply irritation produced by 
the toxsemia of the pneumonia. 

Fig. 30 




A, space between the third and fourth lumbar vertebrae which can be used for puncture ; or B, the 
space between the fourth and fifth lumbar vertebrae. 

Tuberculous meningitis is practically never so sudden in onset as is the true 
epidemic form, and careful physical examination of the patient will usually 
reveal a primary tuberculous focus if meningeal tubercles are present. 
When the inflammation is tuberculous the leukocyte count is not materi- 
ally increased, whereas, in the specific type it may vary from 9000 to 
26,000. 

When cerebrospinal symptoms develop in the presence of an epidemic of 
influenza, the differentiation between true cerebrospinal meningitis and that 
due to influenza may be impossible, although the fact that the case is single 
points to the influenza bacillus as the true cause rather than that the 
attack is a sporadic case of the disease now under discussion. The cerebro- 
spinal symptoms of influenza are rarely so severe or so persistent as those 
due to epidemic cerebrospinal fever. 

The greatest aid that we have in differential diagnosis is by means of 
lumbar puncture. This operation consists in inserting a large hollow needle 



CEREBROSPINAL FEVER 



141 



between the third and fourth or fourth and fifth lumbar vertebrae, a little to 
the side of the median line and just below the spinous process. The needle 
as it enters should be directed upward and inward. In children the fluid is 
reached when the needle is inserted about 2 cm., and in adults w T hen it has 
reached the depth of from 4 to 6 cm. As soon as the membrane containing 
the fluid is punctured it flows from the needle in drops, which should be 



Fig. 31 




Introduction of needle between the last two lumbar vertebrae. The syringe is used as a convenient 
handle for the needle, and is unscrewed after the puncture is made. 

caught in a sterile test-tube in such a way that the fluid does not run down 
its side. If the infection is due to the specific organism, the pressure is greatly 
increased, so that the fluid may escape with a spurt. This fluid is clear if 
tuberculous meningitis is present, but cloudy if the diplococcus of Weichsel- 
baum is the cause of the illness. Under these circumstances, too, the faint 
trace of albumin found in the normal fluid is very distinctly increased. 
The careful staining of a single specimen or a more exhaustive bacterio- 
logical examination may reveal the presence of the diplococcus. 



142 DISEASES DUE TO A SPECIFIC INFECTION 

Demonstration of the meningococcus in the nasal mucus is an important 
addition to other signs, but a number of observers, and more recently Lord, 
have shown that meningitis may occur without the specific coccus being 
present in the nose, and also that a meningococcus rhinitis neither preceded 
nor followed by meningitis is not of exceptional occurrence. 

Prognosis. — The prognosis of true epidemic cerebrospinal meningitis is 
always grave, but its rate of mortality varies in wide limits, namely., from 
20 to 75 per cent. In children under two it is almost always fatal, and before 
puberty its mortality is very high. The most violent cases usually meet 
death by the fifth day, but it is not to be forgotten that many others reach the 
fourteenth day before death occurs. Then, again, it sometimes happens 
that after several days of severe symptoms the general aspect of the case 
improves, but the favorable signs only persist for a few hours and then 
the symptoms return with renewed vigor. Further than this, patients who 
seem about to recover not rarely suffer from a relapse which may prove 
fatal. Koplik asserts that the character of the spinal fluid is of great prog- 
nostic value. If it is thick and purulent the outlook is bad; but if it 
is of a straw color and clear it is good. 

Treatment. — The treatment of true cerebrospinal fever is not very satis- 
factory. We know of no remedies which exercise any true curative influence, 
and all the physician can do is to keep the patient during the acute stages in 
a quiet, darkened room, and give bromides in. sufficiently large doses to pre- 
vent convulsions of sufficient violence to exhaust the patient. Chloral is an 
even more powerful and useful drug for this purpose, being given in the dose 
for an adult of 20 grains by the mouth, or 60 grains by the rectum, in starch- 
water. Unless the nervous symptoms are very severe, it is a great mistake to 
attempt to overcome moderate rigidity or twitchings by full doses of nervous 
sedatives, because they in no way influence the progress of the disease, and 
simply give the stomach the task of absorption and the kidneys the burden 
of elimination. The idea that quinine is of value is probably erroneous. 
The doses usually advised are too small to act in any way as specifics, and 
if large doses are given they serve to distinctly increase congestion of the 
meninges and in the middle ear. Pain is to be relieved, if excessive, by the use 
of morphine in adequate doses, as much as J- a grain being used if needed, 
particularly at night, to give rest and sleep. The morphine, or deodorized 
opium, had better be given by the mouth when this mode of administration 
is possible, as hypodermic injections may cause abscesses. 

Cold, in the form of an ice-bag, may be applied to the head for the relief of 
headache. Blisters have been applied to the nape of the neck in the hope 
of influencing the effusion at the base of the brain, but they are of little 
value. It has been claimed by some practitioners that a very liberal use 
of antidiphtheritic serum exercises a curative influence. 

Mention has already been made of lumbar puncture for diagnostic pur- 
poses. When headache, high temperature, rigors, or stupor are marked, the 
relief of the pressure upon the brain and spinal cord by this means may 
give temporary relief, but that it aids the patient permanently is very 
doubtful. The amount of fluid withdrawn should equal 40 to 50 c.c. 
Very recently several clinicians have reported good results from the injec- 



CROUPOUS PNEUMONIA 143 

tion into the cerebrospinal fluid of an antiseptic substance. The method 
they employ is as follows: after withdrawing about 50 c.c. of cerebrospinal 
fluid by lumbar puncture they inject an equal quantity of normal salt solu- 
tion (0.9 per cent.) through the same needle which has remained in situ 
after the withdrawal of the fluid. They next inject into the spinal cavity 
through the same needle about 10 c.c. of a 1 per cent, solution of lysol. 
After this is done the needle is withdrawn. It is claimed for this plan 
that it causes a fall of the fever, which, however, returns after one or two 
days. The same procedure should be repeated at intervals of two days 
until the cerebrospinal fluid when withdrawn is limpid and clear. 

Relief from the severe pains in the limbs and back may be obtained in 
some cases by immersing the patient for long periods of time in a hot bath 
of plain or salt water at 99° or 100°. 

The fever is rarely high enough to need treatment. If it is above 105°, the 
ice-bag and the use of cool spongings with frictions may be resorted to. 

In all cases the diet should be one which is easily swallowed and easily 
digested, and everything should be done to support the system. This is 
particularly necessary in the prolonged types, in which marked emaciation 
is often present. 

CROUPOUS PNEUMONIA. 

Definition. — There is no condition of the lungs which is so apt to be 
confused in the mind of the student as that designated pneumonia. This is 
because the word "pneumonia" is used by some medical men to designate 
a single disease affecting the lung and by others as signifying any state in 
which, as the result of an inflammatory process, a part of the lung becomes 
congested or consolidated. The latter is the better use of the word, and 
when the physician desires to state that a lesion representing a definite 
infection is present he should specify the type of pneumonia by employ- 
ing an adjective to qualify the noun — i. e., he should speak of the various 
forms of pneumonia as croupous or lobar pneumonia, catarrhal or lobular 
pneumonia, and of tuberculous pneumonia. The term "pneumonia," while 
commonly used to signify croupous pneumonia, means nothing more definite 
than consolidation of the lung. 

Croupous Pneumonia is sometimes called Lobar Pneumonia, Pneu- 
monitis, Lung Pever, or Fibrinous Pneumonia. 

Croupous pneumonia is an acute infectious disease depending for its exist- 
ence, when in its typical form, upon the activity in the body of the specific 
organism known as the Micrococcus lanceolatus, sometimes called the pneumo- 
coccus of Fraenkel. As the result of this infection, there takes place in the 
lung an acute inflammation accompanied by the exudation into the air 
vesicles of an adhesive, croupous, or fibrinous exudate, which produces con- 
solidation of the lobe or lobes affected. In addition to these changes the 
patient suffers from a greater or less degree of toxaemia, due to the poisons 
made by the infecting micro-organisms and from the changes produced in the 
tissues of other organs than the lungs by the growth of the micrococcus or by 
its toxins. This disease is also characterized by the fact that it usually lasts 



144 DISEASES DUE TO A SPECIFIC INFECTION 

about nine days and ends by crisis, although this crisis may occur as early as 
the third day or even earlier in very rare instances. 

Etiology. — The development of croupous pneumonia is dependent upon 
many causes, some of which we do not know. These causes are those 
external to the body which produce conditions in the individual favorable to 
the growth of the specific germ, and internal causes which exert similar 
influences. The importance of these conditions is shown by the fact that 
the pneumococcus is periodically or continuously present in the oral secre- 
tions of a large percentage of healthy human beings. Although the organ- 
ism is capable of rapidly increasing in virulence, this cannot be held to 
account for all cases of infection, as even the most virulent strains are 
sometimes found in normal persons. A valuable contribution to the 
various phases of the pneumococcus question, including the communica- 
bility of the organism from person to person, is the work done under the 
auspices of the Department of Health of New York City, Journal of Ex- 
perimental Medicine, August 25, 1905, vol. vii., No. 5, pp. 401-632. 

So far as season is concerned, there can be no doubt that the summer 
and autumn are the months in which the fewest cases occur. Thus, 
the combined statistics of Seitz, in Munich, and Jurgensen for six large 
German towns, and of Sturgis for Westminster Hospital, London, show 
that in winter the incidence is 31.7 per cent.; in the spring, 34.6 per cent.; 
in the summer, 15.1 per cent., and in the autumn, 18.5 per cent. The 
following chart is based upon 35,828 cases occurring in hospitals in the 
United States, Germany, and Austria, and 19,000 cases occurring in the 
Confederate army during the year 1862, collected by Joseph Jones. 

Exposure to cold was thought for many years to be a cause of croupous 
pneumonia, but we now know that this only acts as a predisposing cause 
which decreases the general systemic, or local, powers of resistance to infec- 
tion; in other words, it is prone to affect all persons whose vital resistance 
is diminished. Living in poorly ventilated rooms is a predisposing cause, 
as is prolonged physical or mental strain, or any condition which saps 
vitality. A very interesting illustration of the effect of fatigue, bad air, and 
exposure in the production of croupous pneumonia has been recorded by 
Connell, of Leadville, Colorado, who reports the common occurrence of 
the disease in miners and others who go on long railway journeys for a 
day's outing and live during that time in badly ventilated railway cars. 

In many cases of acute or chronic disease, death results not from the 
primary malady, but from the superimposed croupous pneumonia which 
attacks the feeble individual, who may be just about to touch the shores 
of convalescence. In these cases it is a true "terminal infection." 

Croupous pneumonia is also a disease peculiarly apt to attack those of 
advanced years, and a very large proportion of deaths among the aged is 
due to this cause, such patients seeming to possess little resistance to its 
attack. This inability to resist the infection depends upon at least two 
causes — viz., a feeble heart muscle which cannot meet the circulatory 
demands of the disease nor resist the depressant effects of its toxins; 
diseased kidneys, or kidneys impaired in function, whereby toxic materials 
cannot be speedily eliminated, and as the general result of which the vital 



CROUPOUS PNEUMONIA 



145 



resistance of all the tissues is diminished, so that not only the Micrococcus 
lanceolatus is permitted full sway, but the patient is also placed in a favorable 
condition for the growth of other infecting micro-organisms which aid 
in producing a fatal issue. It is because of these facts that pneu- 
monia so frequently attacks those 



or 



Fig. 32 



who are already in ill health, 
who are suffering primarily from 
some other malady, and it is for 
these reasons that it so often ends 
in death. Acute and chronic alco- 
holism greatly predispose to croup- 
ous pneumonia, and it is a sin- 
gularly fatal disease in persons 
addicted to alcohol. 

Sometimes an injury to the chest 
wall will be followed by acute 
croupous pneumonia, probably be- 
cause the trauma to the lung ren- 
ders it susceptible to infection. 
Numerous experimental observa- 
tions have confirmed this clinical 
fact, which may be of great im- 
portance from a medicolegal stand- 
point, as well as from the purely 
clinical aspect. Without doubt 
local injury renders a part peculiarly 
susceptible to infection by any 
pathogenic micro-organisms which 
may enter it, and as the pneumo- 
coccus is a constant inhabitant of 
the mouth in healthy persons, a 
source of infection is ever present. 

There can be no doubt that the 
disease is capable of being spread 
from one patient to another. On 
several occasions I have seen pneu- 
monia contracted by the wife, or 
daughter, of a patient who was en- 
gaged in nursing him, and repeatedly it has occurred that the introduction 
of a case of pneumonia into a ward of a hospital has resulted in the de- 
velopment of the disease in other patients. Thus, out of eleven women 
suffering from typhoid fever on admission to my wards in the Jefferson 
Medical College Hospital, no less than eight suffered from croupous pneu- 
monia after the introduction of a single case of this disease. 

Unlike many of the acute infectious diseases, one attack does not protect 
against another, but rather predisposes the patient to subsequent attacks. 

Distribution. — Croupous pneumonia is met with in all parts of the world, 
but it is more common in the temperate than in the tropical zones. In the 
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Chart showing the seasonal incidence of croupous 
pneumonia. 



146 DISEASES DUE TO A SPECIFIC INFECTION 

United States the census for 1900 shows that its greatest mortality occurs 
in the great Northwestern States east of the Rocky Mountains, in which 
district it causes 120, or more, deaths per 1000 deaths from known 
causes. Only a few areas in the States east of this area have so heavy a 
mortality, even if large cities like New York, Philadelphia, and Chicago are 
included. 

Frequency. — Statistics as to its frequency are to some extent vitiated by the 
fact that in many health reports the difference between the various forms of 
pneumonia is not specified. There can be no doubt, however, that it is one 
of the most common and most fatal of all acute infectious diseases, and 
that its frequency and mortality are increasing. The United States census 
for 1900 shows that during that year the total mortality from pneumonia 
was 105,971, of whom 58,340 were males and 47,631 were females. The 
proportion of deaths was 106.1 for each 1000 deaths from all known 
causes. Its average mortality is about 1.5 to 2.3 per 1000 persons living. 

At times croupous pneumonia may occur in epidemic form and cause 
an extraordinary increase in the death rate of a given district. Thus, the 
mortality from this disease in Chicago, as shown by Reynolds in his official 
report covering the period from January 1 to June 1, 1903, became remarkably 
high. There were 2891 deaths from pneumonia, as compared with 1321 from 
consumption and 1238 from all other communicable, contagious, or infectious 
diseases, including diphtheria, erysipelas, influenza, measles, puerperal fever, 
scarlet fever, smallpox, typhoid fever, and whooping-cough. This is an excess 
of 382 pneumonia deaths over the deaths from all the other preventable dis- 
eases — 1570, or 118.8 per cent., more than the deaths from consumption, and 
1653, or 133.5 per cent., more than those from the other specified diseases. 

Riviere found 65 cases of croupous pneumonia in 260 cases reported as 
cases of "pneumonia" occurring in infants under two years. He believes 
that the disease is more frequent in infancy than in early childhood. 

Croupous pneumonia occurs with the greatest frequency between the ages 
of forty and fifty years, but it is also very common between fifty and sixty. 
The mortality is in direct proportion to the age of the patient. It affects 
males far more frequently than females, the proportion being as high as 88 
per cent, in the former to 12 per cent, in the latter (Kerr). This proportion in 
favor of men is probably too high for the average, but it serves to emphasize 
the fact stated, and is approximately correct. The reason probably lies in 
the greater exposure of men to cold and wet and to their abuse of alcohol. 

The relative frequency with which croupous pneumonia affects the right 
and left lung, as based on many thousand cases collected by Meltzer in 
Russia; Jurgensen, Moellmann, and Brach in Germany, and West and Pye- 
Smith in England, is for the right lung, 51.4 per cent.; left, 39.4 per cent., 
and for both lungs, 9.2 per cent. 

In 495 cases examined at autopsy, and collected by Fowler, Osier, Kerr, 
and Steven in this country and England, the disease was unilateral in 83 per 
cent. It is unilobar in the proportion of about 50 per cent. The disease 
affects a lower lobe in nearly 75 per cent, of the cases. 

Prevention. — At the present time we have no means of directly preventing 
development of this disease. It is hardly necessary to state that the sputum 



CROUPOUS PNEUMONIA 147 

of the patient should be received into a spit-cup containing some suitable 
disinfectant, or into a cloth which should be speedily burned. A patient 
suffering from croupous pneumonia should not sleep in the same bed with a 
person who is in health, and should be isolated as much as possible. 

Pathology and Morbid Anatomy. — In studying croupous pneumonia it must 
not be forgotten that the disease is, at least in some cases, a general infec- 
tion with the Micrococcus lanceolatus, the morbid changes being chiefly man- 
ifested in the lungs, just as in typhoid fever they are chiefly manifested in 
Peyer's patches. The pneumococcus is found in the blood during the prog- 
ress of this disease with great frequency, now that proper methods for its 
discovery are employed. Thus, Prochaska has found it in the blood in 38 
out of 40 consecutive cases, and Rosenow has isolated it in 77 out of 83 
cases, and has discovered it in the blood as early as twelve hours after the 
initial chill. On the other hand, the mere presence of the pneumococcus in 
the blood of a patient does not necessarily mean that pneumonia is present, 
for it has been found in the blood in cases of tonsillitis, otitis, arthritis, and 
in pulmonary oedema. Parker and many others have even described cases 
of purulent peritonitis due to this organism. 

While it is true, as already stated, that croupous pneumonia is, in its 
typical form, due to the Micrococcus lanceolatus, it is also a fact that lobar 
pneumonia or consolidation of the vesicular portions of a lobe or lobes may 
arise from infection by other micro-organisms. Such an occurrence is, how- 
ever, rare, the non-specific infection resulting usually in abortive changes in 
the pulmonary parenchyma, or running a course at variance with that com- 
monly pursued by the true infection. 

Engorgement Stage. — The first change taking place in the lung in 
croupous pneumonia is a hyperemia of the intervesicular tissues of the lobe 
or lobes about to be consolidated. This engorgement rapidly becomes more 
marked, and is accompanied by the exudation into the air vesicles of w T hite 
cells (apparently transitional leukocytes) and red blood cells and serum, 
with fibrinous material, which speedily becomes solidified, so that all that 
part of the lung which is affected may, in the course of a few hours, be 
devoid of air and impervious to its passage, except in those bronchial tubes 
which are of some size. 

Stage of Red Hepatization. — The lung is now said to be in the stage 
of red hepatization (Fig. 33) , since the exudate is red from blood-coloring 
matter, and the consistency of the organ to touch and on section resembles 
that of fresh liver; hence it is said to be hepatized or liver-like. 

When a cross-section is made of the solidified lung the surface is seen to 
be granular because of the protrusion of the exudate from the air spaces. In 
some instances the cut surface is found not to be uniformly solid, probably 
because the process is less marked in some places than in others. This 
appearance of the lung on section is also largely modified in young children 
and in greatly enfeebled individuals, in whom the degree of solidification 
may be much less marked. If the exudate is examined microscopically, it 
will be found to contain not only shreds of fibrin, red and white cells, and 
desquamated epithelial cells from the walls of the vesicles, but large numbers 
of pneumococci as well. That the amount of extravasation is in many 



148 DISEASES DUE TO A SPECIFIC INFECTION 

cases extremely large is shown by the fact that a lung may increase in 
weight by six or seven pounds. 

Stage of Gray Hepatization. — Following the stage of red hepatization 
there ensues the stage of gray hepatization. At this time the acute inflam- 
mation in the lung has passed by and the system is beginning the task of 
clearing away the results of the disease, which is accomplished by the 
cells which have been extravasated undergoing fatty degeneration and 
granular change while the fibrin undergoes softening. During this stage 
of resolution the exudate is gotten rid of by absorption and expectoration. 
Finally, the air cells are freed from the exudate with which they were 
filled, the epithelial lining is reproduced, and recovery results. 

Fig. 33 




SLO^ 



Lung ; croupous pneumonia, stage of red hepatization. The centre of the microscopic field is occupied 
by an air vesicle containing a mass of exudate composed of a network of fibrin, red blood cells, and a 
few leukocytes. 

Unusual Changes. — In rare instances the normal process of resolution 
is not followed, and in its place organization of the materials which have 
been extravasated takes place to some degree, new connective tissue is pro- 
liferated into the air vesicles from their walls, and fibrous bands containing 
bloodvessels extend throughout the lungs. Simultaneously a similar growth 
takes place in the interstitial tissues, and so the lung gradually becomes 
consolidated by overgrowth of fibrous tissue. 

Flexner and others have urged the view that unresolved lobar pneumonia 
is due to the fact that, owing to some disproportion between the leukocytes 
and other constituents of the exudate, or other causes as yet undiscovered, 
the normal process of autolysis is not carried out, and so the exudate under- 
goes organization instead of resolution. 

In other instances which are far more rare the process of resolution is sup- 
planted by the development of abscess or gangrene of the lung, which con- 



CROUPOUS PNEUMONIA 149 

ditions are probably due to secondary infection of the lung by the strepto- 
coccus pyogenes, or staphylococcus pyogenes, or other bacteria capable of 
producing such lesions. Sometimes the process of fatty change and death 
of the extravasated cells is so rapid that on section of the lung the vesicles 
exude a purulent matter looking like true pus, which indeed it may be, but 
this in no sense is an abscess of the lung. 

Associated with the changes in the lungs we find adjacent organs involved 
by direct extension of the inflammatory process or by the infection itself. The 
most common of these is inflammation of the bronchi (bronchitis), which 
is practically always present. After bronchitis in frequency comes inflam- 
mation of the pleura, due to direct extension from the underlying lung and 
to infection of the pleura by the specific organism of the disease. Nearly 
always this is manifested by the formation of a plastic fibrinous exudate on 
the serosa and an abnormal amount of fluid in some part of the pleural 
cavity, which fluid is often serous and not infrequently purulent. (See 
Pleuritis.) 

Sometimes the pericardium is similarly affected, and even the endocardium 
may be infected by the specific germ. (See Pericarditis and Endocarditis, 
under Complications.) 

Reference is made elsewhere to the meningitis which sometimes develops. 

It is a great mistake to view the lesions just described as representing all 
the pathology of croupous pneumonia. It is true that these changes are the 
most evident, but it is not to be forgotten that the toxaemia of the malady 
exerts a very great influence in producing symptoms and lesions during life 
which are not so readily seen, but are equally important in their influence on the 
patient. The muscular fibres of the heart and the epithelial cells of the kidneys 
undergo albuminous degeneration, and similar changes occur in the liver. 
When the heart is opened after death we frequently find its cavities, partic- 
ularly those of the right side, almost filled by firm clots, part of which may 
have formed so long before death as to be of the " chicken-fat' ' type. The liver 
is often found to be greatly engorged with blood, because of the impeded cir- 
culation in the vena cava, produced by the difficulty with which the right side 
of the heart empties itself. The bronchial lymph glands also show by the 
swelling of their cells and by their distended sinuses that they have en- 
deavored to prevent the entrance of the micrococcus and its toxins into the 
general system, for in them may be found broken-down cells, red cells, 
pneumococci, and phagocytes containing cells or organisms. 

My colleague, Coplin, has shown that definite changes take place in the 
intercostal muscles in the course of pneumonia and pleurisy. 1. Granular 
degeneration or cloudy swelling of the muscle fibres, which is probably a part 
of the general action of the toxic bodies circulating in the blood. 2. The 
muscle fibres are dissociated, oedema is present, but there is little fibrin-con- 
taining substance. Groups of muscle fibres and bundles show changes that 
cannot be differentiated from the hyaline degeneration described by Zenker 
as occurring in the muscles of the abdominal wall in typhoid fever. 3. In 
addition to the changes already described, leukocytes become abundant, 
bacteria are often present, and, finally, if the inflammatory process is chronic, 
there is an overgrowth of fibrous tissue and fatty infiltration of the muscle. 



150 DISEASES DUE TO A SPECIFIC INFECTION 

Incubation. — The incubation period of croupous pneumonia is forty-eight 
hours. 

Symptoms. — Before describing the symptoms met with in cases of 
croupous pneumonia, it is essential to emphasize the fact that in no other 
infectious disease are the manifestations of illness so variable. These 
variations depend not only upon the virulence of the infecting germ and 
the susceptibility of the patient, but upon his habits, age, and general state 
of health. In some cases the malady develops as a frank, open inflamma- 
tion of the lung. In others it is so insidious as to be overlooked, except 
by the most careful physician. In certain cases the course of the disease 
is markedly sthenic, in others profoundly adynamic. In still others the 
progress is so mild that the patient is never seriously ill, and in some 
instances it springs like a tiger upon a seemingly healthy man and 
destroys him. 

The symptoms of croupous pneumonia may be divided into three stages 
for readiness of description — namely, those of onset, those of the well- 
developed stage, and those of convalescence. 

Stage of Onset. — The patient, usually an adult, is seized after, or without, a 
brief period of general malaise, with a chill, followed by a well-developed fever, 
The chills may be repeated and may vary from a slight feeling of creepiness 
to a severe rigor of sufficient force to shake the patient severely, and to last 
for over an hour. The pulse is quickened, but not as much so as we would 
expect from the sharpness of the onset, and at first may be small, but soon 
becomes full and bounding if the patient has been previously in good health ; 
the respirations are also markedly increased in rate per minute. More or 
less severe pain may be felt in the chest on the affected side. The degree of 
pain, however, varies greatly, some patients bitterly complaining of it, while 
others seem to have little or no suffering, probably because in the latter 
cases the inflammation of the lung is so deeply situated that it does not 
extend to and involve the visceral layer of the pleura. It is important to 
bear in mind the fact that this pain not infrequently is referred by the 
patient to another part of the body. I had a case admitted not long since 
to my wards, on the statement of a well-known physician that she had ap- 
pendicitis, when she was really suffering from a pleuropneumonia of the 
right lower lobe. Children are very prone to refer the pain to the epigas- 
trium. 

If the patient is very feeble it sometimes happens that the onset of the 
malady is insidious and no pain is felt. This is especially apt to be true 
when the disease complicates chronic alcoholism, renal disease, or other 
grave malady. 

The temperature usually makes a sharp and decided rise, immediately 
after or during the chill, to 103° or 105°, and in some cases even higher than 
this, and remains high throughout the disease, the variation in the morn- 
ing and evening temperature not being more than a degree or a fraction 
thereof. (See Fig. 34.) 

The face is usually flushed, particularly over the cheek bones, and it is a 
noteworthy fact that this flush is usually most marked upon the cheek of the 
same side as the lung involved. The expression of the face is apt to be some- 



CROUPOUS PNEUMONIA 151 

what anxious, the skin dry and hot, and a moderate degree of cyanosis may 
be seen in the capillaries of the lips and finger-tips, and about the nose. 

Violent headache may or may not be present. A more or less active delirium 
may also develop at this time, and the patient may be quite restless unless the 
pain in the side makes it more comfortable to lie quietly in bed. An incessant 
unproductive cough is often an early symptom of onset. 

The 'physical signs of the disease in the thorax in the stage of onset are not, 
as a rule, well marked. Inspection may reveal some impairment of expansion 
upon the affected side; palpation may evince some increase in vocal fremitus; 
auscultation will show in many cases fine crepitant rales, increased bronchial 
breathing or tubular sounds, increased loudness of vesicular breathing for a 
few hours, and often some exaggeration of the normal respiratory sounds 
on the sound side. Indeed, this increase in the harshness of the breath 
sounds over the normal side, due to the increased activity on the part of the 
healthy lung, to compensate for the impairment of the diseased lung, may 
mislead the beginner in physical diagnosis into thinking that this is the 
lung diseased. Percussion may also reveal some impairment of resonance 
over the affected area. 

Developed Stage. — The developed stage of the disease is characterized 
by certain conditions and physical signs, some of which are almost pathog- 
nomonic of the malady. The peculiarity of the pulse is that it is quite slow 
as compared to the rapidity of the respirations. Usually when high fever is 
present the pulse rate is as high as 110 or 120, or even higher, while the 
respirations are about 24, but in pneumonia of the croupous type the pulse 
rate is sometimes only 90, while the respirations are as high as 30 per minute. 
More commonly, however, the respiratory rate mounts to as high a point 
as 40 or 50 per minute, while the pulse reaches 110 to 120, the relative pro- 
portion being 1 to 3, while in health it is usually about 1 to 4.5. 

A second peculiarity of this stage is the rusty or bloody sputum, which is 
still more characteristic in that it is sticky and tenacious, and therefore 
difficult to expectorate, and so adherent that even when a spit-cup is filled 
with it the vessel can be held nearly upsidedown without losing its contents. 

A third characteristic of croupous pneumonia at this stage is the develop- 
ment of single or multiple fever blisters, or spots of herpes, upon the lips or 
about the edges of the nostrils. 

Dyspnoea may or may not be present. If present it depends upon the fact 
that so much of the lung is involved that respiration is difficult, or it is due 
to feebleness of the heart from engorgement of its right ventricle by the blood 
which cannot pass readily through the diseased lung; or, again, it may be 
dependent upon actual impairment of the power of the heart as a result of 
the action of the toxin of the disease upon its muscular tissues and nerve 
centres. Dyspnoea in croupous pneumonia may, therefore, be due to pul- 
monary, cardiac, or toxic causes. Cyanosis may be very marked, and not 
uncommonly the jugular and other superficial veins can be seen to be full 
and distended. 

A peculiarity of the dyspnoea of pneumonia is the fact that the patient does 
not seem capable of resting quietly, but continually moves about, making 
exertions which seem scarcely compatible with so much shortness of breath. 



152 DISEASES DUE TO A SPECIFIC INFECTION 

Delirium of an active type is common in this stage, and it may be difficult 
to keep the patient in bed, particularly if he is an alcoholic. 

During the second stage of croupous pneumonia the pulse may become 
hobbling or dicrotic, the heart sounds tumultuous, and the dyspnoea 
severe. In other instances the pulse seems voluminous, but nevertheless 
is very easily compressed to the point of extinction, while the sounds of the 
heart reveal the fact that that viscus is laboriously endeavoring to fill vessels 
which, because of their relaxation, fail to offer the normal resistance to its 
action. In still other instances, if the heart is markedly affected by the 
toxaemia of the disease, the heart sounds will be feeble and difficult to differ- 
entiate, and the pulse be very small and easily extinguished by pressure. In 
still other cases auscultation over the area of the pulmonary valves at the third 
left interspace will reveal accentuation of the pulmonary second sound or a 
murmur due to incompetency of these valves under pressure, while later on 
the labored action of the heart is shown not only in the signs named, but also 
in the pulsating jugular veins, which are distended and full, indicating great 
venous engorgement, as the result of the obstruction of the flow of blood out 
of the right ventricle, or because of inco-ordination of the auricular and 
ventricular contractions, as the result of the formation of a heart clot or 
from toxaemia. 

The physical signs of croupous pneumonia in the well-developed stage are 
quite characteristic in typical cases. Inspection shows an even greater 
impairment of expansion on inspiration on the affected side than in the stage 
of onset, and palpation reveals, when the patient speaks, a distinct increase in 
vocal fremitus over the part of the lung which is diseased. Auscultation gives 
a harsh inspiratory sound, prolongation of expiration, and a large number of 
fine crackling or crepitant rales in the same area, so fine that they may not be 
heard by the careless examiner. They sound very much as does that noise 
which is produced by moistening the tip of the forefinger and thumb with 
saliva, pressing them together, and separating them, or, again, as does the 
sound made by the hair which grows over the examiner's ear when it is 
rubbed between the finger and thumb. Ordinary vesicular breathing over 
the area diseased is absent, and in its place is heard bronchial breathing, 
which is caused by the air in the bronchial tubes, which produces a sound 
which is transmitted through the consolidated lung unmuffled by the vesic- 
ular murmur usually present. Auscultation while the patient speaks will 
also show a distinct increase in vocal resonance. That is to say, the sound 
of the voice will be transmitted through the chest-wall with a greater degree 
of clearness than in health. While auscultation is being performed in cases 
which have a delicately developed chest, as in youths and children, it is 
often noted that the movement of the anterior chest- wall under the ear is 
not uniform, but undulating, one part expanding at an appreciable interval 
before the other. 

Percussion, a most valuable aid in the diagnosis of this disease, reveals, if 
the lesion in the lung is near the surface, marked impairment of resonance 
amounting to dulness, but it is a fact well worth remembering that if the lesion 
in the lung is deep seated, and not near its surface, the percussion note over 
the area diseased may not be impaired or dull, but hyperresonant, or, as 



CROUPOUS PNEUMONIA 153 

Samuel West has said, "boxy" in character. Usually hyperresonance is 
demonstrable all over the lung, except where it is consolidated, and is also 
to be found upon the healthy side of the chest, owing to the increased 
amount of air which is in these parts to compensate for the area of consolida- 
tion; but careful examination will reveal the fact that the hyperresonance 
over the consolidated area, or in its immediate neighborhood, has a different 
tone from that in the healthy and compensating lung, the "boxy" note just 
named. I have frequently been able to determine the presence of deep- 
stated pneumonia by the presence of this sign. By the aid of careful auscul- 
tation and percussion it is usually, but not always, possible to definitely 
determine the exact area of the lung which is involved. 

While in the majority of cases these positive signs of croupous pneumonia 
may be found in a more or less well-developed form, it is not to be forgotten 
that negative signs may be as valuable in making a diagnosis. That is to say, 
there may be absence of any one or all of the signs just enumerated, and a 
total absence of vesicular breathing. In such cases, therefore, the physician 
must exercise care lest the loud and exaggerated breath sounds of the 
healthy part of the chest mislead him into thinking that that portion is the 
one which is diseased. 

In certain instances, in which the action of the heart is very labored, its 
sounds distant, and the pulse is small and insufficient, careful examination 
may reveal a pericarditis with effusion, wmich, by its pressure, interferes 
with the movement of the cardiac muscle. This question as to whether there 
is pressure by pericardial effusion is by no means readily determined, because 
it frequently happens that there is a marked degree of cardiac dilatation 
present at this time, which naturally increases the area of cardiac dulness 
downward and to the right. Further, as it is the right ventricle which is 
most apt to be engorged, the area of cardiac dulness may be abnormally 
great in this direction. Again, it not infrequently occurs that the compen- 
satory fulness of the healthy lung, if the disease is on the left side, pushes 
the heart downward and to the left, or, on the other hand, if the right 
lung is diseased, the unusual expansion of the left lung causes an extension 
of pulmonary resonance to the right, and so increased area of cardiac 
dulness is very effectually masked. 

Patients suffering from croupous pneumonia should always be turned on 
the side when the back is to be examined, as it is dangerous, because of the 
state of the heart, for them to sit up in bed. 

The urinary flow during an attack of croupous pneumonia is usually dimin- 
ished, so that the passage of about twenty ounces of urine in twenty-four 
hours may be taken as the average. This urine is usually highly concen- 
trated, and contains, as does the urine in most febrile diseases, an increased 
amount of urea and an excess of amorphous urates which are deposited on 
standing. It also contains, very constantly, a moderate amount of albumin, 
but the chief peculiarity is its scanty content of chlorides, which may be 
entirely absent. If the albumin be large in amount, or casts are present, 
the probability is that the kidneys were diseased before the onset of the 
pneumonia. 

During the course of croupous pneumonia the function of the alimentary 



154 DISEASES DUE TO A SPECIFIC INFECTION 

canal is rarely seriously disturbed, although loss of appetite because of the 
fever may be a marked symptom. The most important change in any part 
of the digestive system, if it may be so called, is seen in the tongue, the state 
of which is noteworthy, because it gives some idea of the general state of the 
patient. It is, of course, prone to be dry and somewhat coated, caused by 
the rapid breathing through the mouth, and because of the fever; but if it be 
exceedingly dry and red, narrow and pointed at the tip, it possesses a more 
positive significance as to the general state of the patient than if it be broad 
and moist. 

Sometimes when pneumonia is very severe and particularly when toxaemia 
is marked, an excessive degree of tympanites develops, which is of evil 
significance, in that it shows a diminution in vitality and causes interfer- 
ence with the action of the lungs and heart by pressure. I have seen this most 
commonly when the disease has affected those addicted to the excessive 
use of alcohol. 

The nervous symptoms of pneumonia are quite various and depend more 
upon the previous habits of the patient, the location of the lesion, and the 
degree of toxaemia than upon any other causes. Delirium varies in degree 
from mind wandering, as the patient is about dropping off to sleep, to 
active mania, during which it may be very difficult to keep the patient 
in bed. The severity of the delirium depends largely upon the age of 
the patient and his habits. Alcoholic patients nearly always have de- 
lirium in a well-marked degree, and in this class of patients it is grave 
from a prognostic point of view in direct proportion to its constancy and 
severity. 

The type of the delirium also varies very greatly in the strong and in the 
weak. In those who are adynamic from some previous disease or from 
bad habits, it is often of a low muttering type, resembling that sometimes 
seen in toxic cases of typhoid fever, while in other instances it may be vio- 
lent, as already described. 

It is a noteworthy fact that delirium is particularly prone to affect those 
who suffer from pneumonia at the apex of the lung, and I have frequently 
seen in children, who had pneumonia at the apex, a delirium in which 
there seemed to be a constant fear of falling, so that the child clutched its 
mother every time it was moved. Holt's experience, on the other hand, 
leads him to believe that the portion of lung involved has little influence upon 
the production of nervous symptoms, and without doubt the recent advances 
in the study of pneumococcus infection tend to show that the toxaemia and 
not the portion of lung involved is responsible not only for the marked 
nervous manifestations, but also for the dyspnoea and great acceleration of 
the respiration. A peculiarity of the delirium in many alcoholic cases is 
that they labor under the delusion that they are lying in a coffin, and in 
their constant efforts to escape greatly exhaust themselves. This form of 
delirium is exceedingly grave from a prognostic standpoint. Delirium is 
also very much more apt to be marked in those patients who suffer from 
toxaemia than in those in whom a very considerable area of the lung is 
involved, but who have, nevertheless, comparatively slight signs of poisoning 
by the toxin of the pneumococcus. 



CROUPOUS PNEUMONIA 



155 



Very rarely, in young children, the onset of the disease is characterized 
by convulsions instead of by the ordinary chill. 

Insomnia is a very constant symptom of croupous pneumonia, and may 
become so persistent as to require medicinal measures for its relief, par- 
ticularly if it be accompanied by great restlessness. 



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A chart of croupous pneumonia in a girl of six years, showing the little effect produced by sponging 
upon the temperature and the characteristic crisis on the sixth day. 

The skin in an ordinary case of croupous pneumonia is usually hot and 
dry; but if the toxic element in the case is very marked, it may, as death 
approaches, become cold and clammy and even bedewed with sweat. In 
toxic cases, too, it is not infrequently somewhat jaundiced. If this jaundice 
is associated with hamioglobinuria, the prognosis is almost certainly fatal. 
On the other hand, in some instances jaundice occurs apparently as the 
result of the action of the toxin upon the liver, and this type is not so 
grave. 

Profuse sweating nearly always occurs at the time of crisis. The frequency 
with which herpes appears about the mucous membranes and skin of the 
mouth and nose has already been mentioned. 

Stage of Resolution. — As the disease approaches the period of crisis, 
and sometimes not until this event has taken place, it will be noted that the 
rapidity of respiration as compared to the rapidity of the pulse more nearly 
approaches the normal ratio. 



156 DISEASES DUE TO A SPECIFIC INFECTION 

The first change which can be noted in the physical signs in the chest is the 
development of fine moist rales, which indicate the early stages of resolution. 
These rales, when they are first heard, are fine and crepitant, and closely 
resemble those heard in the stage of onset; for this reason they are called 
rdles redux. 

The rales in the chest become more and more coarse and moist in char- 
acter as convalescence is carried on, and the speed with which nature in 
an otherwise healthy individual clears away the exudate is quite extra- 
ordinary, although usually for several weeks after a sharp attack of croupous 
pneumonia, involving the surface of the lung, impaired resonance on percus- 
sion and some prolongation of expiration with harsh inspiration can be 
demonstrated. 

The critical jail of temperature is often preceded by a sharp rise, but 
when the fall occurs it takes place with extraordinary speed, the patient 
being afebrile or with a subnormal temperature within a few hours, or even 
within one hour (Fig. 34) . Sometimes this critical state is accompanied by 
a profuse sweat, and even collapse may develop, with urgent dyspnoea, 
due to vasomotor palsy and vascular relaxation. 

When the fall is quite gradual, extending over a day, it is called a pro- 
tracted crisis ; this very commonly occurs in children. 

Often the day after crisis the temperature returns to slightly above nor- 
mal, and sometimes an apparent crisis fails to reach the normal and the 
fever rises again. Such a pseudocrisis is rarely seen after the fifth day. 

The critical fall of temperature, as has already been stated, usually occurs 
on about the seventh or eighth day of the disease, but it may occur as 
early as the third day (Fig. 35). In feeble persons and in children the 
disease sometimes ends by lysis. 

Complications. — The complications of croupous pneumonia are quite 
numerous. Of these the most frequent is undoubtedly pleurisy. Indeed, 
it may be said that in almost every case of croupous pneumonia a certain 
amount of inflammation of the pleura exists. As an illustration of this fact, 
the statistics of Kerr are of value. Out of 171 cases which came to autopsy 
from croupous pneumonia, no less than 118 showed acute pleuritis. Of 
these, 74 were acute fibrinous pleuritis, 38 serofibrinous pleuritis, and 6 acute 
empyema. In Osier's 103 autopsies pleuritis was present in all but 2 cases. 
The pleuritis is due to the extension of the inflammatory process to the vis- 
ceral layer of the pleura and to infection of the pleural membrane by the 
pneumococcus or by some other organism which is associated with it. (See 
Pleurisy). The inflammation of the pleura manifests itself by an excess of 
pain in the area involved, by a friction sound on auscultation, and later, it 
may be, by the outpouring of a considerable amount of fluid which may 
be serous or purulent. When the fluid is serous it is often absorbed with 
a rapidity only equalled by the absorption of the croupous exudate in the 
lungs. In other instances it persists and actually increases in quantity, 
relief only being obtained when the physician performs paracentesis. In 
4523 cases of croupous pneumonia, occurring in twelve large hospitals in 
the United States and England, pleural effusion is stated to have occurred 
in 233 cases, a percentage of 5.15. 



CROUPOUS PNEUMONIA 



157 



In still other cases the effusion is puru- 
lent from the beginning, and in this way 
an empyema is formed. Like all collec- 
tions of pus, recovery can only be reached 
in the majority of these cases by giving 
vent to the accumulation. The presence 
of the pus is usually manifested by a re- 
turn, or maintenance, of the febrile move- 
ment seen in the early stages of the dis- 
ease, accompanied, it may be, by the ordi- 
nary manifestations of septic poisoning, 
such as chills, sweats, and irregular tem- 
perature. On the other hand, all evi- 
dences of the presence of pus may be 
absent, owing to the non-absorption of 
toxic matters through the pleural mem- 
brane. In 10,076 cases of croupous 
pneumonia collected principally from the 
official reports of hospitals in the United 
States, England, and Germany, empyema 
is stated to have occurred in 208 cases, a 
percentage of 2.06. 

In all cases in which speedy recovery 
from croupous pneumonia does not take 
place and where marked impairment of 
resonance persists upon the diseased side, 
pleural effusion or empyema should be 
strongly suspected, and the tests for the 
purpose of determining these complica- 
tions be instituted. Sometimes the pres- 
ence of a pleural effusion is not suspected 
because it produces no symptoms until, 
by the increase in its quantity or the 
taking of moderate exercise by the 
patient, it produces dyspnoea by inter- 
fering with respiratory movements. (See 
articles on Pleural Effusion and Em- 
pyema.) It is a noteworthy fact that if 
the empyema be due to the pneumococ- 
cus the prognosis is more favorable, both 
as to complete recovery and to speediness 
of cure, than if it be due to some other 
infecting micro-organism. 

Hydwpneumothorax has occasionally 
been recorded as a complication, but it 
is very rare. 

Gangrene and abscess formation in the lungs are two very important 
and serious lesions which, fortunately, are not of common occurrence in 



















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Chart showing day of crisis in acute 
croupous pneumonia, based on 2166 cases in 
hospitals in the United States, England, 
and Germany. The black area shows the 
proportion (percentage) which have their 
crisis on any given day. The percentages 
for third and fourth days are taken from 
Aufrecht's statistics alone, as they could 
not be ascertained in all the other cases. 



15S DISEASES DUE TO A SPECIFIC INFECTION 

connection with cases of croupous pneumonia. Eisendrath has analyzed 96 
recorded cases of pulmonary abscess, gangrene, and bronchiectasis following 
croupous pneumonia. When the totals are computed as to percentage of 
recovery, the result is quite striking, especially in the more acute cases. Of 
25 cases of acute single abscess, 96 per cent, recovered and 4 per cent, 
improved; of 28 cases of acute gangrenous abscess, 71.4 percent, recovered, 
7.2 per cent, improved, and 21.4 per cent. died. Of 14 cases of chronic 
simple abscess, 42.8 per cent, recovered, 21.4 per cent, improved, and 35.8 
per cent, died; while in 26 cases of chronic putrid abscess with bronchiec- 
tasis 50 per cent, recovered, 15.3 per cent, improved, and 34.7 per cent. died. 

Eisendrath found, from his review of the subject, that the symptoms 
usually came on after the crisis and consisted in a post-critical rise in tem- 
perature, which then became remittent in type. The sputum became puru- 
lent, and there was a distressing cough, accompanied by expectoration of pus 
in large quantities. If the abscess cavities do not communicate with a bron- 
chus there is but little expectoration. There is in all cases emaciation, loss 
of appetite, and a rapid decline in strength. If the abscess becomes chronic 
there may be recurrent attacks of fever, with profuse expectoration. 

Physical examination in these cases is rather disappointing. The lesions 
are most frequently in the lower lobes, and this is of some aid in diag- 
nosis. There are no typical physical signs, owing to the fact that the 
cavities, be they due to abscess, gangrene, or bronchiectasis, may be near the 
surface, or quite deeply situated, and may or may not communicate with 
a bronchus. Dulness, decreased respiratory murmur, decreased vocal 
resonance, and decreased fremitus are present in the majority of cases, but 
bronchial breathing may be heard. The most reliable sign is the presence 
of large, moist rales, not infrequently metallic in character. Another striking 
feature is the variability of the physical signs, so that dulness and then 
tympany may alternate at the same spot. Clubbed fingers develop quite 
early, as do also symptoms produced by pressure on the heart, liver, and 
spleen. 

Gangrene must be suspected when there occurs a rise of temperature, a 
few days after the crisis, and the breath becomes fetid. The sputum is 
also fetid and divides itself into three characteristic layers. (See Gangrene 
of the Lung.) 

The frequency of haemoptysis in cases of gangrene is due to the fact that 
the vessels are more apt to pass freely through the cavity, owing to the 
more rapid destruction of tissue. 

In bronchiectasis following pneumonia the sputum may be fetid at times, 
but the odor is not so penetrating as in gangrene and there are no elastic 
fibres. There is usually a history of long-continued expectoration of large 
quantities of pus. This, however, is not characteristic, for the same history 
may be true of chronic simple abscess. 

Pericarditis is not a very infrequent complication of pneumonia. In the 
majority of instances it is of such mild degree that it does not jeopardize the 
patient's life; but in other instances, when the effusion which follows it is 
profuse, it may, by mechanical pressure, produce great cardiac disability. 
When the accumulation is extensive, a definite increase in the area of cardiac 



CROUPOUS PNEUMONIA 159 

dulness is usually demonstrable. Not rarely, however, the presence of this 
complication may be unsuspected during the patient's life. Thus, Thayer 
was only made acquainted with the presence of pericarditis in one of his 
cases of croupous pneumonia when the autopsy disclosed a thick layer of 
pyogenic membrane over the visceral pericardium, with a large quantity of 
pus in the pericardial cavity. Some statistics seem to show that pericarditis 
varies in frequency in from 5 to 16 per cent, of all cases, but in 21,383 cases 
of croupous pneumonia collected by me principally from the official reports 
of hospitals in the United States, England, Germany, and Austria, peri- 
carditis is stated to have occurred in only 266 cases of croupous pneumonia, 
a percentage of 1.24. (See Pericarditis.) 

Endocarditis is a rare complication, occurring much less frequently than 
pericarditis. In a considerable number of cases the pneumococcus is re- 
sponsible for the lesion. It often affects the aortic valves, and it is gener- 
ally of the ulcerative type. In 14,510 cases of croupous pneumonia col- 
lected from several series of cases reported by German, English, and 
Swedish physicians, and from official reports of hospitals in the United 
States, England, Germany, and Austria, endocarditis is stated to have 
occurred in 106 cases, a percentage of 0.73. Norris in 500 cases found it 
recorded five times, while Sears and Larrabee, in Boston, found it 9 times 
in 940 cases. Aufrecht, in 1500 cases, met with endocarditis only once. Out 
of a total of 5738 cases of croupous pneumonia von Brach found less than 
0.2 per cent, complicated by endocarditis, and less than 0.5 per cent, of them 
complicated by pericarditis. Preble, from an exhaustive study, places the 
average at 1 per cent, in all cases and 5 per cent, in fatal cases, and 
these figures are probably correct. Osier found 16 instances of endocarditis 
in 100 fatal cases. Preble believes that while pneumonia is more common in 
males than in females, endocarditis due to this infection is most common 
in females. (See Endocarditis.) 

Two apparently distinct types of meningitis are found as complications 
of croupous pneumonia; one appearing at the onset of the disease, the other 
during the active or post-critical stage. The former variety is seen most 
frequently in children, and is probably symptomatic; it is rarely fatal, and 
therefore its pathology is somewhat uncertain, On the contrary, meningitis 
developing during the course of the well-developed infection is generally the 
result of meningeal infection and is very frequently associated with endo- 
carditis. (See Cerebrospinal Meningitis.) 

Numerous cases are on record of croupous pneumonia in children which 
at the onset simulated meningitis, cerebrospinal meningitis, and even hemi- 
plegia. But the subsequent appearance of local physical signs, the pulse 
and respiration ratio, and the crisis, marked by a sudden fall in temperature 
about the eighth day, have confirmed the diagnosis of croupous pneumonia. 
The favorable termination in many of the reported cases has not permitted 
an adequate pathological investigation, although meningitis due to the pneu- 
mococcus is well recognized. 

Disturbance of the nervous system over and above the signs of meningeal 
irritation or true meningeal inflammation may occur. Hemiplegia in croup- 
ous pneumonia was recorded by Huxham; later it was described by Charcot, 



160 DISEASES DUE TO A SPECIFIC INFECTION 

Lupine, and Vulpian as hemiplcgie pneumonique. It may occur early in the 
course of the disease, or may not develop until the period of convalescence. 
Such a paralysis has been observed in cases as early in life as the eighteenth 
month and as late as the seventy-sixth year. 

Pierre Boulloche has collected 56 cases of paralysis resulting from croup- 
ous pneumonia. In this analysis the type of paralysis was found to be nearly 
always hemiplegic. In advanced years death nearly always ensued upon this 
complication, while in the young the mortality was very much lower, recovery 
being the rule. In one case occurring at the age of fifty-eight years, hemi- 
plegia, with aphasia, developed during the course of the disease, but ended 
in recovery. 

In some instances the paralysis is monoplegic, and this is well illustrated 
by a case described by Boulloche in a patient thirty-two years of age, who, 
from the onset of the disease, was delirious and who presented a typical 
right-sided croupous pneumonia. Paralysis of the right arm and right side 
of the face was discovered upon the sixth day of the disease. Movements of 
the right leg were entirely retained. There was aphasia, but no loss of con- 
sciousness, neither was there any disturbance of sensibility; twelve days 
later the fever had subsided, the aphasia had diminished considerably, and 
the muscles of the face were less drawn. Sensation in the pharynx returned 
and a day later the aphasia disappeared. The facial paralysis passed off; 
the relative strength of the two arms showed only a decrease of 10 degrees 
in the affected side, and at the expiration of twenty days the monoplegia had 
entirely disappeared. 

Transitory aphasia is a complication reported by Chantemesse. This 
observer has found that aphasia usually occurs about the second or third 
day of the disease, that it is ordinarily preceded by headache and giddiness, 
even to the verge of syncope; in some cases numbness or a sensation of pricking 
in the right side of the face and right arm is experienced; in other cases it 
may set in abruptly without loss of consciousness or become manifest after 
a typical apoplectiform seizure. The characteristics of the speech impair- 
ment do not differ from those dependent upon an organic lesion of the third 
frontal convolution upon the left side of the brain. The paralysis may 
involve the entire right side of the body, but usually only the inferior portion 
of the right side of the face, the right half of the tongue, and the right superior 
extremity are affected ; as a rule, sensation and the reflexes are not altered. In 
pronounced cases the paralyzed parts may be the seat of increased redness 
and an cedema, which is more or less circumscribed and increased by heat. 
The phenomena persist commonly for from a few hours to a few days, and 
seem in no way to influence the primary disease. 

It is doubtful whether the clinical picture and pathology of these cases of 
transitory aphasia differ in any particular from many of the cases already 
described as hemiplegic. They probably represent the cases in which no 
lesion is found postmortem. 

Softening of the brain has occurred in some cases. In one case, reported by 
Suckling, it was due to thrombosis of the basilar artery, and thrombosis of 
the circle of Willis ; with plugging of the superficial arteries of the left hemi- 
sphere. While these lesions have been found as the causative agents in pro- 



CROUPOUS PNEUMONIA 161 

(hieing hemiplegia, there are also cases on record in which the autopsy has 
been negative. In other words, hemiplegia with lesions and hemiplegia 
without lesions occurs. In the former case hemiplegia results from either 
meningitis or softening, or is due to thrombosis or embolism. In the second 
class the paralysis is like that of diphtheria — that is, of the toxic type. It is 
important to remember that it is possible for hemiplegia to develop in pneu- 
monia without there being any relationship between the two conditions. 

The fact that these marked nervous manifestations sometimes come on 
early in an attack of croupous pneumonia emphasizes the importance of 
examining the chest in all cases of paralysis, not only because pneumonia is 
competent to produce hemiplegia or other localized palsy, but also because 
these conditions are quite competent to produce secondary pulmonary 
lesions. In other words, pulmonary lesions may be the cause of hemiplegia, 
and hemiplegia may be the indirect cause of croupous pneumonia. 

Neuritis, occurring chiefly as a sequel to croupous pneumonia, has been 
described by several observers. These cases resemble those described by 
Boulloche as paralysis with muscular atrophy, coming on during the period 
of convalescence. 

Until Weichselbaum isolated the pneumococcusfrom the pus aspirated from 
the synovial sac of joints involved during the course of croupous pneumonia, 
the occurrence of arthritis was considered a coincidence, but since 1888 
arthritis and osteoarthritis have been recognized as being not rarely due to a 
pneumococcus infection. Herrick has collected 52 cases from the literature 
of the subject, including some of his own, but it is interesting to note that 
in 2292 cases of pneumonia collected by me, treated by various Swiss and 
German physicians, only 2 cases of arthritis occurred. 

In regard to the frequency with which different joints are involved in this 
complication, the following quotation from Herrick's paper is of interest: 
"In 23 of 52 cases the upper extremities alone were involved; in 18 cases 
the joints of the lower extremities alone; in 11 there was involvement 
of joints of both the upper and lower extremities. These figures show a 
slight preponderance' in favor of limitation to the upper extremity, but so 
slight that little or no significance can be attached to it. In fact, the knee 
seems to be the joint oftenest affected, being involved in 22 of the 52 cases, 
in 3 of which both knees were affected, so that out of a total of 84 joints the 
knee makes up 25, or about 30 per cent. The involvement of other joints 
was as follows: the sternoclavicular, eight times; the shoulder, twelve times; 
the elbow, nine times; the wrist, eight times; the metacarpophalangeal, twice; 
the hip, three times; the knee, twenty-five times; the ankle, three times; the 
metatarsophalangeal, three times. The arthritis was monarticular in thirty- 
two instances, or in 61.5 per cent, of the cases. The joints thus solitarily 
involved were: shoulder, ten times; knee, nine times; wrist, five times; elbow, 
twice; sternoclavicular, four times; and the hip, ankle, metacarpophalangeal, 
and metatarsophalangeal, each once. Of the remaining cases there were in- 
volved: two joints, nine times; three joints, four times; four joints, once; 
more than four, three times." These figures bring out the fact that the 
larger joints are more often affected than the smaller ones. 

The process in subacute cases is sometimes highly destructive to the joint. 
11 



162 DISEASES DUE TO A SPECIFIC INFECTION 

It is a noteworthy fact that the prognosis as to life is grave, the mortality 
amounting to 65 per cent., chiefly because this lesion is associated, as a rule, 
with affections of the serous membranes elsewhere, and particularly in the 
endocardium. 

Venous thrombosis is an exceedingly rare complication of pneumonia. 
Steiner could find only 38 cases recorded, and reports 3 of his own. In 27 
of these the thrombosis occurred during convalescence. In 1 case it 
occurred at the time of crisis and in 4 during the course of the disease; 
and in the cases collected by him the lower extremities were always involved. 
The left lower extremity was involved in 16 cases; the right in 10, and both 
legs in 7. The more frequent involvement of the left extremity is attributa- 
ble in this disease, as in typhoid fever, to the greater length and obliquity 
of the left common iliac vein and its passage beneath the right common 
iliac artery. Adding Steiner's 3 cases to the 38 which he found in the 
literature, making 41, we find that recovery occurred in 25, death in 9, 
and that no definite information is given of 7, 

Gangrene of a limb due to arterial thrombosis or embolism has been 
recorded by Zuppin, Benedict, Grimm, and Nielsen. 

Parotitis, while a rare complication of croupous pneumonia, may occur, and 
not infrequently goes on to suppuration. Most of the cases so far reported 
have not been due to the pneumococcus ; but to the staphylococcus or strepto- 
coccus. 

Otitis media is quite a common complication of croupous pneumonia in 
children, the infection taking place through the Eustachian tube. 

A relapse in croupous pneumonia is practically never met wdth, but recur- 
rence is very common. 

Duration of Croupous Pneumonia. — It is important to remember that while 
croupous pneumonia often runs a course of from seven to ten days, it not 
infrequently reaches its crisis at a much earlier period. As already pointed 
out, crisis may occasionally occur as early as the third day, and by no means 
infrequently takes place as early as the fifth. While it is true that early 
crisis usually occurs in comparatively mild attacks of the disease, it is also a 
fact that the patient may seem seriously ill throughout the whole course 
of these cases of comparatively short illness. 

Varieties of Croupous Pneumonia. — Croupous pneumonia varies much in 
its character with the condition of the patient that is attacked. I have 
already mentioned the type which occurs in persons who are addicted to the 
excessive use of alcohol. In other individuals the disease is accompanied by 
such marked symptoms of adynamia that the patient seems to be suffering from 
typhoid fever, so far as his general symptoms are concerned. This form is 
known as typhoid pneumonia, in that it is typhoid in character; but this term 
does not necessarily imply that typhoid infection is associated with that by 
the pneumococcus. On the other hand, it sometimes happens that patients 
suffering from typhoid fever also have a pneumococcic infection of the lung, 
and this, of course, is another form of so-called typhoid pneumonia. True 
croupous pneumonia also occasionally, although rarely, complicates malarial 
fever, acute articular rheumatism, and pulmonary tuberculosis. Sometimes, 
too, it occurs as a sequel to the administration of ether as an anaesthetic. 



CROUPOUS PNEUMONIA 163 

This is probably due primarily to the chilling and irritation of the lung by 
the drug, and secondarily to the inhalation of pneumococci from the mouth, 
where, as already stated, they are almost constantly present even in healthy 
persons. 

Diagnosis. — Croupous pneumonia is to be carefully differentiated from 
acute tuberculous pulmonary infection, from lobular or catarrhal pneu- 
monia, from infarction of the lung, accompanied by bloody expectoration, 
due to cardiac disease, from pleurisy with effusion, and from chronic inflam- 
mation of the pleura, with marked thickening of that serous membrane. 
Finally, it is to be separated from hypostatic congestion due to cardiac 
feebleness arising in the course of acute diseases or chronic ailments. 

The differentiation from acute pneumonic phthisis may be quite impos- 
sible until the development of profuse sweating, a feeble and rapidly acting 
heart, and the appearance of yellow elastic tissue and tubercle bacilli in the 
sputum takes place. From pulmonary infarction it is to be separated by 
careful examination of the heart, which may reveal valvular lesions, and by 
the fact that in infarction the onset of pulmonary disorder is instantaneous 
and the sputum contains bright blood. From pleural effusions it is differ- 
entiated by the development of the physical signs of that condition. (See 
Pleurisy, with Effusion.) Hypostatic congestion of the lungs is discovered 
by the character of the sputum, which may be blood-stained, although it 
is usually serous, by the fact that the lesions are usually bilateral, and 
also by the fact that the heart is primarily very weak. Catarrhal or lobular 
pneumonia is recognized by the absence of the typical rusty sputum, by the 
history of the presence of some primary disease prior to the onset of the 
pneumonic consolidation, and by the wide distribution of the lesions and 
the more diffuse physical signs. 

An important aid to the diagnosis of croupous pneumonia is the increase 
in the number of the polymorphonuclear white cells, the so-called leukocytosis 
of croupous pneumonia. In this disease in most instances the increase in 
these particular white cells causes a leukocytosis of from 18,000 to 20,000. 

The blood serum of these cases is capable of causing agglutination of the 
pneumococcus and the degree of agglutinative power seems to be greatest 
about the time of crisis, but there are technical difficulties about the test 
which render it of little value in diagnosis. 

It is of the greatest importance that the severe pain sometimes described 
as being in the belly at the onset of pneumonia is not mistaken for that due 
to appendicitis. Cases frequently occur in which pain due to thoracic disease 
is thought to be abdominal, particularly if the base of the lung is involved. 
The presence of pain on pressure over McBurney's point, of some fixation 
of the abdominal muscles, and of a high leukocyte count may be so misleading 
as to lead the physician to operate for disease of the appendix. 

It is characteristic of croupous pneumonia that the chlorides in the 
urine are greatly decreased. 

The physician should always be on his guard lest he overlook a "central" 
or deep-seated pneumonia, which presents no marked physical signs. 

Prognosis. — The prognosis in croupous pneumonia is always to be governed 
by the recollection of the fact that its mortality in adults is usually high, and 



164 



DISEASES DUE TO A SPECIFIC INFECTION 



again by the condition and habits of the patient. It is to be remembered 
that the prognosis in a case of croupous pneumonia is grave in direct pro- 
portion to the years of the patient. In young children, unless it is compli- 
cated by some grave accident, the disease has a very low mortality. By 



Fig. 36 



PERCENTAGE 

UNDER 5 YEARS 

OF AGE 

BETWEEN 
5 AND 10 


BETWEEN 

10 AND 20 

BETWEEN 

20 AND 30 

BETWEEN 
30 AND 40 

BETWEEN 

40 AND 50 


BETWEEN 
50 AND 60 

BETWEEN 
60 AND 70 


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Chart showing the morbidity and mortality of croupous pneumonia at different ages, based on 868 
cases in the Presbyterian Hospital, New York, and Guy's Hospital, London. Solid line, morbidity; 
dotted line, mortality. 

far the greater number of children recover, whereas in advanced years 
the disease is exceedingly fatal (Fig. 36) . As an illustration of how low the 



CROUPOUS PNEUMOMA 105 

mortality may be when young, healthy persons are affected by the disease and 
come under skilful treatment early in its course, Osier states that in 40,000 
cases occurring in the German army the mortality was only 3.6 per cent. 

If the mortality percentage is based upon the total number of deaths from 
this disease, it may be stated to be as high as from 25 to 40 per cent. ; but if, 
on the other hand, those cases which would naturally fall victims to its 
ravages are excluded, the mortality is probably only about 10 per cent., if 
we accept the large statistics of Townsend and Coolidge, who excluded 
patients over fifty years of age and those who were delicate or suffering 
from some other disease primarily present. In private practice the mortality 
varies from 6 to 18 per cent. 

Aside from advanced years the other causes which render the prognosis 
especially grave are renal disease, with secondary cardiovascular lesions, alco- 
holism, and diabetes. Indeed, these three states contribute a very large pro- 
portion of the number of cases which suffer from this malady, and also the 
largest proportion of deaths in the statistics. 

It is stated by some authors that any history of previous ill health 
distinctly increases the danger from croupous pneumonia. While this 
may be true in certain cases in which vitality is greatly depressed, it is 
also a fact that pneumonia in chronic invalids frequently runs a com- 
paratively mild course unless the cause of their ill health be renal or 
cardiac disease, whereas it may speedily produce death in robust, power- 
ful, muscular men, who frequently succumb to its ravages far more rap- 
idly than more lightly built and apparently delicate individuals. Indeed, 
the physician of experience dreads the onset of this disease in powerful, 
well-developed men much more than when it attacks those who are less 
given to active exercise and feats of physical strength. Stout persons 
also seem much more susceptible to the lethal influences of the disease 
than those who are lean. This probably depends upon two causes: first, 
the heart and lungs may be overweighted by fat, and, second, such persons 
usually contain in their tissues a large amount of serum, in which, perhaps, 
specific micro-organisms find an opportunity to grow and to prepare their 
toxic product in large quantity. 

Cases of croupous pneumonia characterized by moderately high fever do 
not possess the unfavorable outlook of other diseases which suffer from hyper- 
pyrexia; that is, a temperature in the neighborhood of 106°. On the other 
hand, it not infrequently happens that cases running a temperature course 
varying from 101° to 102° are more severe as to toxaemia than those which 
range in the neighborhood of 103° or 104°, or even 105° for a short time. If, 
with the drop in temperature which occurs at crisis, the general condition of 
the patient does not markedly improve, the prognosis is bad. If in place of 
the ordinary rusty sputum it is of the color of prune-juice, it is usually con- 
sidered that the disease is malignant. 

An important prognostic point in any given case is the degree of toxaemia 
which is present. In other words, the prognosis depends not so much upon 
the area of lung which is involved as it does upon the quantity of toxic 
material which the infecting micro-organisms seem to be producing. 
Again and again death occurs in apparently otherwise healthy individuals 



166 DISEASES DUE TO A SPECIFIC INFECTION 

who present a small area of consolidated lung and almost no typical signs of 
pneumonia, but who are apparently overwhelmed by great toxaemia. 

An absence of leukocytosis in a case of croupous pneumonia usually pos- 
sesses an evil import, since it seems to indicate a degree of toxaemia with 
which the system of the patient finds it difficult to deal. Indeed, in some 
fatal cases the leukocyte count may not only not be increased, but very much 
diminished. 

As to the prognostic value of finding the pneumococcus in the blood, 
there is much difference of opinion. Some observers assert that its pres- 
ence is of evil import, while others think it of little significance, unless the 
infection is manifestly severe. The latter view is probably correct. 

Treatment. — The treatment of a case of croupous pneumonia varies greatly 
with the condition of the patient who is suffering from the disease. When 
it attacks the stout and robust, the only duty of the physician, in a large 
number of instances, is to watch the patient's symptoms; to insist upon rest in 
bed in a well-ventilated and quiet room, and to administer a sufficient quan- 
tity of bromide, Dover's powder, or morphine to relieve pain, if that symp- 
tom is excessive. If, on the other hand, the patient is one who has been 
addicted to the use of alcohol in excess, whiskey or brandy should be given 
him in amounts varying with the quantity which he had been accustomed to 
ingest daily. Not only does his system require the effects produced by 
this drug, but its use is also necessary to prevent the rapid development of 
delirium tremens, which is a most fatal complication in these cases. An 
active stimulation is also usually required in many cases of croupous pneu- 
monia in which the patient is just recovering from some other severe infec- 
tion, such as typhoid fever. 

It is, however, a fatal mistake to think that every patient suffering from this 
disease should be stimulated. The physician should always bear in mind 
the important rule not to meddle with the course of the disease unless symp- 
toms are so pressing as to require interference. There can be no doubt that 
one of the best stimulants in the average case of croupous pneumonia is 
alcohol, in some form which will agree well with the stomach. The dose of 
this drug in the form of whiskey or brandy must depend upon the needs of the 
individual. Rarely will any patient require more than 8 to 12 ounces in the 
twenty-four hours, and many will do best on much less than this. Valuable 
adjuvants to alcohol are the aromatic spirit of ammonia, given in the dose of 
30 minims, well diluted, every two or three hours; and should any sign of acute 
cardiac failure develop, Hoffmann's anodyne, in the dose of 1 or 2 drachms, 
in water, every hour or two, is an invaluable remedy. 

For the condition of acute cardiac weakness, the value of strychnine 
should also be borne in mind. Under these circumstances it is often 
invaluable, and if need be may be given in full dose, frequently repeated, 
by a hypodermic needle, until the patient rallies. Usually -£$ to ■£■$ grain, 
repeated once or twice, at an interval of two or three hours, approximates 
the proper dose. At the present time it has become fashionable for 
physicians to administer strychnine as a cardiac stimulant throughout 
the whole course of pneumonia. This is an abuse of a good remedy. 
Strychnine is not a direct cardiac stimulant. It increases the activity of 



CROUPOUS PNEUMONIA 167 

the heart by rallying the nervous system and acting as an indirect whip to 
the circulation. If its use is persisted in it soon loses its so-called stimu- 
lant effects, and is apt to produce a condition of nervous irritation, par- 
ticularly in the aged, which may be quite distressing. Its constant use 
deprives the physician of a valuable remedy for meeting critical moments 
in the course of the disease. 

The value of digitalis for the purpose of combating cardiac failure in acute 
croupous pneumonia has been questioned. It is a well-known fact that 
digitalis loses a large amount of its power over the heart in the presence of 
high fever; and fever is nearly always a marked symptom in this disease. 
It is also coming to be a well-recognized fact that digitalis is of little value 
in those cases in which the heart muscle has undergone degenerative 
change, and the toxaemia of pneumonia often produces such alterations in 
the muscle fibre of this viscus. In cases in which there is marked vascular 
relaxation and cardiac dilatation, I have known it to do good when given 
in a few large doses, particularly if strychnine and atropine were simultan- 
eously administered. Although it is a drug which contracts the bloodvessels, 
the vasomotor dilatation or relaxation of advanced pneumonia is often so 
marked that digitalis seems to be unable to raise the arterial pressure, and I 
am convinced that in many instances death occurs more largely because of 
the relaxed condition of the bloodvessels than by any direct effect of the dis- 
ease upon the heart. When I use digitalis, therefore, I am in the habit of 
prescribing 5 or 10 drops of a physiologically tested tincture every eight or six 
hours, and the same quantity of tincture of belladonna every three or four 
hours, in order that the belladonna may increase the tone of the vessels. 
This treatment, however, is rarely instituted before the fifth or sixth day, or 
at the approach of crisis. 

If cardiac failure is the result of cardiac dilatation due to the obstruc- 
tion of the flow of blood through the lung, digitalis may be advantageous, 
but when the cardiac weakness is due to toxaemia it is probably of little 
value, and if a clot has formed in a cardiac cavity it is manifestly use- 
less. Sometimes when the fever is high and digitalis fails to act, it is 
well to aid its effect by quieting the heart through the application of 
an ice-bag placed upon the preecordium. I have also known the reduc- 
tion of temperature by the local application of the ice-bag and by cool 
sponging of the body, with friction, to be followed by the manifestation of 
a distinct digitalis influence. If moderate doses of 5 or 10 minims of a 
physiologically tested tincture, three or four times a day, fail to produce 
good effects under these circumstances, I feel quite confident that larger ones 
will not be of any value. 

Should sudden collapse come on, a hypodermic injection of strychnine and 
atropine should be given, and it may be wise to introduce under the skin, by 
hypodermoclysis, a pint of normal saline solution, containing 1 drachm of a 
1 : 1000 solution of adrenalin chloride. The normal saline solution, under 
these circumstances, cannot do much good directly because the relaxation 
of the bloodvessels is so great that even if it is absorbed its influence will not 
be felt, but it forms a reservoir from which the adrenalin chloride will be 
slowly absorbed and so raise arterial pressure by stimulating the w r alls of the 



16S DISEASES DUE TO A SPECIFIC INFECTION 

bloodvessels when the toxaemia of the disease has perchance paralyzed the 
vasomotor centre When the skin becomes relaxed and bedewed with sweat, 
atropine is often a life-saving drug. 

In cases in which the heart is laboring, where there is evidence of dilata- 
tion of its right cavity with pulsating jugulars and other evidences of 
venous stasis, free venesection may be practised with advantage, and 
sometimes gives wonderful relief; but in cardiac failure without these 
signs of venous obstruction, venesection is practically of no value whatever. 

The value of inhalations of oxygen gas is problematical. I always em- 
ploy them because they seem to give comfort both to the patient and his 
friends. The oxygen should not be given through an inhaler, but be allowed to 
escape, through the opening of the rubber tube or glass nozzle, about the lips 
or nose of the patient, for the ordinary individual who is suffering from 
dyspnoea in this disease will not permit one of his nostrils to be blocked 
or his mouth closed by such an inhaler, as his desire for ordinary air is too 
great. If the dyspnoea is due to toxaemia, the oxygen is probably useless. 
If it is due to a large area of the lung being incapacitated by consolidation, it 
is conceivable that oxygen can do great good. 

The value of saline infusion also depends upon the degree of toxaemia 
which is present and upon the activity of the kidneys. If, in a given case, 
the urinary secretion is scanty and toxic symptoms develop, a pint of normal 
salt solution may be given by hypodermoclysis every six or eight hours for 
twenty-four hours with advantage. If, on the other hand, the pneumonia 
complicates renal disease, and there is any tendency to oedema of the sub- 
cutaneous tissues, this method of treatment may be disadvantageous, in that 
it tends to increase the dropsy, and perhaps increases the tendency to pul- 
monary oedema. As marked toxaemia is usually associated with renal 
inactivity, this method of treatment should be borne in mind. Direct 
infusion of a saline solution into a vein is probably not advisable in the 
majority of cases, since it is usually absorbed with sufficient rapidity from 
the subcutaneous tissues. 

The treatment of the fever during the course of croupous pneumonia is 
not of as great importance as it is during the course of a more prolonged 
malady, like typhoid fever. Indeed, there is some evidence to show that 
fever within moderate bounds may be an effort on the part of the organism 
to protect itself from the infecting germs. If the temperature does not exceed 
102.5° to 103°, antipyretic measures need not be instituted, although spong- 
ing the patient with tepid or cool water three or four times a day will control 
the temperature somewhat, allay peripheral nervous irritation, keep the skin 
clean, and often produce sleep. These spongings are, therefore, useful in the 
ordinary case of pneumonia with a temperature jf 103° or more, but they 
are not to be carried out with the same vigor, either as to the activity of the 
rubbing or degree of cold, as is employed in typhoid fever, for the temperature, 
as a rule, does not resist the cold, and if it is applied too freely the patient 
may be thrown into collapse by a sudden fall of fever. Nearly every case 
of acute pneumonia will be benefited if an ice-bag is kept applied to the head, 
and if the action of the heart is very rapid when the fever is high an ice- 
bag over the praecordium, as already stated, is often advantageous. 



CROUPOUS PXEUMOXIA 169 

The administration of antipyretic drugs to patients suffering from pneu- 
monia is absolutely inexcusable. In the first place, antipyresis by drugs is 
rarely if ever needed. In the second place, there is overwhelming clinical 
and experimental evidence to show that the use of these drugs materially 
diminishes the vital resistance of the patient, decreases the ability of his blood 
to convey oxygen to his tissues, reduces its ability to destroy infecting micro- 
organisms, lowers vascular tone, depresses the heart, and is altogether evil 
in its influence, probably also diminishing the elimination of toxic materials 
by the kidneys, and certainly giving these organs the additional labor of 
eliminating the antipyretic drug, which, perchance, may be irritating to them. 

Quinine is employed by some practitioners with the idea that it possesses 
antipyretic power, and there is no objection to its use in small doses; large 
doses, which produce cinchonism or irritation of the stomach, are valueless, 
and may do harm by irritating the stomach, producing cerebral congestion 
and meningeal irritation, or irritating the kidneys. 

When croupous pneumonia is of the typhoid type and asthenia is marked, 
valuable results can be obtained very frequently by the hypodermic injection 
of \ to 1 grain of camphor, dissolved in sterilized olive oil. This injection 
may be given once, twice, or thrice in twenty-four hours for one or two 
days, but ought not to be continued too long; first, because it rapidly loses 
its effects if used too frequently, and, second, because in these doses there 
may be some danger of camphor poisoning. Camphor is to be regarded as 
a remedy for an emergency, and is to be reserved for critical periods. 

If great mental and nervous excitement is present and persistent, life can 
often be saved by the administration hypodermically of J. J, or \ grain of 
morphine. This will often produce several hours of desired sleep, from which 
the patient awakens much refreshed and perhaps free of the delirium which 
before the administration of the morphine was an annoying symptom, in 
that it produced physical exhaustion through the constant activity of his 
body and mind. 

The employment of nitroglycerin in the treatment of pneumonia is limited 
to those cases which have a high arterial tension. The drug, under these 
circumstances, is of great value in that it diminishes the work of the heart by 
removing the vis a fronte. If, on the other hand, vascular spasm does not 
exist, the drug is useless, for it is not, as some have thought, in any sense a 
direct cardiac stimulant. 

The question of the employment of circulatory sedatives in the early stages 
of acute croupous pneumonia is one which has been widely debated, particu- 
larly in this country. There are many excellent practitioners who consider 
that full doses of veratrum viride or aconite in the earlier stages of croupous 
pneumonia are advantageous. Statistics, or, to speak more correctly, wide 
personal experience on the part of many physicians, seems to justify the use of 
this drug in some cases, namely, in those instances in which the physician sees 
the patient during the first hours of the attack, and if the patient is a strong, 
sthenic individual, w T ith a full, bounding pulse, and great flushing of the face. 
Under these circumstances the relaxation of the general vascular system 
produced by the veratrum viride and the quieting of the excited heart seems 
distinctly advantageous. Whether such treatment in any way aborts, or 



170 DISEASES DUE TO A SPECIFIC INFECTION 

jugulates, or diminishes the violence of the subsequent attack is difficult to 
determine. In a few instances of acute croupous pneumonia and acute 
pleurisy, seen in the very early stages, I have noted good results from such 
treatment. But in the vast majority of instances the physician does not see 
the patient for nearly twenty-four hours, by this time the disease is well 
started on its way, and the symptoms of great circulatory excitement 
have usually passed by, so that circulatory sedatives are distinctly contra- 
indicated. 

As the rapid development of the signs of circulatory depression can 
be aided by the administration of sedative remedies, the use of chloral 
and the bromides as nervous sedatives in the course of croupous pneumonia 
is usually inadvisable. Chloral in particular is contraindicated, because of 
its well-known depressant effect upon the heart and its irritant action upon 
the kidneys. 

The diet should be liquid and consist of milk, with a little pancreatin 
and bicarbonate of soda, to aid in digestion, and of animal broths 
and gruels made of wheaten grits, oatmeal, rice, or barley, the digestion of 
these starchy foods being aided by the administration of small quantities of 
taka-diastase or pancreatin. I am quite convinced that we too infrequently 
resort to these cereal fluids in the treatment of diseases of this nature, since they 
possess much nutritional value and, if their digestion is aided, agree with the 
vast majority of patients, and enable us to change the diet so that the patient 
does not become tired of any one particular kind of food, w T hich is a great 
advantage. 

Care should be taken in cases of croupous pneumonia that the patient 
receives an adequate amount of water to drink, so that the kidneys may 
be well flushed with fluid in each twenty-four hours; but it is important 
that only small amounts of fluid be taken at a time, as distention of the stomach 
may cause fatal cardiac embarrassment. The bowels should also be moved 
each day in the early stages of the attack by full doses of calomel, and in the 
later stages by salines, or, if the patient is too weak for the use of these purga- 
tives, by a rectal injection of water or of glycerin and water. 

The administration of expectorants in croupous pneumonia is useless 
until the stage of resolution is reached. Even then they are probably of 
little value in clearing up the exudate in the vesicular portions of the lung. 
But the chloride of ammonium, the oil of sandal-wood, guaiacol, and terpin 
hydrate often prove useful at this time in aiding in removing the symptoms 
of chronic bronchitis which exist, a state which results in the formation of 
a good deal of thick, tenacious bronchial mucus, which the patient may have 
difficulty in expectorating. 

Excessive cough in all stages of croupous pneumonia is best controlled 
by the administration of Dover's powder, codeine, paregoric, or the newer 
drug, heroin. In the stage of resolution cough sedatives should not be 
administered unless the physician is certain that the cough is in excess of 
the needs of the patient in getting rid of the materials in his chest which 
should be gotten rid of in this way. 

Meningeal symptoms are to be treated by the application of cold to the 
head, and sometimes it is wise to apply a blister to the nape of the neck. 



DIPHTHERIA 171 



DIPHTHERIA. 



Definition. — Diphtheria is an acute infectious disease, which chiefly affects 
children under puberty. It is due to the Klebs-Loeffler bacillus, and is char- 
acterized primarily by an acute local inflammatory process which affects, as a 
rule, the pharynx, larynx, or nasal mucous membrane, and which is peculiar in 
that it is associated with the development of a false membrane due to a 
fibrinous exudate. From the spot upon which this condition develops the 
general system becomes affected, not by the micro-organism of the disease, 
but by the poisons or toxins produced by the specific organism at the site of 
primary infection. Other infections may occasionally cause the production 
of a false membrane, but the discovery of the presence of the Klebs-Loeffier 
bacillus determines that the affection is diphtheria. All cases in which a 
false membrane develops on a visible mucous membrane should be considered 
to be cases of diphtheria and treated as such until proved to be non-diph- 
theritic, because in this way the spread of the disease is prevented and the 
use of the specific remedy, antitoxin, will save life if the disease is present 
and do no harm if it is not. 

In the great majority of cases the disease primarily affects the pharyngeal 
mucous membrane, or the mucous membranes immediately adjacent thereto, 
and from this area spreads to the nose or larynx, where the results of its 
development are very fatal. The specific inflammation and false membrane 
may, however, develop on any exposed mucous membrane, and even upon 
the true skin if the epiderm be removed intentionally or by accident. 

It is possible for bacteriologists to find the Klebs-Loeffler bacillus in cases 
of sore throat in which there is no false membrane and no systemic symptoms 
of diphtheria, and in some of these instances even local disturbances may 
be absent because of the resistance offered to this infection by some persons. 
These cases are not to be considered instances of diphtheria, although they 
are entirely capable of conveying the completely developed disease to others. 

On the other hand, cases are not rarely seen in which the physician finds 
a shaggy false membrane on the throat associated with signs of great sys- 
temic toxaemia, and in which the bacteriologist fails to find the specific micro- 
organism of diphtheria. This condition is called diphtheria by the physician 
and pseudodiphtheria by the bacteriologist. The streptococcus is probably 
responsible for some cases of the latter type, while in other patients the 
pneumococcus causes a similar effect. These instances are met with most 
commonly as complications of scarlet fever or more rarely of measles, and 
also occur as manifestations of severe tonsillitis or angina. 

History. — Diphtheria has been recognized for many centuries as a disease, 
but it was not until the clinical observations of Bretonneau, of Tours, that 
its separate identity was established under the name of "diphtherite." 
He classed all cases of "putrid sore throat," "cynanche maligne," and 
"suffocative augina" under this one heading, and much more recently those 
cases heretofore called "membranous croup" have also been very properly 
put in the class called "diphtheritic." This sweeping classification is not 
scientifically justifiable, as has just been pointed out, but from a clinical 



172 DISEASES DUE TO A SPECIFIC INFECTION 

standpoint it is proper because in the majority of instances the false 
membrane' is due to this cause. 

Distribution. — Diphtheria is a disease which occurs in nearly all parts 
of the world, but is much more prevalent in the temperate zones than 
elsewhere. It occurs in epidemics and in sporadic cases, and is endemic 
in nearly every large city„ While common in cities, it is even more common 
in country districts. No special influence upon its development is known 
to be exercised by bad drainage, although such drainage may, by diminish- 
ing vital resistance, very greatly increase susceptibility to the malady. 

It is a disease of the poor rather than of the rich, and when it occurs 
in the well-to-do it is usually sporadic and its source can often be traced to 
some single exposure. The reason for this does not lie so much in greater 
susceptibility of the poor as in greater exposure to the infection, for when 
the children of the well-to-do are attacked they succumb as readily as 
their otherwise less fortunate fellows. 

Diphtheria occurs much more frequently between the ages of two and 
five years than at any other time of life (Fig. 37). 

Etiology. — Diphtheria is due, as has already been stated, to a specific 
bacillus first described by Klebs in 1883, and later isolated by Loeffler. 
This micro-organism is from 1.5 to 3.5 or rarely 4.5 micromillimetres in 
length, and from 0.3 to 0.8 in breadth. It usually appears singly, in groups 
of two or three, but true chains are said not to occur; the organisms may 
lie side by side or at an angle. They are slightly curved with straight, 
rounded ends, sometimes branched, and commonly beaded or barred. 
They do not give off spores, and flagella are absent. They may contain 
highly refractive bodies which cause them to stain irregularly. The best 
stain is that of Loeffler, the oval bodies in the organism staining more highly 
than the rest of the bacillus. They are grown best in Loeffier's blood serum, 
but develop in all the laboratory media. The organism is non-motile and 
almost purely aerobic. 

All cases of diphtheria are due to the entrance into the body of this specific 
bacillus originally derived from some patient ill with the disease. The 
transfer is made in a multitude of ways. Sometimes it is by the clothing, 
by books, by foodstuffs, or drinks, or drinking-vessels, by pencils, or by the 
coughing of an individual, who may have the bacilli in the throat, in such 
a way that the infectious agent is driven into the respiratory passages or 
mouth of the other person. Convalescent patients may in this manner act 
as disseminators of the disease long after they are apparently entirely well, and 
healthy persons w r ith the bacilli in the mouth may also carry the in- 
fection. 

Thus it is entirely possible for a nurse who has been in charge of a case of 
diphtheria to carry in the crypts of the tonsils the specific micro-organism, 
to have no sign of the disease, and yet infect a child or adult whom she 
may care for soon after leaving the first case. It is evident, therefore, that 
while the infection is not carried by the air, as in smallpox, it is very easy for 
a patient who sneezes or coughs to distribute the infectious agent broadcast 
by its falling on neighboring substances which act as agents of conveyance. 
These are some of the causes that result in the rapid spread of the disease 



DIPHTHERIA 



173 



in tenement houses, schools, and other public places where children are 
congregated. 

As the specific bacillus possesses great vitality, the relationship between 
cause and effect may not be readily discovered. Thus, if the bacilli fall on 
a garment they have been found to remain capable of producing the disease 
six months later, and they have been found in the throat many months after 
perfect health has been established. So, too, the dust of the room may carry 
the infection, and even the hair or beard of the physician may do likewise, 
if the patient expels any secretion upon it. Finally, as already intimated, 
milk may act in this manner, and cheese made from contaminated milk 



Fig. 37 



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Showing the age incidence of diphtheria, based on 3360 cases collected from various sources. 



may even convey the bacillus. Pet animals, such as cats and dogs, 
also act as distributors, and rodents, such as rats and mice, may do 
likewise. 

While all the diseases of birds, cats, and calves characterized by the for- 
mation of a false membrane are not communicable to man, the possibility 
of a true diphtheritic infection, in domestic animals, cannot be denied. 

There are a number of causes existing in the patient which exercise a 
predisposing influence in connection with this infection. Some of these 
are at present obscure and probably depend upon a lack of anti-bodies in 
the blood and tissues, but others are equally active, readily recognizable 



174 DISEASES DUE TO A SPECIFIC INFECTION 

and in many cases remediable. There can be no doubt whatever that 
chronically enlarged tonsils, overgrowth of the so-called pharyngeal tonsil 
and chronic catarrh of the nasopharynx very materially increase the suscep- 
tibility of a child to diphtheria. For this reason these conditions should 
not be allowed to exist in otherwise healthy children. Further than this 
the crypts of the tonsils when diseased may harbor the Klebs-Loeffler bacillus, 
until a time when the system of the patient is favorable for its growth and 
then develop rapidly, or on being expelled cause the malady in another 
individual. 

None of the pathogenic organisms seems to possess a greater degree of 
variance in virulency than the one under discussion. In some instances 
it fails to exert any malign effect beyond a local influence, and even this 
may amount to nothing more than a sore throat. In other cases it attacks 
the patient with a virulence which is perfectly terrifying. 

It is not probable that sex has any influence as a predisposing cause. 
Statistics vary, however, some showing that a greater number of cases occur 
among boys than among girls. That these differences are merely fortuitous 
is exemplified by the fact that of 22,005 cases collected from various sources 
11,006 occurred among boys and 10,999 among girls, a difference of only 
seven cases. 

Pathology and Morbid Anatomy. — In studying the pathology and morbid 
anatomy of diphtheria it is essential to remember that the disease is primarily 
local and secondarily systemic; that the local area of infection is the site 
at which the specific organism multiplies and produces local changes by 
its growth, and at the same time elaborates a toxin which, being absorbed, 
acts on distant parts and so endangers life. The bacillus enters the blood 
stream in a relatively constant percentage of cases. 

Local Lesions. — The local change produced by the growth of the bacillus 
is now well understood, for a large number of researches in Europe and 
America have given us clear conceptions of it, Of these researches by far the 
most noteworthy is that carried out by Councilman, Mallory, and Pearce in 
Boston. 

The poison produced by the specific bacillus in the mucous membrane 
of the throat results in the death of the tissues and in this necrotic mass 
the bacilli then very rapidly develop. The epithelium in many cases 
manifests more or less proliferation, becomes hyaline and necrotic, eventu- 
ally fragmenting and disintegrating. The inflammatory exudate which per- 
meates the mucosa and even the submucous stratum is very rich in fibrin 
elements, and when brought in contact with the necrosing structures forms 
a fibrous reticulum entangling within its meshes the cells and bacteria. 
The membrane formed by the coagulation necrosis and hyaline degeneration 
of the cells may be so transparent as almost to escape detection during life 
(hyaline type) , or it may be granular or fibrillar. The necrosis may extend 
into the superficial epithelium only or penetrate the submucosa, in some 
instances involving the parenchyma of the tonsil or even the submucous 
muscular structures. This necrotic membrane is subject to a number of 
important changes. It may disintegrate and form a mass of shreddy detritus 
on the surface or it may be thrown off by being elevated by the exudate 



DIPHTHERIA 175 

which forms beneath it. In the latter process a very thick, false membrane 
formed of consecutive layers may be produced. The membrane always 
develops on a necrotic surface, but it may extend a short distance over the 
surrounding mucous membrane. 

The depth of the destructive process is not very great in the majority 
of cases, but in rare instances it has become deep enough to erode the 
carotid artery. In many, if not all, such instances other organisms play 
an important part in the spread of the necrosis and add to the intoxication 
their own poisonous products. It is important to bear in mind in diphtheria 
that the infection is "mixed" in the vast majority of cases; that is, the false 
membrane not only holds in its meshes a multitude of the specific bacilli 
but many other micro-organisms as well, many of which possess a power 
for evil, as, for example, the streptococcus. 

The membrane is closely attached to the tissues beneath and is stripped 
off with great difficulty except when it develops in the larynx and bronchi, 
when it is dislodged quite readily. 

The false membrane may develop on any mucous membrane or upon 
any wound or abrasion, but it most frequently appears on the tonsils. 
According to Lennox Browne, of London, the relative frequency of its 
appearance is as follows: 

Above the larynx, 84.1 per cent.: 841 cases. 

Fauces (including tonsils) alone ..... 672 cases. 

Nose alone ......... 2 cases. 

Fauces and nose . . . . . . . .165 cases. 

Mouth or lips alone ........ 1 case. 

Hard palate alone ........ 1 case. 

Involving larynx, 15.9 per cent.: 150 cases. 

Larynx alone ......... 4 cases. 

Larynx and fauces 100 cases. 

Larynx, fauces, and nose ....... 46 cases. 

The growth of the membrane, whatever its site, varies greatly in rapidity, 
in the area covered, and also in its thickness, but the virulence of the systemic 
infection is not always in direct ratio to the size of the diphtheritic patch. 
On the other hand, the degree of secondary infection depends largely upon 
the particular surface involved, and if it develops in the nasopharynx the 
toxaemia is apt to be profound. In many severe cases the accessory nasal 
cavities are infected, particularly the antrum of Highmore. 

Visceral and Systemic Lesions. — The action of the toxin of diphtheria 
is chiefly expended upon the heart, the nervous system, and the kidneys, 
The heart suffers from an acute myositis or inflammation of its interstitial 
and muscular tissues, and this may be followed by conversion of the muscle 
fibres into hyaline masses. In a large proportion of the cases in which 
sudden death from heart-failure occurs the cause lies in the effect of the 
poison upon the nervous mechanism of the heart, possibly to a greater 
degree than its effect upon the myocardium. In some of these cases, how- 
ever, death is due to thrombi in the heart cavities (see Sequelae), or, 
again, portions of these thrombi are swept out of the heart and produce 



176 DISEASES DUE TO A SPECIFIC INFECTION 

embolism in the coronary arteries, in the pulmonary vessels or in the gen- 
eral arterial system. As would be expected from the effects upon the 
heart, just described, the bloodvessels are also affected. An acute arteritis 
often occurs and affects particularly the intima. 

The nervous system is involved chiefly in its peripheral portions. The nerve 
trunks suffer from acute toxic neuritis and less commonly autopsy reveals 
hemorrhage into the spinal cord and its membranes as a result of the vascular 
action of the poison. A much more common spinal lesion is, however, an 
acute anterior poliomyelitis, that is, involvement of the cells in the anterior 
horns of the gray matter. Sometimes, too, the posterior nerve roots in the 
cord may be also affected. The special cranial nerves are also involved in 
many instances and loss of function in the oculomotor, vagus, hypoglossal 
and spinal accessory fibres takes place. It is, however, interesting to note 
that while paralysis, due to peripheral diphtheritic neuritis, may be absolute 
and widespread, it usually gets well unless the function of some vital part 
is so interfered with that death speedily ensues. The brain is very rarely 
affected. 

The kidneys are more or less affected in all cases of diphtheria. In some 
there is only a mild albuminuria produced by the irritative effect of the 
toxin upon the renal epithelium. In more severe cases an acute toxic 
nephritis develops. This nephritis primarily is parenchymatous, involving 
the Malpighian tufts and the tubules, but it speedily becomes diffuse. 
Hyaline degeneration also takes place in the renal vessels, as elsewhere in 
the body. 

The spleen is enlarged, markedly congested, and minute hemorrhages 
are to be seen beneath its capsule. The liver may be found, on cross-section, 
to be dotted with small areas of coagulation necrosis. 

As the infection is most marked in the throat the cervical lymph glands 
are usually infiltrated and the poison may also cause enlargement of the 
lymphatics in the mediastinum and in the retroperitoneum. The inflamma- 
tion of the lymph nodes, however, rarely ends in suppuration or extensive 
necrosis. 

The lungs are often the site of bronchopneumonia resulting from a com- 
plicating pneumococcus infection, but true croupous pneumonia is a rare 
complication. When great dyspnoea is present because of laryngeal stenosis 
compensatory emphysema may develop. In the laryngeal form the mem- 
brane may extend to the smaller bronchi. 

The blood is affected very deleteriously by the poison of diphtheria, so 
that a great diminution in the number of the red cells takes place with 
a corresponding fall in haemoglobin. A leukocytosis occurs except in the 
very malignant forms of the disease. Myelocytes are said to be present in 
severe cases, and Engel states that in those cases in which they appear in 
as high a percentage as 2 per cent, death occurs. 

Symptoms. — After a period of incubation varying from two to seven days 
the disease has its onset in the form assumed by most acute infections, 
namely, with general malaise, chilliness, and fever, the temperature often 
reaching 102° or even 103° in the first twenty-four hours. The severity of 
these symptoms varies greatly. In some cases they are so mild that the child 



DIPHTHERIA 177 

is scarcely thought to be ailing, and the physician at his second visit is 
shocked on examining the throat to find distinct local lesions. In other cases 
the disease is fulminating in its onset. I have seen a small patch of mem- 
brane on a tonsil within twelve hours involve the larynx and necessitate 
tracheotomy, the membrane involving the external edges of the wound in 
less than twelve hours more. In nearly every case there is some complaint 
of sore throat, or of difficulty in swallowing arising from this cause. The 
pharyngeal mucous membrane is reddened and upon the tonsil or tonsils 
is seen a tiny patch, which is the beginning of the membrane, but which may 
be due to the exudate thrown out by a follicular tonsillitis. This membrane 
rapidly spreads and may extend to the pillars of the fauces, the pharynx, 
nasopharynx, and the uvula. It is grayish or light mouse color in hue, and 
in many cases speedily becomes shaggy and dirty looking. If the physician 
attempts to remove it it is found to adhere to the mucous membrane, and 
it can be taken off by only tearing it loose, so that a raw, bleeding surface is 
exposed over which a false membrane speedily reforms for reasons given 
when discussing the pathology and morbid anatomy of the disease. 

There is nearly always some enlargement of the glands at the angle of the 
jaw. 

The degree of systemic disturbance depends in every case upon the virulence 
of the infecting bacillus and the rapidity with which the toxin is absorbed. 

Some patients who present on examination a large area of membrane 
suffer slightly in a comparative sense. The fever does not rise above 
102° or 103°, the pulse does not go above 100 or 110, and the general state 
of the patient is favorable. In other instances from the very onset the gen- 
eral systemic state is bad, even when the local changes may seemingly be 
slight. Even in severe cases, however, the fever is not prone to be high, and 
often it never rises above 101°. 

The nervous symptoms consist in restlessness, sometimes in delirium, and 
rarely convulsions come on. As the disease approaches a fatal issue, the 
child becomes apathetic and it may be difficult to rouse it. 

The circulation is feeble and irregularity of the pulse is a very frequent 
symptom. In White's recent exhaustive study of 946 cases this irregularity 
was present in 60 per cent. The younger the patient the greater the 
frequency of irregularity of pulse. Endocardial murmurs, systolic in point 
of time, occurred in 94 per cent. 

Albuminuria is a very constant symptom in these cases, appearing as 
early as the third day. The albumin may appear in considerable quantities, 
but the urinary flow is in many cases not greatly increased, although the 
presence of granular and hyaline casts shows that a true nephritis is present. 
Dropsy is uncommon. 

In cases which are not complicated or treated by antitoxin, and which 
spontaneously recover, the membrane ceases to grow by the fifth or sixth 
day, and gradually separates at about the seventh or tenth day, leaving at 
its former site a bright-red surface which bleeds easily, The nasal false 
membrane persists longer than that in the pharynx, and often comes away 
in one mass. 

After this period convalescence gradually goes on, the patient being pro- 
12 



178 DISEASES DUE TO A SPECIFIC INFECTION 

foundly weak and anaemic and in great danger of sudden death from heart- 
failure if any sudden change in posture is made. A great many cases thought 
to be on the high road to recovery meet an unexpected fatal ending at this 
time. 

Special Forms. — There still remain to be described the special symptoms 
connected with those cases of diphtheria in which particular portions of 
the respiratory mucous membrane are involved, or in which the disease 
presents conditions which may be considered aberrant. In nasal diphtheria 
the false membrane may be so hidden by the swollen turbinated bodies 
that it is overlooked until it extends well forward into the nostril, when it 
may completely occlude the nares. Only a careful rhinoscopic examination 
will reveal this form in its early stages. Because of the importance of insti- 
tuting treatment in all cases of this disease at the earliest possible moment 
the nasal cavities should always be examined at the same time the throat 
is investigated, and any signs of nasal obstruction taken as of importance. 
A valuable sign of nasal diphtheria, but one which unfortunately does not 
manifest itself until the disease is well advanced is a nasal discharge which 
may excoriate the upper lip. 

It is never to be forgotten that nasal diphtheria is a very malignant 
type of the disease in nearly every instance in which it occurs, and it is 
particularly prone to affect infants or very young children. 

Laryngeal diphtheria manifests itself chiefly by the marked respiratory 
obstruction which it produces very shortly after the pathological process 
begins in the mucous membrane of the larynx. Hoarseness on speaking, 
or crying, and a harsh cough of a metallic sound, sometimes called " brassy," 
develops. Following these symptoms it is noted that there is slight inspira- 
tory stridor which is accentuated at intervals by what seems to be asso- 
ciated laryngeal spasm. This is followed by persistent stridor, harsh 
breathing, and manifest unrest and respiratory anxiety. The child may 
grasp its throat with its hands as if endeavoring to remove the obstruction, 
and as it becomes livid, partly from mechanical failure of respiration and 
partly from toxaemia, it often grinds its teeth and looks from side to side for 
relief, presenting at the same time signs of profound toxaemia. Its pallid 
skin may be bedewed with sweat. As the disease advances the child becomes 
more and more limp, and struggles less and less for its breath. In children 
old enough and strong enough to cough violently in an effort to dislodge 
the membrane it often happens that they expel pieces of false membrane, 
and in some instances they may expel complete casts of the larynx. The 
fever in this type of diphtheria may not be at all high after the larynx has 
become infected, but, as would be expected, the pulse is usually exceedingly 
rapid and small. 

Laryngeal diphtheria rarely occurs without extension to the pharynx, so 
that at the time of death the membrane usually covers a wide area. When 
the pharyngeal and laryngeal symptoms are very marked there is usually 
great enlargement of the cervical glands. 

Bronchopneumonia, due to the inspiration of septic material, is a frequent 
complication of this type. 

Like nasal diphtheria, laryngeal diphtheria has a very high mortality, 



DIPHTHERIA 179 

partly because it causes suffocation and partly because it is associated 
with toxaemia of a grave type. Sometimes laryngeal diphtheria results in 
diphtheria of the bronchial tubes. 

Diphtheria of the conjunctiva may occur as a complication or as a primary 
lesion. 

Complications and Sequelae. — The complications, involving the cervical 
glands, the lungs, heart, kidneys, and nervous system, have already been 
mentioned. Nevertheless it is proper to say something more concerning them. 

Sudden heart-failure toward the close of the attack, or after convalescence 
is established, sometimes occurs on the slightest exertion. The child sits 
up to take a drink, or to grasp a toy, or becomes angry, and drops over 
dead. 

In other instances, instead of almost instantaneous cardiac failure with 
sudden death, a more gradual manifestation of grave heart disease is devel- 
oped. A patient apparently on the high road to convalescence, except for 
the reddened throat and profound anaemia, is found to have developed a 
weak pulse, which flags, and he presents unduly feeble heart sounds. 
Endocardial murmurs may be present. Sometimes the pulse is abnormally 
slow. In other cases it is too fast, and, with these circulatory symptoms, 
some epigastric distress or even vomiting occurs. The pulse becomes 
weaker and weaker and arhythmia increases, the face is more and more 
pallid, and cardiac dyspnoea with lividity comes on. Auscultation reveals 
fetal heart sounds or there may be a "delirium cordis." Death finally 
closes the scene at the end of twenty-four or forty-eight hours in the presence 
of gradually deepening asthenia and a mind which is clear almost to the 
very last. Acute cardiac dilatation may occur. 

There are three causes for the types of heart-failure which arise as a 
result of diphtheria. When the heart fails in the course of an attack it is 
usually the result of cardiac thrombosis. When it occurs after an attack it 
is due usually to a toxic myocarditis or to the failure of the nervous supply 
of the heart through bulbar paralysis or paralysis of nerve fibres. Some 
statistics indicate that thrombosis is the most common cause of death after 
disappearance of the membrane. Of course all three of these factors may 
be present simultaneously. It is probable, however, that thrombosis is 
more frequently the cause of sudden death than is generally thought. Bar- 
bier in 71 autopsies on cases of sudden death in diphtheria found an ante- 
mortem cardiac thrombus in no less than 52 per cent. These thrombi were 
commonly found on the right side of the heart, usually in the right auricle. 

Sometimes death is due to paralysis of the phrenic nerve, so that dia- 
phragmatic paralysis ensues. 

The septic condition of the throat, the labored respiration, the decreased 
vital resistance of the patient, and the feebleness of the pulmonary circula- 
tion in severe cases very greatly predispose the patient to bronchopneumonia, 
and this complication or sequel of diphtheria is the cause of death in a very 
large number of young children. 

Local or widespread paralysis often follows an attack of diphtheria, and 
if it involves vital nerves causes death. On the other hand, these palsies 
are noteworthy because of the fact that they usually recover. It is by no 



180 DISEASES DUE TO A SPECIFIC INFECTION 

means uncommon to see a child so paralyzed that it can neither move 
hand nor foot or even move its head, that lies perfectly limp in its 
mother's arms, entirely recover muscular power. These palsies are not 
usually immediate sequences of an attack of diphtheria, but are all the more 
alarming because they may manifest themselves from one to three weeks 
after an attack. Again, it often happens that a very mild attack of the dis- 
ease is followed by this distressing sequence, although as a rule severe cases 
usually have this result. The palate is the part most commonly paralyzed, 
and this results in difficulty in swallowing, regurgitation of liquids through 
the nose, and in a peculiar tone to the voice. When the throat is examined 
the palate is seen to hang relaxed and motionless when the patient attempts 
to phonate, and it is also somewhat anaesthetic, so that the contact of food 
is not well recognized. 

The time of onset of the paralysis varies somewhat with the parts involved. 
The form that occurs most frequently and which affects the muscles of the 
pharynx and eyes and extremities, or even that of the heart or the muscles 
of respiration, is a late palsy of the seventh to the twenty-first day of con- 
valescence, whereas that form which affects the palate is more frequently 
met with at the end of the first week. 

True facial paralysis very rarely occurs except as a result of otitis media 
arising secondarily from the diseased state of the pharynx. 

Statistics as to the frequency with which paralysis accompanies or follows 
diphtheria vary. Hoppe-Seyler states it to be 27 per cent. Johannessen, 
for all Norway, 12.5 per cent.; the report of the Metropolitan Asylums 
Board of London for 1900, 18.5 per cent. 

The collective investigation of the American Pediatric Society based on 
3384 non-hospital cases treated with antitoxin showed that 328 cases of 
paralysis occurred, which gives a percentage of 9.6. 

Hemorrhage from the ulcerative process in the nose may be sufficiently 
free to seriously exhaust the patient. When subcutaneous hemorrhages 
appear they are always a sign of very profound toxaemia. 

When that practically constant sequel of diphtheria, profound ancemia, 
remains persistently present and is but little improved under treatment, the 
possibility of renal disease being a serious sequel is to be recalled. 

Diagnosis. — There is no disease in which it is more important for the 
physician to make a correct diagnosis promptly than diphtheria, because if it 
be recognized in its earliest stage it can be cured by antitoxin in the majority 
of instances. On the other hand, there is no disease which is more diffi- 
cult of prompt diagnosis in some cases. As. diphtherial infection may be 
present without marked formation of membrane, all cases which manifest 
sore throat during an epidemic or, after exposure, should receive antitoxin 
as a preventive, and the throat should be swabbed and the secretion obtained 
examined bacteriologically for the bacillus. 

In every large city at the present time the health authorities provide tubes 
and swabs for the transmission of cultures from the patient to a laboratory. 
Usually the swab is delivered in a sterile tube and the culture medium is 
placed in a second sterile tube. The directions issued by the New York 
Board of Health are as follows : " The patient should be placed in a good light, 



DIPHTHERIA 181 

and, if a child, properly held. In cases where it is possible to get a good 
view of the throat, depress the tongue and rub the cotton swab gently but 
freely against any visible exudate. In other cases, including those in which 
the exudate is confined to the larynx, avoiding the tongue, pass the swab far 
back and rub it freely against the mucous membrane of the pharynx and 
tonsils. Without laying the swab down, withdraw the cotton plug from the 
culture-tube, insert the swab, and rub that portion of it which has touched 
the exudate gently but thoroughly all over the surface of the blood serum. 
Do not push the swab into the blood serum nor break the surface in any 
way. Then replace the swab in its own tube, plug both tubes, put them in 
the box, and return the culture outfit at once to the station from which it 
was obtained." 

A loss of valuable time is prevented during the bacteriological test by 
using antitoxin, but many hours need not be lost if the bacteriologist is 
skilful. Dr. Park, of New York, who has done such excellent work along 
these lines, has this to say in regard to this matter: "The examination by a 
competent bacteriologist of the bacterial growth in a blood-serum tube 
which has been properly inoculated and kept for fourteen hours at the body 
temperature can be thoroughly relied upon in cases where there is visible 
membrane in the throat, if the culture is made during the period in which 
the membrane is forming, and no antiseptic, especially no mercurial solu- 
tion, has lately been applied. In cases in which the disease is confined to 
the larynx or bronchi, surprisingly accurate results can be obtained from 
cultures, but in a certain proportion of cases no diphtheria bacilli will be found 
in the first culture, and yet will be abundantly present in later cultures. 
We believe, therefore, that absolute reliance for a diagnosis cannot be 
placed upon a single culture from the pharynx in purely laryngeal cases/' 

Diphtheria is to be separated from tonsillitis with exudation from the 
follicles of the tonsils and from the diphtheroid false membrane produced 
by the streptococcus and by an organism closely allied but not identical 
with the Klebs-Loeffler organism, which is found in scarlet fever, typhoid 
fever, and measles. Sometimes this can be done only by the bacteriological 
test. 

In follicular tonsillitis the exudate may be scattered over the openings 
of several follicles, it is rarely as dark in hue as the true membrane, it can be 
wiped off with an applicator more readily than the membrane of diphtheria, 
and the tonsillar swelling is marked, The systemic symptoms are, however, 
of little value in differentiation, because tonsillitis is a disease charac- 
terized by very severe symptoms as compared to its gravity, for aching in 
the back and limbs, high fever, and great evidence of systemic depression 
are frequently seen during its course. Holt has pointed out the fact that the 
surfaces of the wound left after tonsillotomy may for a few days closely 
resemble tonsillar diphtheria, and I have seen the free application of a 
strong solution of silver nitrate to the pharynx produce an appearance 
which might readily be mistaken, if examined in a poor light, for diphtheria. 

Reference has been made on several occasions to diphtheroid conditions 
of the throat. These states are probably in a large number of instances 
due to the streptococcus pyogenes. The false membrane, if none of the true 



182 DISEASES DUE TO A SPECIFIC INFECTION 

bacilli of Klebs and Loeffler are present, is usually more soft and creamy 
in its consistency, it is not so tightly adherent to the underlying mucous 
membrane, and is often very foul. Occurring as a complication of grave 
infectious diseases such as scarlet fever and typhoid fever, it is dangerous, 
but otherwise the mortality is not high, being about 2.5 per cent., if we 
can take the New York city statistics as representative of all cases. 

Prognosis. — At the present time it may be said that the prognosis of diph- 
theria depends entirely upon the promptness with which antitoxin is used. 
Without antitoxin the death rate varies greatly in different epidemics. In 
some it reaches the appalling rate of 50 per cent., while in others it is not 
more than 30 per cent. It is very much more fatal in babies than in older 
children. Symptoms of evil prognostic import are grinding of the teeth, 
gallop rhythm of the heart sounds, epigastric pain, and vomiting. 

The cases manifesting laryngeal and nasal involvement are always grave 
as to prognosis. The physician should also be most guarded as to his prog- 
nosis as the disease passes its most active period, because everyone of experi- 
ence knows that an attack of sudden heart-failure often occurs as the child, 
once more feeling strong, attempts to sit up. A rapid or gradual heart- 
failure may come on during convalescence. (See Sequelae.) 

Prophylaxis. — ^-As the intimate association of a person, or garments, bear- 
ing the specific bacillus with another individual who is susceptible to the 
disease is essential for its spread, it is evident that by proper quarantine 
and isolation perfect prophylaxis is possible. All patients who have diph- 
theria should be isolated at once, and the attendant who nurses the child 
or adult who is affected should not associate with other persons until after a 
bath has been taken, the face and head well shampooed and the pharynx 
and nasal cavities well douched. After the patient is convalescent, it is 
to be recalled that the specific bacillus may remain in the nasopharyngeal 
mucus for a long period and so isolation is still essential. The child should 
not play with other children for at least two weeks, and during this period 
should have its nasopharynx sprayed daily with some bland antiseptic wash 
such as Dobell's solution, alkathymol, or normal saline solution. Whenever 
it is possible, particularly in public institutions, the nasopharyngeal secre- 
tion should be examined bacteriologically during convalescence to prove 
the presence or absence of the specific infecting germ before the child is 
discharged. As illustrative of this fact the results of the New York Board 
of Health investigation are of interest. Out of 605 cases examined it was 
found that the bacilli were not present in 304 on the third day after the 
membrane disappeared, in 176 they were present for seven days, in 64 for 
twelve days, and in 36 cases for fifteen days. Twenty-one days after the 
membrane was gone 12 showed bacilli, and 4 cases showed them for twenty- 
eight days. Another set of 4 cases yielded bacilli for thirty-five days, and 
2 for sixty-three days. 

It seems hardly necessary to add that the garments, bedding, and toys of 
all diphtheritic patients should be destroyed or thoroughly disinfected by 
steam or formaldehyde. The floors and walls of the room and the furniture 
should also be treated with formaldehyde, and it should be done as thor- 
oughly as if the case had been one of smallpox. All discharges from the 



DIPHTHERIA 183 

patient should be received in a vessel containing bichloride solution, or, if 
cloths are used, these should be burned. 

A very important measure in all cases in which the disease arises in a 
family of children is the use of immunizing doses of antitoxic serum for the 
protection of the well from the disease. There is no doubt whatever that 
this is a most efficient, never-to-be-neglected measure. The dose is not 
less than 500 to 1000 units and the protection lasts about three or four 
weeks. Nurses as well as children should be protected by its use. 

When treating or examining the throat the physician and nurse may 
protect themselves from the discharges by looking through a pane of glass 
held before the face of the patient. 

Treatment. — The treatment of diphtheria at the present time is more 
scientifically accurate in its basis and in its results than that of any other 
malady save malarial fever, in which we know not only the cause but the 
remedy for its removal. The keystone of the treatment is the liberal use o) 
antidiphtheritic serum derived from the horse. 

It is not necessary in a work of this character to give massive accumu- 
lations of statistics to prove that this plan is based not only on scientific 
laboratory investigations, but upon bedside experience as well. A few 
instances may, however, be cited as illustrative of the facts. Thus it is 
interesting to note that a decided decrease in the mortality of diphtheria 
occurred immediately after the introduction of antitoxin. 

The first statistics furnished by Roux are interesting because they permit 
a comparison to be made between the death rate of the two great children's 
hospitals of Paris for a certain length of time during which the cases in 
one w T ere treated by antitoxin — while those in the other did not receive it. 
From February 1 to July 24, 1894, the mortality at the Hopital des Enfants 
Malades, where antitoxin was used, was 26 per cent., while the mortality 
during this period at the Hopital Trousseau, where serum w T as not employed, 
was 60 per cent. From October 1, 1894, serum therapy was practised at the 
Hopital Trousseau, with the result that at the end of two months the death 
rate had fallen to 14.85 per cent. Similar results have been obtained 
wherever antitoxin has been used. In Geneva the death rate fell from 35.7 
to 9 per cent., and the report of the American Pediatric Society, based on 
5794 cases, gave a percentage of 12.3. The largest and most valuable 
statistics are those of Bayeux, who collected more than 200,000 cases from 
all parts of the world and found that the average mortality rate was 16 per 
cent. Making a most conservative estimate of a general mortality of 35 per 
cent, in preantitoxin days, Bayeux's figures prove a reduction in mortality 
of more than 50 per cent, since the introduction of antitoxin. In the first 
nine years during which antitoxin was used in the treatment of diphtheria 
in Chicago the mortality was 6088, while during the nine years preceding 
the use of antitoxin the mortality was 11,488, a decrease of 5400, or 47 per 
cent., although the population had increased nearly 600,000, or 52 per 
cent. If this increase in population is taken into consideration, the decrease 
in the mortality of the disease under this plan of treatment is 63 per cent. 
In New York City, out of 1702 cases injected on the first day, including 
moribund cases, only 85 died — a case mortality of 4.09 per cent. The 



184 



DISEASES DUE TO A SPECIFIC INFECTION 



following figures, which are Baginsky's, show the decrease in mortality 
according to age: 

Before the introduction of antitoxin the mortality of diphtheria accord- 
ing to age was — 



to 2 years 
2 to 4 years 
4 to 6 years 



602 
512. 

38.0 



6 to 8 years 

8 to 10 years 

12 to 14 years 



22.9. 
28.8. 
18.5. 



Since the introduction of antitoxin the death rate is- 



to 2 years 
2 to 4 years 
4 to 6 years 
6 to 8 years 



25.88. 
1712. 
17.24. 
11.39. 



8 to 10 years 
10 to 12 years 
12 to 14 years 



5.17. 
10. 
13.3. 



The physician who fails to use antitoxin, when it is to be had, is guilty 
of a gross lack of professional knowledge or is atrociously careless of his 
patient's welfare. 

There are several points to be borne in mind in regard to the use of 
antitoxin, namely (1) it must be employed early in the attack to get the 
best results, for it is manifest that after the disease has existed long enough 
to do permanent damage to the tissues no antidote can be satisfactory. No 
one would expect to give the antidote for arsenic two days after the poison 
was taken and get good results. Nevertheless, when antitoxin has not been 
used early it must be given freely in the hope of its aiding the patient 
sufficiently to help him withstand the infection. (2) The antitoxin should 
be given liberally. A few large doses in the onset of the attack not only 
are of great value, but are really economical so far as cost is concerned. 
(3) It must be given in particularly large doses in cases of nasal and laryngeal 
diphtheria, because these are forms in which rapid absorption of the toxin 
of the disease and respiratory obstruction takes place and the malady must 
be most actively opposed. In these cases it may be useful to give it intra- 
venously. (4) Whenever a person is exposed to diphtheria he should receive a 
moderate dose of antitoxin to protect him from infection. The dose should 
be about 500 units, repeated in two weeks, if exposure continues. (5) When 
diphtheria is suspected to be present it is well to give antitoxin at once 
rather than run the risk of waiting for a sure diagnosis. In administering 
antitoxin the following rules should be followed: 

1. The skin over the outer surface of the thigh or over the flank or 
lateral abdominal wall should be cleansed with soap and water and alcohol. 

2. The serum should be injected, by means of a syringe or bulb, through 
a large hypodermic needle which is inserted through the skin where it has 
been cleansed. 

3. The injection should be made slowly and quietly and the swelling 
which results should not be rubbed, 

4. At least 1500 to 2000 units of antitoxic serum should be given at the 
first dose and repeated in four to eight hours, according to the severity of 
the case. 



DIPHTHERIA 185 

5. In nasal and laryngeal cases 3000 or more units for the first dose is 
usually necessary. 

The result of this plan of treatment is often magical. The symptoms of 
general systemic disturbance, such as a rapid pulse and fever, become 
modified, the membrane ceases to grow and loses its tenacious hold of the 
subjacent tissues, becoming not only loose but softened, and speedily 
disappears. 

The only disagreeable effects of using antitoxin in large doses is the 
subsequent development of some pain or soreness in the joints or the appear- 
ance of a roseolous rash ; but even if these symptoms appear they are not 
serious and need give no alarm. 

The local treatment of diphtheria consists in the application to the false 
membrane of peroxide of hydrogen by means of a spray or swab. This 
active disinfectant disintegrates the exudate and aids in its removal. The 
other local applications which have been used in the past are painful, 
injurious, or ineffective as compared to this agent. 

The systemic treatment, aside from the use of antitoxin, consists in the 
employment of foods which are easily swallowed and which will maintain 
the vitality of the patient to the highest degree, such as concentrated broths 
fortified by barley-gruel or rice-gruel, which are digested in great degree 
by the administration of 2 to 4 grains of taka-diastase. 

When the pulse flags, small doses of aromatic spirit of ammonia or 
Hoffmann's anodyne (10 to 30 drops in water may be used) or brandy 
which is old enough to have a "bouquet" may be given. Full doses of 
strychnine should also be used for the same purpose. Perfect rest of mind 
and body should be obtained if possible and great care taken during the 
illness and during convalescence that no sudden exertion, which may cause 
cardiac failure, is permitted. 

When obstruction of the larynx takes place the patient's life may often 
be saved by intubation or tracheotomy. In these cases the patient should 
be kept in a room the air of which is moistened by steam. 

The complications and sequelae are treated in the following manner: 
The anaemia is to be controlled by the use of moderate doses of reduced 
iron. Large doses are unnecessary and tend to cause constipation and 
disorder digestion. A quarter grain three times a day is quite sufficient, 
given in a small chocolate-coated tablet or placed in a gum-drop. In some 
instances 3 to 5 minims of tincture of the chloride of iron is equally good; 
y^-q grain of arsenous acid in a sugar-coated granule may be given simul- 
taneously or in alternate weeks. This treatment is also advisable for the 
relief of the local or general paralysis which is usually associated with 
marked anaemia. In other instances the syrup of the hypophosphites may 
be used, and phosphorus is often of value in the dose of y^-Q- grain three 
times a day. Another remedy of great value as a roborant is cod-liver oil. 

In regard to the use of strychnine, which is so largely used as a circu- 
latory and nervous stimulant in all conditions of depression, it should be 
remembered that it is never a stimulant which in any way increases the 
nutrition of the part involved. It simply acts as an irritant stimulant. 
If there is reason to believe that a "whip" is needed to spur atonic nerves 



186 DISEASES DUE TO A SPECIFIC INFECTION 

to greater effort, it may be used, but if there is any evidence of nervous 
irritation it is better not to employ it. Aside from the treatment already 
named there is nothing which can be done to benefit the paralysis. 



GONORRHEAL INFECTION. 

There are still some roue's, and ignorant persons, who lie under the 
delusion, at one time prevalent, that an attack of gonorrhoea is of little 
more gravity ''than a bad cold." A considerable number of both classes 
learn by experience sooner or later that this is a most mistaken conception 
of the disease. It must not be forgotten that within the last few years 
it has been proved again and again that the gonococcus may find entrance 
into the general system from the urethra and there cause the most disastrous 
consequences. Further than this, while systemic dissemination of the 
gonococcus usually is secondary to venereal infection, it is to be remembered 
that gonococcal inflammation of any susceptible mucosa, as the conjunctiva, 
may afford a point of entrance. Heimann has reported a case of gonococ- 
csemia in which he thinks infection occurred through a wound, and Kimball 
believes the mouth or upper air-passages may constitute portals of entry. He 
has also reported a series of cases of gonorrheal pyaemia due to vulvo- 
vaginitis in children, some cases being only three months old. If it gains 
access to the joints, it may not only produce a temporary gonorrheal 
arthritis, but it may also cause a chronic arthritis which is usually mul- 
tiple, and sometimes is so widespread that the patient is crippled hand 
and foot, finger and toe, for the balance of his life, the incapacity of the 
patient being even greater and more rapid in its onset than if he were 
suffering from rheumatoid arthritis. 

Symptoms. — The appearance of a joint suffering from gonorrhceal inflam- 
mation does not differ materially from that of acute rheumatic fever. It 
is swollen and exquisitely tender. The skin about the joint is hot, but 
often it is not much reddened; on the contrary, in some cases it presents 
a peculiar leaden hue. The temperature of the body in general is usually 
normal, but there is often, at the time of onset, some fever. In some cases 
there is a notable serous para-arthritis. 

Gonorrheal arthritis, as a rule, attacks the large joints. It is most 
commonly multiple, but it may be single. I have seen not only all the 
large, but the small joints infected simultaneously. Even the sacroiliac, 
maxillary, and sternoclavicular joints may be involved. This is a note- 
worthy point when we remember that infection of the maxillary joint almost 
never occurs in ordinary rheumatism. 

According to French statistics the knees are attacked more frequently 
than any other joint in the body — 83 times out of 119 cases; the ankle 
32 times, fingers and toes 23 times, the hips 16 times, the wrist 14, the 
shoulder 12, and the elbow 11. 

It must be distinctly understood that gonorrhceal arthritis has no relation 
whatever to acute articular rheumatism. The tendency on the part of 
many physicians to call all swellings of joints rheumatism is to be deplored. 



GONORRHEAL INFECTION 187 

The mere presence of heat, swelling, and pain in a joint, with or without 
fever, does not necessarily indicate that rheumatism is the cause. 

Suppuration of a joint as a result of gonorrhceal infection very rarely 
occurs, but ankylosis, due to thickening of the synovial membranes, liga- 
ments, and periarticular tissues, and atrophic changes in the cartilages and 
in the ends of the bone are met with. In other words, gonorrhceal infection 
of a joint may result in fibrous ankylosis or in atrophy or in overgrowth 
of bony tissue, as in rheumatoid arthritis. 

The fascia in different portions of the body may also be infected. This 
is particularly apt to occur in the plantar region and not infrequently stiffen- 
ing and inflammation of the tendo Achillis is met with. 

A second serious consequence of gonorrhceal infection is the development 
of a gonorrheal endocarditis. As long ago as 1854 Brandes recorded two 
cases of gonorrhoea with arthritis and endocarditis, and in 1862 Traube 
reported another of gonorrhceal endocarditis without joint infection. None 
of these cases were proved to be due to the gonococcus because this organism 
was not known at that time, but in 1893 Leyden proved the presence of 
the gonococcus in the heart. Since then many more cases have been reported 
in which the gonococcus has been isolated from the endocardium or the 
circulating blood. Perhaps the most noteworthy paper was that of Thayer 
and Lazear in 1899. 

There is no special time in the course of the attack of gonorrhoea at 
which the endocardial involvement takes place. Occasionally it has come 
in the stage of onset, but in most cases it occurs at about the fifth week. 
In others it is postponed for weeks, or even for months. In a case reported 
by Finley and McCrae a fatal endocarditis developed nine months after 
the onset of the urethral discharge, and when that discharge was no longer 
present, although a microscopic examination of the urethral mucosa revealed 
gonococci. 

While it is true that these cases are comparatively rare when we consider 
the frequency of gonorrhoea, it is probable that they occur with more fre- 
quency than has been generally thought, and it is a noteworthy fact that 
in those cases in which the physician is skilful enough to examine the blood, 
or the endocardium, for the gonococcus, that it is found as a pathogenic 
micro-organism much more frequently than in those cases in which the 
physician does not possess such pathological training. With improvements 
in technique, general gonorrhceal infection will probably be recognized as 
being by no means as infrequent as it has been thought in the past. 

Males are very much more frequently affected by systemic infection of 
this character than are women. 

Systemic gonorrhceal infection follows not only the primary disease in the 
urethra or vagina, but has been met with in infants suffering from 
ophthalmia neonatorum due to the gonococcus. In some cases the infec- 
tion is pure; in others it is mixed. 

Diagnosis. — The statement of a patient suffering from an acute arthritis, 
acute ophthalmia, or, indeed, an acute endocarditis, that he, or she, is 
also suffering from gonorrhoea will do much toward making the diagnosis 
of the condition clear. But in the majority of instances the patient neglects 



188 DISEASES DUE TO A SPECIFIC INFECTION 

to give this important information, and in a considerable number of cases 
denies gonorrhoeal infection of the genitalia, thinking that it can have no 
bearing upon the inflammations elsewhere, and that therefore it is unneces- 
sary to mention the fact that such a local infection exists. Not rarely patients 
will deny the existence of a local genital lesion, and it can only be discovered 
upon careful examination. It may be necessary in some cases to examine 
the secretions of the urethra or the vagina by staining and by the microscope. 

It may be said that in every male suffering from acute arthritis between 
the ages of fifteen and sixty the possibility of gonorrhoeal infection should 
be considered as having almost equal rank with the possibility of acute 
articular rheumatism, and the development of endocarditis should not be 
considered as indicative of one condition more than the other, although 
as a matter of fact endocarditis is, of course, infinitely more common in true 
articular rheumatism than it is in gonorrhoeal infection. On the other 
hand the mere discovery by the physician of a presence of a purulent dis- 
charge from the urethra does not by any means prove that the patient has 
gonorrhoeal arthritis. It is entirely possible for him to have acute articular 
rheumatism and gonorrhoea, and, again, it sometimes happens that gouty 
persons have a purulent discharge from the urethra which does not depend 
upon the gonococcus. Rarely, too, a purulent urethral discharge is found, 
in persons who are not gouty, w T hich does not depend upon the gonococcus, 
but is due to another form of infection. 

A therapeutic test of some value lies in the fact that full doses of the 
salicylates usually cause remarkable improvement in the arthritis of rheu- 
matism, and affect in no way whatever the arthritis of gonorrhoea. Again, 
it is characteristic of true rheumatism to leave one joint as it affects 
another; whereas, in gonorrhoeal rheumatism it is rare for the inflammation 
to diminish in the joint primarily affected when other joints become involved. 

Prognosis. — The prognosis in gonorrhoeal rheumatism is favorable in the 
majority of instances, provided the infection is not very severe, and is not 
persistent. The physician, however, must be most guarded in expressing 
an opinion as to ultimate complete recovery, for, as already stated, some of 
the severest cases of chronic multiple arthritis are met w T ith as the result 
of this infection of the joints. The prognosis is also influenced to some 
extent by the history of the patient. If he has already suffered from previous 
attacks of gonorrhoeal arthritis, the probability of complete recovery is not 
as good as in primary attacks. 

Endocarditis due to gonorrhoeal rheumatism is a very serious condition 
and often results in death. 

Treatment. — The treatment of gonorrhoeal arthritis consists, first, in the 
cure of the local area of primary infection as rapidly as possible. For this 
purpose the ordinary forms of treatment for gonorrhoea are to be followed. 
The arthritis is to be relieved by the use of a splint and by the application 
of a 50 per cent, ichthyol ointment to the joint. If the inflammation is 
exceedingly acute an ice-bag may be employed, and if the effusion is con- 
siderable aspiration may be needed to relieve pressure. In some instances 
the best results are obtained by opening the joint and permitting free 
drainage. Should the physician place the limb of the patient suffering 



ERYSIPELAS 189 

from gonorrhoeal arthritis upon a splint, it should not remain so fixed 
for any length of time, as ankylosis is particularly prone to ensue. The 
splint is used only for the relief of pain in the acute inflammatory 
stages. 

As already stated, the salicylates are useless in gonorrhoeal arthritis. 
Indeed, they are worse than useless in that they in no way influence the 
infection and they are apt to disorder the stomach. Rest in the acute 
stages and the treatment of the local infection is the most that can be 
done for the patient aside from local applications. Later, passive move- 
ments of the joints and the use of the iodides or of the syrup of the 
iodide of iron, if anaemia is also present, must be resorted to. Endocar- 
ditis is to be treated as is ordinary ulcerative endocarditis. 



ERYSIPELAS. 

Definition. — Erysipelas is an acute infectious disease due to the entrance 
into the skin in its deeper layers of the Streptococcus pyogenes, sometimes 
called the Streptococcus erysipelatis. The skin of the part affected becomes 
dusky, red, and swollen. A peculiarity of the area of redness is that it has 
a sharp line of demarcation separating it from the surrounding healthy 
tissue, which is usually of its natural color and appearance. The line of 
demarcation cannot only be seen but can be felt by the finger-tip, and if the 
affected area be punctured and the serum which then exudes stained with 
methylene blue the chains of streptococci can readily be found under the 
microscope. Erysipelas is sometimes called "St. Anthony's Fire." 

Frequency. — Erysipelas is found in nearly all parts of the world and is 
not infrequently present in epidemic form in hospitals and other institutions 
in which large numbers of persons, with impaired health, are together in 
wards and dormitories. Under these conditions it spreads rapidly from 
patient to patient, particularly if wounds afford an entrance into the body. 
For this reason the outbreak of the disease in an institution should be fol- 
lowed by the immediate isolation of the patient and a thorough disinfection 
of the entire ward in which he has been lying. The disease occurs most 
frequently in the spring months, particularly in April, but is met with at all 
seasons of the year. 

Etiology. — As already stated the cause of erysipelas is the entrance into 
the deeper layers of the skin of the streptococcus in a form which cannot 
be separated from that which sometimes produces purulent infection in 
other parts of the body. The anatomical and many of the clinical features 
of this disease may be produced by several closely allied bacteria, but 
the clinical manifestations of erysipelas are so constantly associated with 
the Streptococcus erysipelatis that the different infections may be ignored 
or grouped with this one. Two additional factors are nearly always 
active in the production of the disease, namely, a break in the skin or in a 
neighboring mucous membrane, so that the streptococcus gains access to 
the tissues, and, secondly, some cause, local or general, which diminishes 
vital resistance to such a degree that the tissues afford a favorable site for 



190 DISEASES DUE TO A SPECIFIC INFECTION 

the growth of the micro-organism. Thus erysipelas may be due to the 
infection of a small pimple, by scratching it with the finger-nail, and it is 
not uncommonly met with in those who are suffering from renal disease, 
from diabetes, from alcoholism, or from some condition which distinctly 
decreases the ability of the body to protect itself from infection. 

Sometimes the resisting power is decreased by local causes, as by exposure 
to great cold, but it is very doubtful if this cause alone, with the presence 
of the streptococcus, is capable of causing the disease unless the general 
systemic vital resistance is impaired. 

The course to be followed in cases of early erysipelas is to examine 
into the state of the urine at once, and, even if this be found normal, to 
examine it repeatedly for evidences of renal disease or diabetes, since such 
causes render the patient very susceptible. Search for other causes of 
impaired health should also be made, because erysipelas is a malady 
which is particularly prone to attack those who are already ill, even if the 
primary illness is not apparent. Occasionally the physician meets with a 
case in which there is no underlying dyscrasia which predisposes to the 
disease. In these instances the patient may have repeated attacks, due 
apparently to general susceptibility to this infection, the streptococci 
remaining inactive in the tissues in certain cases for weeks at a time. 
Women during the puerperal period are especially susceptible to the infection. 

Pathology and Morbid Anatomy. — Primarily the lesion of erysipelas con- 
sists of a hyperemia ; later, an exudate composed of cells and fluid appears 
in the layers of the true skin, associated with a rapid growth of the strep- 
tococcus in the lymph spaces in the margin of and often beyond the inflam- 
matory zone. In severe cases the lesion spreads with great rapidity and may 
affect not only the deeper layers of the skin, but the underlying connective 
tissue as well. The destructive action of the bacterial toxin may lead to the 
formation of sloughs, gangrenous erysipelas, or the polymorphonuclear 
leukocytes may accumulate in such numbers as to constitute pus, forming the 
so-called phlegmonous erysipelas. In rare instances the streptococcus, after 
entering the body through some solution of continuity in the skin or mucous 
membrane, is carried by the blood or lymphatic system to distant parts, 
causing a development of the disease far from the site of the primary lesion. 

The accompanying visceral lesions may be due to the absorbed toxin or 
to streptococcsemia. The former may cause degenerative changes, such as 
focal, or even diffuse, necrosis in the liver, spleen, kidneys, or myocardium. 
The entrance of the streptococcus into the blood may be manifested in an 
endocarditis, pericarditis, nephritis, pleuritis, meningitis, arthritis, osseous 
or pulmonary infections, or other evidences of colonization of the germ in 
the various organs or tissues. 

The onset of erysipelas is associated with a leukocytosis of polymor- 
phonuclear cells, except in malignant cases in devitalized persons. 

Incubation. — The period between the introduction of the streptococcus 
and the development of the disease varies greatly in different cases. Usually 
the period of incubation lasts from three to seven days. 

Symptoms. — In the great majority of cases erysipelas affects the skin of 
the face about the corners of the nose or near the ear. A tingling of the 



ERYSIPELAS 191 

skin is felt which speedily becomes an intense burning, and is increased 
by rubbing or scratching the part. This reddened area spreads rapidly 
and is characterized at the end of twenty-four hours, or before, by the pres- 
ence of a sharp line of demarcation, which marks the advancing line of 
inflammation, a margin which can often be felt as a slightly indurated and 
raised edge. Sometimes the inflammatory process projects well-defined 
areas of extension into the healthy skin. Palpation of the diseased skin 
also reveals the fact that it is hot and somewhat brawny and tender. The 
color of the part is not a bright red, but is dusky in hue. The swelling of the 
face when well developed is sufficient to render the patient unrecognizable, 
and the eye, or eyes, may be completely closed by the infiltration of the eye- 
lids. The ears when involved become swollen to an extraordinary degree 
and the skin seems very tense and indurated. Not infrequently blebs or 
blisters form over the inflamed area. 

After the early stage of onset it has been my experience that patients 
rarely complain very greatly of pain and burning. 

The amount of systemic disturbance varies very much in different cases. 
In those who have previously been in moderate health the local lesion and the 
degree of systemic disturbance may be so slight as to be scarcely noticeable. 
The patient may complain of a slight chilliness, the pulse may be slightly 
accelerated, and the temperature roAsed one or two degrees. In other 
cases in which vital resistance is poor and the infecting germ virulent in 
form, the symptoms just described are very severe in degree, so that rigors, 
high fever, a rapid pulse, delirium, and great prostration may be present. 
In still other cases, not so common, when by reason of great diminution of 
vital powers the general health has been greatly undermined, as in advanced 
diabetes or Bright's disease, the disease attacks the patient so vigorously 
that he sinks beneath its onset without having enough stamina to resist the 
infection, and may pass into semi-coma or even convulsions followed by 
collapse due to the apparent exacerbation of the underlying malady by the 
secondary infection. In rare instances the part involved may become 
gangrenous and death follow from sepsis and exhaustion. 

In cases of ordinary severity the fever lasts about five days and ends 
by crisis. 

One attack of erysipelas does not protect but rather predisposes the 
patient to another. 

Under the name erysipelas migrans a form of the disease is met with 
in which the disease spreads from part to part and, in the course of its 
wandering, may affect successively almost the entire surface of the body. 

Complications and Sequelae. — When erysipelas attacks individuals who 
are greatly impaired in health the results are often grave, not only because 
the onset of erysipelas is dangerous in itself, but because it is an indication 
in many cases of a grave disease, hitherto unrecognized, which may 
speedily cause the death of the patient by an exacerbation. Thus the devel- 
opment of erysipelas in cases of chronic Bright's disease not only means 
that the renal lesion has resulted in poor resistance, but in addition the task 
of eliminating the toxins of the new malady may so overwhelm the kidneys 
that they may cease to perform their function. 



192 DISEASES DUE TO A SPECIFIC INFECTION 

Again in cases of greatly impaired health the inflammatory process goes 
on to suppuration and the deeper tissues become filled with pus, forming 
the phlegmonous form of the disease. In other instances septic embolism 
occurs in the lungs, brain, kidneys, liver, and spleen. 

A focus of erysipelatous inflammation also results sometimes in the pro- 
duction of ulcerative endocarditis or even purulent pleuritis or pericarditis, 
but these complications probably are of less common occurrence than has 
been thought. In 1674 cases of erysipelas collected by Anders from the 
records of five large hospitals and from private practice, endocarditis 
occurred only once, and pericarditis not at all. Pleurisy was present in 
seven cases. Roger, of Paris, did not have a single case either of endo- 
carditis or pericarditis in 957 cases, and only one case of pleurisy. 

In 2631 cases of erysipelas croupous pneumonia is said to have occurred 
in 17 cases, and the catarrhal form in 2. Of these cases 957 occurred in the 
practice of Roger, of Paris, and the remaining 1674 were collected by Anders, 
and represent chiefly the statistics of five large American hospitals. 

Prognosis. — The prognosis in a case of erysipelas depends largely upon 
the general state of the patient. As already stated the presence of grave 
visceral disease, as of the liver or kidneys, renders it very dangerous, but in 
the great majority of cases, when it occurs in otherwise healthy persons, the 
outlook is very favorable. Anders' statistics give the mortality at 7 per cent, 
for hospitals and 4 per cent, for private practice. When it recurs frequently 
or develops in different parts of the body consecutively, it may cause death 
by exhaustion, but in nearly all these cases there is a chronic malady as a 
predisposing cause. 

Treatment. — The treatment of erysipelas is local and systemic. If the 
bowels are not active they should be freely moved by a dose of 2 grains of 
calomel followed in twelve hours by a saline purge such as a Seidlitz powder 
or a half-ounce of Rochelle salts. As soon as the bowels have been evacuated 
thoroughly the patient should receive 10 minims of the tincture of the 
chloride of iron, well diluted with pure water, every three or four hours, or 
30 minims four times a day. The excess of water protects the stomach 
from being disordered by the drug and also aids in flushing the kidneys, 
the activity of which prevents the accumulation of toxic material in the body. 
The diet should be as easily digested and as nutritious as possible, in order 
that the vital resistance of the patient may be maintained, and such foods 
as eggs, rare meats, broths, and milk should be freely given if the digestion 
of the patient is capable of dealing with them. If it is not, the food should 
be given in small quantities every two or three hours, and if necessary it 
should be predigested by a peptonizing tablet or powder 

The local treatment is a very important factor in these cases. For many 
years I have used with excellent results an ointment of equal parts of 
ichthyol and lanolin, or lard, smeared over the inflamed area and the 
adjacent skin, and kept in contact with the skin by also smearing this 
salve on a mask of gauze or lint which is applied to the part so that 
the medicinal effect is continuous. By this means the pain and burning is 
almost entirely relieved and a very definite and distinct influence for good 
is exercised both in curing the inflammation and preventing its spread. 



SEPTICEMIA AND PYEMIA 193 

In cases in which the general systemic state is very much impoverished 
and the vitality of the patient is impaired, sufficient quantities of a good 
whiskey or brandy should be given to sustain the flagging powers. Moderate 
doses of quinine (about 3 grains t. i. d.) may also be useful at this time to 
support the system, but large doses are useless and produce headache and 
a disordered digestion without causing any benefit. If the fever is excessive 
it may be controlled by the use of an ice-cap and cold sponging with friction. 
The coal-tar antipyretics should never be used, as they decrease vital 
resistance. 

SEPTICEMIA AND PYEMIA. 

Definition and Etiology. — Septicaemia and pysemia are terms which are 
dependent upon antiquated ideas of septic processes, and do not strictly 
represent the states they are now used to describe. Septicaemia originally 
meant that putrid material was in the blood and pysemia that the blood 
contained pus. We now know that blood infection is due to the presence 
in it of bacteria (bacteriaemia) or to the entrance into this fluid of poisons 
made by micro-organisms not in the circulation (toxaemia). The older 
terms are placed at the head of this article because they are still commonly 
applied. 

Pyaemia, as it is understood to-day, is that state in which bacteriaemia 
is present with associated septic foci, or, in other words, metastatic 
abscesses. As a rule these abscesses appear chiefly in the tissues which are 
not far removed from the seat of primary infection. But this is by no means 
always true, for a septic process in the foot may cause metastatic abscesses 
in the lungs, kidneys, or liver. 

Cases are not rarely seen in which the patient is unable to give any history 
of even a small abscess or minute break in the skin through which germs 
may enter the circulation, and yet a diagnosis of septicaemia or pyaemia may 
be made even when no point of entry can be found. 

The obscurity of most of these cases depends upon our inability to find 
the portal of entry, which may be the genito-urinary organs, the facial or 
cranial sinuses, the middle ear or mastoid, the mouth or pharynx, possibly 
the alimentary canal, the biliary passages or gall-bladder, an unrecognized 
appendicitis or other point of slumbering infection which may or may not be 
recognized during life or determined with certainty even at a postmortem 
examination. 

Pathology and Morbid Anatomy. — The results of septicaemia are not seen 
in equal degree in all cases. In some they may be so slight as not to be 
readily recognized, except by careful bacteriological or microscopic exam- 
ination. In other instances the secondary results are so patent that the 
most careless observer cannot fail to be impressed by their character. 
Thus, it not infrequently is found that septic infection is the cause of a 
severe inflammatory process in any one of the serous membranes, so that 
pericarditis, peritonitis, meningitis, or pleuritis may occur. Septic inflam- 
mation of these parts results either in a distinctly fibrinous or serofibrinous 
exudate or in one which is purulent. The synovial membranes and other 



194 DISEASES DUE TO A SPECIFIC INFECTION 

connective tissues of the joints are frequently infected, so that septic 
arthritis develops. 

Examination of the veins may reveal thrombi near or remote from the 
primary seat of infection, and these thrombi may be soft and even purulent. 
It is important that a clear distinction be made between simple or bland 
thrombi and septic thrombi. Emboli of the former type cause infarction 
when they plug terminal vessels and mechanically disturb the circulation, 
whereas septic emboli not only plug the vessel and so disturb blood supply, 
but as they contain bacteria they constitute new foci of infection. 

Very intimately associated with the subject of septicaemia and pyaemia, 
so called, are the subjects of vital resistance and terminal infection. By 
vital resistance is meant that power, or property, possessed by the living 
body of protecting itself from the various micro-organisms which are con- 
tinually gaining access to the system. This power lies largely in the ability 
of the blood to exercise its so-called bacteriolytic, or bacteria-destroying, 
power, and to the ability of the cells of the body to destroy invading micro- 
organisms by phagocytosis, and manufacture certain other antibodies by 
the action of which bacterial toxins may be antagonized, neutralized, or 
rendered inert. A number of valuable papers on the presence of bacteria 
in the blood have been published within recent years (see Rosenberger in 
the American Journal of the Medical Sciences, January to July, 1903, for 
facts and references). When, because of diminution of vital resistance the 
invading pathogenic micro-organisms obtain a foothold and multiply, w T e 
have developed an infection. When a patient suffers from some malady 
which saps his vitality and so causes the approach of death, even in a 
remote degree, these micro-organisms at once attack his debilitated body, 
and the patient now suffers from what is called a "terminal infection/' 
Very commonly this terminal infection is the actual cause of death, so that 
it has been well said that death is "rarely due to the primary cause of the 
illness." 

Symptoms. — The symptoms of septic infection vary greatly with the par- 
ticular organs which may be the seat of the primary or secondary lesions. 
The manner of their onset varies likewise. In some instances the earliest 
manifestations consist in a rigor or chill, more or less severe, followed by 
fever which varies in its degree with the severity of the infection and the 
vitality of the patient. The chill and fever are followed usually by a period 
of normal, or nearly normal, temperature, and this is again followed by 
chill and fever. In this way the dominant symptoms of the case may closely 
resemble the quotidian malarial infection, a resemblance which is still 
further emphasized by the frequent occurrence of a distinct sweat as the 
fever falls. These sweats may be very profuse. 

Not rarely the pus in the primary focus of infection changes its char- 
acter, and becomes less healthy looking. It is thinner and more ichorous, 
that is, to use a word now rarely heard, it is no longer "laudable pus." 
The infection causes general malaise, rapid loss of weight and loss of appetite 
with gastric distress and perhaps vomiting. Anosmia is rapidly developed, 
the skin of the hands and face becomes not only pallid but develops a 
peculiar cadaveric hue, an appearance difficult to describe, but alluded to 



SEPTICAEMIA AND PYEMIA 195 

by those of experience as the "septic facies." Sometimes the skin may be 
slightly jaundiced. 

If the septic process develops secondarily in any special organ, localized 
symptoms may at once appear, but it is noteworthy that they do not always 
ensue. Severe pain in the chest may betoken the presence of a septic pleurisy 
or pneumonia, or if the pain develops in the left side it is often due to 
septic infarction of the spleen. A physicial examination of these organs 
may reveal the typical signs of these affections. 

As the case progresses pilmcnary abscess, empyema, or suppuration of 
the kidney follows as the result of emboli in these organs. The pulse 
becomes more and more rapid, the general state more and more feeble, 
and the patient dies from general asthenia or from one of the acute 
complications just named. 

There are other cases in which the onset of the systemic infection is not 
so pronounced, the chill, fever, and sweat being absent, but in their place 
a rapid extension of the local inflammatory process with the absorption into 
the general system of the poisonous products of the germ growth as well as 
the organisms themselves. In such cases the patient may speedily become 
not only feeble, but suffer from stupor and finally die unconscious within 
a few days of the beginning of the illness. These cases are usually those 
which, suffering from nephritis or diabetes, offer no vital resistance to 
infection, and die not only from this cause but by reason of rapidly increas- 
ing evidences of the primary disease as well. 

Still a third class of cases may be called subacute or chronic, and last for 
weeks. Not rarely these cases tax the diagnostic acumen of the physician 
to the utmost. A child was brought to me in July with the statement that 
in the previous March she had acute articular rheumatism, but no cardiac 
complications. The fever of the disease in onset had lasted but a short 
time, and in its place only a slight evening rise of temperature took place. 
The acute swelling of the joints disappeared, but they remained tender, 
and the child was unable to walk. There was marked pallor, a septic hue 
of the skin, and a large boil on the buttock with smaller ones on other parts 
of the body. Occasional attacks of vomiting occurred. A diagnosis of 
chronic septic infection was made, and on the child's death six weeks after 
evidences of the correctness of this view were found in nearly every organ 
of the body, although in none of them were distinct purulent foci discovered. 
Circumstances prevented bacteriological examination of the blood either 
before or after death. 

Diagnosis. — The presence of chill, fever, and sweat in any case should 
recall the fact that these symptoms may be due to sepsis as well as to other 
forms of infection. It must be recalled that a history of an infected wound 
is not needful to reach the conclusion that infection has occurred, for it 
may take place by a needle-prick, or through a small blister due to a badly 
fitting shoe, or through a break in the mucous membrane of the alimentary, 
respiratory, or genito-urinary tract. Typhoid fever often fails to cause death 
of itself, but a terminal septic infection following it may cause death. In 
other cases a fatal general infection follows gonorrhoea, and in tubercu- 
losis of the lungs the septic symptoms are due to the pyogenic organisms 



196 DISEASES DUE TO A SPECIFIC INFECTION 

which are associated with the tubercle bacillus, rather than to that organism 
itself. So, too, gallstones with septic infection of the gall-blackler may 
afford the opening for infection. Finally, whenever a patient presents 
acute arthritis the physician should think first of sepsis rather than rheu- 
matism, and when he has a chill, fever, and sweat which does not promptly 
yield to quinine, he should also think of sepsis or tuberculosis. 

Treatment. — The treatment of these states consists first in seeking and 
removing the cause and in the support of the vitality of the patient by every 
possible means, such as fresh air and sunshine, and good food which is 
easily digested and absorbed. Second, many cases are undoubtedly aided 
in combating infection by the use of tonic doses (5 grains t. i. d.) of quinine, 
with or without whiskey. In some instances well-diluted whiskey certainly 
seems to benefit the patient, and it is surprising how much can be taken 
without producing any signs of intoxication. Great care that doses large 
enough to be toxic are not given, for if they are, the toxaemia of alcohol aids 
the toxaemia of the infection. Full doses of tincture of the chloride of iron 
are valuable. The coal-tar products are never to be used, as they decrease 
vital resistance, increase sweating, and do not give any comfort or relief. 

If abscesses form they should be opened and drained as early as possible. 

When bacteriological tests reveal the presence of streptococci as the 
cause of the trouble, antistreptococcus serum should be used. 



ACUTE RHEUMATIC FEVER. 

Definition. — This disease, also known under the name of acute articular 
rheumatism, or acute inflammatory rheumatism, is an acute infectious, non- 
contagious, febrile malady characterized by acute inflammation of the syno- 
vial membranes and adjacent tissues about the joints of the extremities. 
It is to be distinctly separated from the various forms of septic arthritis. 

Distribution. — Acute articular rheumatism is a disease which is found 
chiefly in the temperate zone and rarely occurs in the tropics or in the 
far North. At present we lack reliable statistics concerning its frequency 
because in many countries its occurrence is not reported, and in those 
in which records of the frequency of rheumatism are preserved, so many 
cases are reported which are not true acute articular rheumatism that the 
statistics are valueless. Osier states that he saw more cases in Montreal 
than in Philadelphia and Baltimore while connected with hospitals in those 
cities. I was firmly convinced from my experience in English hospitals 
that the disease was more prevalent in England than in the United States, but 
when I came to the study of the statistics of the relative frequency of acute 
rheumatism in these two countries, I found that out of 74,808 medical cases 
in hospitals in London, there were 3822 cases of acute rheumatism, a per- 
centage of 5.1, and out of 73,839 medical cases in hospitals in different 
cities in the United States, there were 4153 cases of acute rheumatism, a 
percentage of 5.6. It would seem, therefore, that no marked difference in 
frequency exists in these parts of the world. 



ACUTE RHEUMATIC FEVER 



197 



Etiology. — The influence of season upon the occurrence of the disease is 
marked. It is more common in the cool, damp months of the year than at 
other times. In London its greatest prevalence is in September and October, 
whereas in Montreal it is most frequent in March and April. 

The influence of age upon the frequency of the disease is notable. It 
is met with in a very large proportion of the cases between twenty and 



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Chart showing age incidence of acute articular rheumatism, based on 4328 cases. 



thirty-five years of age and is very rare in children below five years. After 
forty-five years it is also rarely met with, comparatively speaking (Fig. 38). 
It must be remembered, however, that infection with the specific organism 
of this disease is probably more frequent in adolescents than is commonly 
supposed, and it may cause very mild arthritic symptoms and yet make 
a serious attack upon the heart. 



198 DISEASES DUE TO A SPECIFIC INFECTION 

Males are more frequently affected than females, but this proportion is 
reversed when the patient is under twenty years of age, at which time 
females suffer more frequently. 

The question of the influence of heredity is still undecided. It is 
probable that it plays a very unimportant part in the causation of the 
malady. 

Of the immediate etiological factors we must include exposure to damp- 
ness and cold. These influences are not provocative of the disease unless 
the specific micro-organism is present, nor unless the exposure reduces the 
vital resistance of the joints so that the specific organism is enabled to 
multiply and induce its pathological effects. 

Acute rheumatic fever is a disease which is endemic, but it has periods 
in which it is distinctly epidemic. In other words, it is much more frequent 
in some years than in others. 

There can be no doubt that the infection usually gains access to the 
general system through the tonsils. 

The old theory of acute rheumatism being due to uric acid is now 
exploded. The excess of uric acid present in the urine in this disease 
is the result, not the cause, of the affection. 

Bacteriology. — A very large number of investigators have endeavored to 
isolate the specific micro-organism of this disease, but until recently no satis- 
factory proof that this had been accomplished was forthcoming. About fifteen 
years ago Achalme asserted that he had done this, and later Triboulet and 
Wassermann made similar claims. Up to the present time it would appear 
that Poynton and Paine have come nearer to success in this line of research 
than any of their predecessors, and Meyer has also carried out studies which 
seem to prove the correctness of their conclusions. Still more recently 
Walker and Beaton have further confirmed the correctness of the views of 
Poynton and Paine. These last investigators believe it is impossible to 
separate this special organism, for which they advise the name Micrococcus 
rheumaticus, from the ordinary streptococcus. Meyer succeeded in obtaining 
it in a form which produced all the lesions found in the course of the disease, 
and found the same organism in the sore throat, in the inflamed endocardium, 
in the pleura, and in the inflamed joints of persons attacked by this malady. 
More recently still Poynton has further enforced his views. The most 
that we can say at present is that acute articular rheumatism appears to 
be a streptococcic infection. Until, however, the supposed exciting cause 
can with certainty be differentiated from the streptococcus found in other 
lesions, the propriety of giving to it a special name must be regarded as 
doubtful. 

It is a fact worthy of note that the introduction of many pathogenic 
micro-organisms into the body will result in endocarditis and arthritis, but 
these states are not true acute articular rheumatism. 

Morbid Anatomy. — The changes produced by an attack of acute rheumatic 
fever are not pathognomonic. On the contrary, the condition of the synovial 
membranes is one of more or less intense hyperemia with the effusion of 
fluid into the surrounding tissues and into the joint itself. The synovial 
liquid is turbid and contains leukocytes and some small flakes of fibrin. 



ACUTE RHEUMATIC FEVER 199 

The secondary changes produced by the disease are vegetative endocarditis, 
acute pleuritis, and pericarditis, but there is nothing about these lesions 
which is peculiar to this specific infection. (See Endocarditis.) 

Symptoms. — The symptoms of acute articular rheumatism are usually 
sudden in onset. With or without premonitory signs of illness the patient 
awakes to find that one or more of his larger joints is acutely inflamed 
so that any movement causes great pain, and the part may be so sensitive 
to the touch as to prevent any thorough examination by palpation being 
made. 

The skin over the affected part is usually dusky red in hue, and quite 
puffy in appearance because of the presence of subcutaneous exudation, and 
the inflamed area is much more hot to the touch than adjacent tissues. 
Sometimes, however, no local redness is seen, but in its place swelling and 
a peculiar sodden and livid hue of the skin. With the development of this 
arthritis a distinct febrile movement begins, and the fever may reach 102° 
or 103° on the first day in many cases. This level of temperature is not 
usually exceeded, but the variations in its course are very marked in that 
it is subject to great remissions, particularly if the sweating is profuse. 
The fever ultimately falls by lysis. 

The tongue is coated, the bowels are usually confined, and the skin is 
hot and dry, or at times bathed in a profuse sweat. This sweat breaks out 
in paroxysms and is exceedingly acid, possessing a peculiar acid odor. It 
is probably an effect at elimination, but it does not develop in all cases. 
The urine is nearly always scanty and concentrated, highly acid, and on 
standing deposits urates in excess. 

Acute articular rheumatism is characterized by the speedy spread of the 
arthritis to joints in other parts of the body. In some instances the involve- 
ment of a second joint is followed by diminution of the inflammation in the 
joint first affected, but in many instances the patient suffers from a pro- 
gressively developing arthritis which soon involves almost all the larger 
joints. This fugitive character of the inflammation, wandering from joint 
to joint, is so very characteristic, that the presence of a monoarticular 
inflammation is a point against the disease being true rheumatism. The 
smaller joints, such as the fingers and toes, usually escape, but they are 
often apparently affected by reason of the fact that the swelling of the 
tissues extends from the large joint above so that it covers the smaller ones. 
In other instances, however, the joints escape severe infection, and the 
synovial coverings of the tendons suffer chiefly, so that parts near the joint 
may be swollen, and the swelling is purely periarticular. The vertebral 
and clavicular joints are very rarely affected. 

There is no form of acute arthritis which seems to give the same amount 
of severe pain as does that of this disease, and the close of the attack usually 
leaves the general system of the patient considerably shattered because of 
the severity of his suffering, his marked anosmia, and the exhaustion caused 
by the sweats and the lack of sleep. The pain is also peculiarly trying 
because the state of the joints is such that movement is impossible and the 
patient gets bed-sore and bed-frantic. 

In some cases a subacute type of the disease develops in which all the 



200 DISEASES DUE TO A SPECIFIC INFECTION 

symptoms, in the joints at least, are very mild, but these cases are very 
prone to manifest cardiac complications later on. This is particularly true 
in children. 

One attack usually predisposes to another. It certainly in no way pro- 
tects the patient from subsequent attacks. 

Duration. — The disease may run its course in a week or be continued 
over a very long period of time, lasting a month and causing great dis- 
couragement of both the physician and patient. In some instances, the 
arthritic state merges by degrees into one of chronic arthritis without fever, 
and the patient never fully recovers the free use of his joints, but this is 
fortunately very rarely the case. Even when the amount of inflamma- 
tory exudate seems very large gradual and complete absorption usually 
occurs. 

Complications. — The complications of acute articular rheumatism are the 
means by which it produces fatal results, and they are most frequently found 
in the heart muscle, in the cardiac valves, or in the pericardium. The infection 
attacks the endocardium with great constancy, and even in those cases in 
which the arthritic changes are slight, it often plays the greatest havoc in 
the heart, so that we frequently see young persons with grave cardiac 
lesions who have presented such mild articular symptoms that the pres- 
ence of rheumatism has been overlooked. Of 842 cases of acute articular 
rheumatism, all of which were first attacks, valvular heart lesions were 
present in 420, or 50 per cent. Of these lesions, 390 were mitral, 16 
aortic, and 14 mitral and aortic. 

The following table arranged from the statistics of Church at St. Barthol- 
omew's Hospital illustrates not only the frequency of cardiac complications 
but also the age incidence as well: 

Number of Number in which Percentage of 

Age. cases. heart was affected. heart affection. 

Under 10 years 25 20 80 

10 to 20 years 244 170 69.16 

20 to 30 years 241 124 51.1 

30 to 40 years 115 35 30 

40 to 50 years 41 9 21.39 

Over 50 years 17 7 41.03 

683 365 48 78 

This table includes pericarditis as well as valvular lesions. 

It is generally recognized as a fact that heart lesions arise less frequently 
in the old than in the young, and therefore the percentage of 41.03 given 
for cases over fifty in this table is probably excessive. 

These lesions are rarely lethal during their acute stage. They develop 
into subacute or chronic lesions, and days, weeks, or years after the patient 
has recovered from the acute illness become active agents in destroying life 
or incapacitating him for work. The reason for this lies in a continua- 
tion of the endocarditis, in a subacute or chronic form, for days or weeks 
after the acute symptoms have passed by, with the result that the valves 
become shrunken, and so are unable to perform their proper functions; or 



ACUTE RHEUMATIC FEVER 201 

they become glued together, and in this way their action is interfered with. 
Acute articular rheumatism with cardiac complications may therefore cause 
death many months or years after the acute attack. (See Endocarditis.) 

Pericarditis is by no means as frequent as endocarditis. It is usually of 
the fibrinous or serofibrinous type, and occasionally it is purulent, particu- 
larly in the case of children. In rarer instances a myocarditis develops. , 

It is of the greatest importance that the physician in charge of a case 
of acute articular rheumatism be continually on the lookout for cardiac 
complications. He can do something toward preventing these by following 
the directions given under Treatment, and by insisting upon absolute rest. 
The vast majority of cases of acute articular rheumatism manifest some- 
time during their course a more or less well-defined mitral murmur, and 
sometimes a pericardial friction sound. In many instances, instead of these 
lesions increasing in severity, they disappear with the subsidence of the 
joint symptoms. 

Pulmonary complications are not exceedingly common. Stephen Mac- 
kenzie found that pneumonia, or pleurisy, occurred in about 10 per cent, 
of 3433 cases. Not infrequently slight pulmonary congestion of the bases 
occurs. 

The nervous complications in acute articular rheumatism arise from 
three causes: the high fever, the profound toxsemia, and the nervous 
irritation and exhaustion produced by many hours of suffering. Delirium 
is not commonly met with. An active, noisy delirium sometimes develops 
as a result of the administration of large doses of the salicylates. Such 
mental disturbance is said to not infrequently complicate the development 
of rheumatic pericarditis. Sometimes, too, excessively high temperature is 
associated with delirium. 

Meningitis occurs as a very rare complication. 

The relationship between chorea and rheumatism is not clear. There 
can be no doubt that they bear some relationship one to another, but whether 
rheumatism is to be regarded as an etiological factor in chorea is undecided. 

The skin lesions of acute articular rheumatism consist chiefly in the 
development of urticaria and erythema. Purpuric rashes sometimes appear, 
hence the somewhat old-fashioned term " purpura rheumatica ;" but it is 
probable that these extravasations under the skin are due to an associated 
infection rather than to the rheumatism itself. Another very interesting 
lesion occurring as a sequence of acute articular rheumatism are rheumatic 
nodules which vary in size from a small pinhead to a large pea, and develop 
chiefly on the hands and wrists and about the elbows and knees, and 
sometimes upon the back over the spine. They often last for months, and 
are seen more frequently in children than in adults. Indeed, they are so 
characteristic in children that they may be regarded as a positive sign that 
rheumatism has at some time been present. They are not, however, path- 
ognomonic of rheumatism in all cases, for they appear in gouty and rheu- 
matic subjects who have never suffered from the acute form of the disease. 

Diagnosis. — The diagnosis of acute articular rheumatism is by no means 
easy in all cases, but the presence of fever with progressive involvement 
of one joint after another is very indicative. The great difficulty lies in 



202 DISEASES DUE TO A SPECIFIC INFECTION 

separating the various nearly related forms of septic arthritis from true 
rheumatism. If there is present a pre-existing septic focus from which 
septicaemia may arise, the probability is that the malady is not the specific 
disease we are discussing. Thus, a multiple arthritis, with or without 
fever, often follows or complicates gonorrhoea, and follows scarlet fever, 
typhoid fever, and dysentery, or any disease which, by providing a source of 
infection, exposes the joints to the invasion of micro-organisms. 

The chief conditions, aside from gonorrhceal rheumatism and ordinary 
septic arthritis, that we must carefully exclude are acute osteomyelitis, 
which usually affects the femur, and which if it is not recognized early may 
destroy the patient's life; monoarticular inflammation, which is often due 
to syphilis, and acute gout, in which case the history of previous attacks of 
pain in the smaller joints will be present and the inflamed area will prob- 
ably be in the ball of the thumb or in the joint of the great toe. In children 
an acute arthritis with little fever sometimes develops and soon suppurates. 
It is undoubtedly due to septic infection. Finally, let it be borne in mind 
that the mere presence of heat, pain, swelling and fixation, in a joint should 
not be called acute articular rheumatism until all other possibilities are 
excluded. Perhaps no more frequent error occurs than the calling of all 
forms of acute arthritis " acute rheumatism." 

Prognosis. — Death very rarely ensues as a result of acute articular rheu- 
matism without any complications. This is well shown by the following 
statistics. In 8431 cases of acute articular rheumatism collected from 
the official reports of several American and English hospitals there were 
127 deaths, which gives a percentage of 1.5. From the years 1880 to 1903 
1524 cases were treated in the Pennsylvania Hospital with only 14 deaths, 
a mortality of 0.9 per cent. While, therefore, acute rheumatism rarely causes 
death during its presence in the active stage it is nevertheless true that no 
acute disease causes death so frequently in after years because of secondary 
changes in the heart. 

Treatment. — The treatment of acute articular rheumatism is at times 
eminently satisfactory and at others equally disappointing. In a certain 
proportion of cases, in which treatment fails to produce good results, the 
condition is perhaps maintained by the presence of associated infections 
which help to produce the arthritis. While no true specific exists for acute 
articular rheumatism, the salicylates act in some cases with a degree of 
celerity which is most gratifying, and therefore they are always to be 
considered as the most important remedies when the physician is called 
upon to treat a case of this disease. The chief objects of the physician 
under these circumstances are the alleviation, modification, and shortening 
of the disease, and, second, the protection of the heart from the secondary 
affections of its endocardium, its muscle, and its pericardium. For the 
relief of the pain and of the inflammatory processes in the joints the best 
remedy is the salicylate of strontium in the dose of 15 to 20 grains from 
three to six times a day. It should be given in capsules and followed by 
a copious draught of water or milk to prevent it from irritating the stomach. 
Sometimes a few swallows of the emulsion of sweet almonds may be taken 
to protect the stomach from irritation. 



ACUTE RHEUMATIC FEVER 203 

If full doses of the salicylates, sufficient to produce distinct physio- 
logical symptoms, such as fulness in the head and some deafness, do 
not produce signs of improvement in the course of five or six days, they 
will probably fail to cure, and had better be discontinued, as after this 
time they are apt to increase the discomfort of the patient, to disorder 
his stomach, and to increase the sweats. In their place the patient may 
receive 10 minims of the wine of colchicum root and 15 grains of iodide 
of potassium three times a day. While the salicylates are being given 
it is always advisable to give not less than 40 to 60 grains of sodium 
bicarbonate or bicarbonate of potassium in each twenty-four hours. The 
sodium bicarbonate seems to aid the stomach in withstanding the salicy- 
lates, and provides the body with a certain amount of alkali which is 
advantageous. 

Copious draughts of water are always to be given in rheumatism for 
the purpose of flushing the kidneys. 

For the prevention of endocarditis and pericarditis from four to six small 
fly-blisters may be placed over the prsecordium, and their influence as pre- 
ventive measures is thought to be aided by the free use of the sodium bicar- 
bonate just named. If pericarditis develops and the action of the heart is very 
excessive, small doses of aconite may be cautiously given to act as a cardiac 
sedative. But this drug is not to be used if the patient is markedly depressed. 
Sometimes an ice-bag placed over the heart acts equally well. 

The joints are best treated by anointing them with ichthyol and lanolin in 
equal parts, applying an excess of this ointment, and then wrapping them in 
cotton-batting. When the patient suffers pain because of the twitchings of 
his muscles, which in turn move his inflamed joints, some relief and comfort 
can be given by applying a splint to produce fixation of the joint. 

The acute inflammatory process in the joint is usually severe enough 
to make the patient content to remain in bed. But it not infrequently 
happens that as the pain in the joint diminishes the patient is most anxious 
to get about and return to his usual pursuits. Nothing can be more 
dangerous than the pursuance of such a policy. A very large proportion 
of cases of valvular heart disease are due to the fact that the patient has 
suffered from rheumatism, and has returned to his occupation before the 
endocarditis produced by the rheumatic poison has entirely disappeared. 
For a time he may be able to perform his customary duties, but the increased 
labor thrown upon his heart by exercise causes a delay in the healing of 
the lesions in his endocardium, and as a result he suffers from mitral stenosis 
or mitral regurgitation, which sooner or later will make him a cardiac invalid. 
Even if these symptoms are not manifested for some time after the attack 
of rheumatism has been present, they may nevertheless become dangerously 
active when with advancing years cardiac compensation is lost. The 
physician should therefore impress upon every patient, with acute articular 
rheumatism, who insists upon rising as soon as he feels well, the fact that 
he is taking his life in his hands by so doing. Even after all articular 
symptoms are passed by, the patient who has had this disease should remain 
in his bed for at least two or three weeks, and this advice holds good even if 
during the attack no signs of an endocardial murmur have been manifest. 



204 DISEASES DUE TO A SPECIFIC INFECTION 



CHOLERA. 

Definition. — The word cholera when strictly applied is used to designate 
a disease which is characterized by profuse serous purging, cramps, 
vomiting, and extreme prostration, and which is due to an infection 
of the bowels by the specific micro-organism of this disease, called the 
Spirillum choleras asiaticce, which, as it is often broken into short, curved 
rods, is frequently incorrectly termed the "comma bacillus." When it is 
desired to indicate that the true disease is present the term "Asiatic cholera" 
is used to distinguish the malady from other forms of serous diarrhoea of 
a severe type, such as cholera morbus or cholera infantum. 

History. — Prior to 1817 cholera was confined to certain parts of India and 
never infected districts far removed from them. It is probable that the dis- 
ease has occurred for many centuries, but it is a noteworthy fact that, unlike 
most epidemic diseases of pronounced characteristics and high mortality, 
no clear description of its presence was placed on record. Since 1817, 
when an epidemic of unusual severity broke out in India, it has been known 
to be constantly present in endemic form in some parts of that country, and 
it has from time to time been carried thence along well-travelled routes 
by pilgrims and travellers, or by their possessions, until many parts of the 
earth removed thousands of miles from the original focus have suffered 
from it. Seven distinct invasions of Europe have occurred since 1817, and 
the last one from 1891 to 1895. The disease was first introduced into 
America by emigrants who landed in Quebec and New York early in the 
decade of 1830 to 1840. 

Distribution. — The geographical area of origin has already been described. 
The disease may occur in any part of the world to which the specific germ 
may be conveyed. 

Etiology. — The cause of epidemic cholera is the spirillum which was first 
isolated by Koch. It is spiral shaped or assumes the form of segments of 
a spiral, or short curved rods and S forms. 

The degree of curve varies greatly; sometimes the organism is almost 
straight, at other times it forms a partial circle. Bizarre forms also occur. 
It is active, motile, and flagellate. The bodies described by Hueppe as 
spores have not been so considered by other observers. 

Cholera is distinctly a water-borne disease in the vast majority of epidemics. 
The specific organism gains access to the body through contaminated drinking 
water or soiled food. In the Hamburg cholera epidemic of 1892, about 18,000 
persons were stricken, and of this number 8000 died. In the city of Altona, 
which is really a part of Hamburg, and which also derives its drinking water 
from the Elbe, there were only about 500 cases of cholera in a population of 
150,000. Hamburg had no filtration plant at the time, while Altona had a 
sand filtration plant. It is only by water and food that cholera can be 
transmitted, except that if choleraic stools are desiccated, and the dust is 
blown on food or into the mouth, it is conceivable that the infection may 
occur. Aside from the rarity with which this accident takes place, the fact 
that the bacillus speedily dies, when dried, militates against it being active 



CHOLERA 205 

under these circumstances. A more possible and indeed probable method 
by which the infecting agent may reach the food is its carriage by flies, 
for in the body of the common house-fly the specific organism may exist for 
twelve days. 

Hot weather favors the spread of the disease. As in all infectious maladies, 
all causes which decrease vital resistance, such as alcoholism, exposure, con- 
valescence from other diseases, and even profound mental depression, dis- 
tinctly increase the susceptibility of the patient. 

Prevention. — It is evident from what has been said that there is no reason 
why cholera cannot be prevented, and it may be said of deaths from cholera, 
as it is said of deaths from typhoid fever, that every one is preventable if proper 
care is taken to destroy all the specific organisms the moment they escape 
from the body of a patient suffering from the malady. That they are not 
destroyed in cholera is all the more to be condemned by reason of the fact 
that they escape only in the stools, whereas in typhoid fever the specific 
bacillus escapes by the urine, the skin, and perhaps the saliva. The cholera 
spirillum is exceedingly susceptible to bactericides and particularly to acids, 
under favorable circumstances succumbing to such weak acids as vinegar. 

All dejecta from cholera patients should be destroyed by heat or by the 
action of chlorinated lime, or formaldehyde, or of corrosive sublimate, con- 
tact with a solution of which should be complete and prolonged for at least 
one hour, for in the latter instance the mercury salt may combine with the 
albumin, or be decomposed by the gases in the stools. 

During the presence of the disease no food should be taken in the raw 
state, and it should be cooked immediately before it is eaten, in order that 
there may be no time for it to become infected after it is cooked. With these 
precautions the danger to physicians and nurses is reduced to a minimum. 
When there is a possibility of negligence, a valuable prophylactic is the use of 
dilute sulphuric acid in the dose of 5 to 10 drops in water three times a day 
after food. This does good, by reason of the fact that dilute acids kill the 
comma bacillus, and again because this acid acts as an astringent remedy 
in diarrhoea. Care should be taken during an epidemic that bad food and 
exposure are avoided, as this may prepare the way for infection. 

Through the researches of Haffkine in India, it would seem that it is possible 
to immunize human beings against cholera, but this plan of inoculation is of 
no value when the disease has once developed. 

During the years 1894 and 1895 Haffkine inoculated 3951 individuals 
with his anticholera vaccine. Of this number, 33, or a little less than 1 per 
cent., contracted the disease, whereas, of 9335 individuals who were uninocu- 
lated and similarly exposed to the infection, 210, or 2.24 per cent., were 
stricken. These observations were made in India. 

In July, 1902, an epidemic of cholera broke out in the prefecture of 
Nagasaki, Japan, and preventive inoculations were at once begun. Of 
21,334 persons who were inoculated, 110 contracted the disease. In previous 
epidemics the number of persons affected ran well up into the thousands, 
but it is but fair to state that in this epidemic only 741 cases occurred in 
that prefecture among the uninoculated. As the number of uninoculated 
inhabitants is not stated, we cannot judge of the real value of the plan. 



206 DISEASES DUE TO A SPECIFIC INFECTION 

Haffkine's conclusions as to the result of anticholera inoculations are as 
follows : 

1. The inoculation produces an effect within four days. 

2. During these four days a difference in susceptibility shows itself in favor 
of the inoculated. 

3. After the expiration of the four days and during a period of at least 
fourteen months, a high degree of resistance to attack is observed in the 
inoculated. 

4. The proportion of deaths to cases is not influenced by the inoculation. 
Pathology and Morbid Anatomy. — After death from cholera postmortem 

rigidity comes on very rapidly, and is persistent to such a degree that dis- 
tortions of the limbs and body may be present. In typical cases the entire 
body appears shrunken and wasted and the dependent portions rapidly 
become livid. Not rarely a postmortem rise of temperature takes place. 

When the body is incised the tissues are found to be devoid of their normal 
moisture, and the blood in the great vessels is thick and dark in hue. 
The stomach is empty, its mucous membrane is congested, and, in some 
instances, ecchymoses may be present. 

The chief changes are to be found, however, in the lower part of the 
small bowel. Its mucous membrane is boggy or sodden, and covered by a 
glutinous material which is readily detached. Not rarely the mucous mem- 
brane is stripped off in patches or shed in flakes. These changes may 
extend as high as the duodenum, and in the lower ileum Peyer's patches 
and the solitary glands are found to be swollen and congested. There 
may be present a diphtheritic exudate, which is adherent in part, and in 
part is fleecy or flocculent in appearance. Deeper ulcerations and perfora- 
tions are exceptional. Hemorrhages may also be found in the mucous mem- 
brane at this place. 

Notwithstanding the active purgation, the large bowel in cholera is not 
as much altered as is the ileum, the only change, as a rule, being an acute 
catarrh of the mucous membrane. 

It is important to the student to recall the fact that cholera is character- 
ized by changes in the small bowel, whereas dysentery is chiefly characterized 
by changes in the colon. 

The intestines are contracted, their coats thickened, and the peritoneum 
possesses a peculiar rosy hue. The mesenteric glands are enlarged and 
infiltrated. 

Granular changes in the large glandular viscera are present in a certain 
percentage of cases, and a complicating nephritis is occasionally seen. The 
kidneys may be enlarged and the vessels congested. Under the micro- 
scope the uriniferous tubules are seen to be filled with granular casts, but 
the tufts are not materially changed. The great loss of fluid by the serous 
discharges and the lessened absorption of liquids causes concentration of 
the blood and greatly interferes with the excretion of poisons by the kidneys. 

The liver is not enlarged but rather shrunken, and its cells show, under 
the microscope, cloudy swelling, with patches of fatty degeneration. The 
spleen is usually small. The heart is flaccid and the lungs shrunken. 

The cholera organism is found in immense numbers in the contents of the 



CHOLERA 207 

bowels and in the discharges of patients suffering from this disease, but, 
unlike the typhoid bacillus, it is not usually widely disseminated through the 
body (Figs. 39 and 40). 

Fig. 39 



♦••*■ 



*v** 



fe*. 






*i" 







* V * 9 fi $4 



I 






Comma bacilli in the fundus of a gland of Lieberkuhn in the small bowel in a case of 
Asiatic cholera. (Kast and Rumpler.) 



Fig. 40 



:- F& 



V ~ " : -A * * 



*2m 












■# 






;*?#■ 



Comma bacilli in the intestinal contents. (Kast and Rumpler.) 

Symptoms. — The symptoms of cholera develop in from a few hours to ten 
days after infection has occurred. The average period of incubation is 
usually three to six days. 

The earliest symptoms, aside from a feeling of depression, is the onset of 
watery diarrhoea, which may be associated with pain. The patient suffers 



208 DISEASES DUE TO A SPECIFIC INFECTION 

from the weakness and depression characteristic of ordinary watery diarrhoea, 
and if the passages are very profuse there may be great feebleness and even 
collapse. In the majority of cases, however, the onset of the disease is more 
abrupt than that just described. With almost no indication of impending 
illness the patient is seized by active vomiting and purging, by severe cramps 
in the extremities and trunk, and passes into collapse. The stools, as soon 
as all the ordinary intestinal contents have been washed out, are rice-water 
in character, that is, on standing they separate into two layers, the upper 
clear and opalescent, the lower full of flakes of mucus and exfoliated 
necrotic mucosa. 

The amount of serum lost by the purging is very large, and it is expelled 
with considerable force. Because of the large quantities of fluid lost by this 
means the urine becomes scanty and suppressed. This loss of fluid, com- 
bined with the changes in the kidneys, results in uraemia, which, of course, 
aids greatly in increasing the toxaemia of the disease. The vomiting is not 
only violent, but persistent retching may greatly exhaust the patient. The 
cramps in the muscles are due to the rapid abstraction of fluid from their 
tissues and perhaps, in part, to the toxaemia of the disease. 

In about half the cases recovery begins to take place at this stage by a 
gradual modification of the symptoms, but if the patient is too ill to recover, 
the second stage, or that of collapse and profound asthenia, now develops. 
This stage may last from a few hours to two days. As it proceeds the patient 
becomes so feeble that the respirations become shallow. The fluid stools 
pass from the bowel involuntarily, escaping rather by relaxation of the 
sphincter than by the conscious act of the patient. Feeble attempts at 
emesis may still persist, and the cramps may be more severe than before. 

As the exhaustion deepens the pulse becomes a mere thread at the wrist, 
and may even be imperceptible in the great vessels. The heart sounds 
become more and more indistinct, and occasionally soft murmurs are 
heard. 

The face now bears the Hippocratic expression, the nose is pinched and 
pointed, the eyes sunken and surrounded by dark rings, the mouth is partly 
open, the teeth covered with sordes, the skin of the entire body is livid and 
often bedewed with a cold sweat. The voice is whispering, the thirst exces- 
sive, and the mind clouded. Toward the close of life stupor or coma merci- 
fully relieves suffering. Finally, with a continued fall of bodily temperature, 
death takes place. 

When the stage of reaction develops, before these grave symptoms threaten 
death, the pulse becomes a little stronger, the passages are less frequent and 
less copious, and the respirations grow deeper. Bodily heat is gradually 
restored, and the patient recovers, unless some of the complications men- 
tioned farther on ensue. 

Variations from the Ordinary Course. — The patient may have so mild an 
infection as to be but slightly ill and never forced to go to bed. In other 
instances the serous diarrhoea is excessive, but the urine is not suppressed, 
and the general debility does not become marked. These cases are some- 
times called cases of " cholerine." They may speedily recover or rapidly 
proceed to the fully developed malady. In still another class the toxaemia of 



CHOLERA 209 

the disease exceeds all other symptoms. The diarrhoea may be absent, and 
the patient, overwhelmed by the poison, sinks into unconsciousness and 
death. This is called " cholera sicca." 

The degree of stupor varies greatly. In some patients the mind, at the 
well-developed stage of the disease, is remarkably clear; in other instances 
it is, almost from the first, stupid from toxaemia. 

In some instances high fever develops. This is a very unfavorable sign. 
In others an urticaria or erythema is seen. 

Complications and Sequelae. — Aside from the grave complication of urinary 
suppression followed by uraemia, the profound infection may result in local- 
ized gangrene of the toes and fingers. (Edema of the lungs often causes 
death, and infectious arthritis and parotitis may develop. Profound weak- 
ness and feebleness may persist for a long time in convalescence, and second- 
ary nephritis may ultimately cause death. 

Diagnosis. — The diagnosis of cholera is not difficult if the well-developed 
type of the disease is present, but in the early stages, or in the aberrant forms 
just described, the determination of the cause of the illness may not be easy. 
True cholera is to be separated from cholera nostras or cholera morbus, 
but in the presence of an epidemic of Asiatic cholera this may be impossible 
without bacteriological tests, for severe cholera morbus may not only be 
manifested by purging and vomiting, but by collapse as well, and even cramps 
may appear in the more severe types. Cholera must also be separated during 
an epidemic from the profuse watery purging sometimes met with in cases 
of Bright's disease, when the purging is due to an effort at elimination* 
Various poisons may also cause choleraic diarrhoea, notably antimony. 
Indeed, it is impossible to separate acute antimonial poisoning from cholera 
during an epidemic of the latter disease, because the symptoms are identical. 
Nothing but a chemical analysis, on the one hand, or a bacteriological test, 
on the other, can determine this question. 

It is important to remember that while the presence of the spirillum of 
cholera is characteristic of cholera, that inability to discover it in the dis- 
charges is not positive proof that cholera is not present, because in rare 
instances it may be temporarily undemonstrable. A very valuable method 
of diagnosis is the test of agglutination of cholera bacilli by the blood of the 
patient in a manner similar to that of the Widal test in typhoid fever, 

Prognosis. — The prognosis in cholera, whenever the symptoms are well 
developed, is always grave, for the mortality in most epidemics is about 50 
per cent. In the old and very young the outlook is worse than in a well- 
developed person in the prime of life. 

There are three facts aside from the severity of the disease which increase 
the gravity of the prognosis very materially, namely, alcoholism, renal dis- 
ease, and disease of the liver. In addition, it must be remembered that any 
pre-existing disease which decreases vital resistance increases the gravity of 
the case. 

In respect to the disease itself, it may be said that abruptness of onset, 

early hebetude, and rapid development of signs of collapse are the three 

facts that promise evil tendencies. If to these is added renal inactivity, 

pulmonary consolidation, or an abnormally low temperature, the case is to 

14 



210 DISEASES DUE TO A SPECIFIC INFECTION 

be regarded as almost hopeless. Contrariwise, there are several signs of 
good omen, namely, the presence of a good pulse and the maintenance of 
bodily heat, the return of a fecal color to the stools, and the absence of the 
great emaciation and wasting which severe cases usually manifest. 

Treatment. — The three most important details in the treatment of cholera 
are the control of the diarrhoea, the maintenance of strength, and the con- 
servation of body heat. All persons who have any tendency to diarrhoea 
during a cholera epidemic should at once be treated by astringent mixtures, 
which should be increased in their efficiency by the addition of a few drops 
of sulphuric acid. By this method of treatment the development of cholera 
can be probably prevented in a considerable number of persons. The use 
of an astringent and acid substance like sulphuric acid is far more advan- 
tageous than the employment of opium, because the acid is destructive to 
the comma bacillus, and it does not interfere with other functions of the 
body as does opium. If the diarrhoea is already active 10 to 15 drops of 
aromatic sulphuric acid, with double that quantity of spirit of camphor, 
should be administered, well diluted with water or with brandy, every 
three hours, and counterirritation in the form of a mustard plaster or sina- 
pisms or capsicum drafts should be applied over the abdomen. If these 
cannot be obtained a turpentine stupe may be used with advantage. 

It seems scarcely necessary to add that even in mild cases the patient 
should be kept in bed and the greatest possible amount of rest enforced. If 
vomiting is an active symptom it may be necessary to avoid all medication 
by the mouth and give stimulants hypodermically. Under these circum- 
stances a grain of camphor dissolved in sterilized olive oil may be given by 
means of the hypodermic needle every eight hours. Such a method of treat- 
ment will usually do much toward the maintenance of active circulation, but 
should the circulation fail the physician must employ not only the camphor 
injections named, but give brandy and strychnine hypodermically, and 
more important still, for the purpose of compensating for the loss of much 
fluid by the bowel, hypodermoclysis should be resorted to. It is best to 
employ " concentrated sterile saline," one ounce of which when added to 
a quart of pure water makes normal salt solution. But if this cannot be 
obtained ordinary common salt in the proportion of a drachm to the pint 
may be injected by hypodermoclysis. This fluid should of course be first 
sterilized by boiling, and the injection should be made slowly, the fluid 
being at the temperature of 100°. It is quite remarkable how rapidly the 
thirsty tissues will absorb this fluid, which not only compensates for the 
loss by purging, but also aids in overcoming suppression of urine by sup- 
plying the bloodvessels with fluid. There can be no doubt that hypoder- 
moclysis is a most valuable life-saving measure in the treatment of this 
disease. 

The body heat should be maintained by the application of hot bottles 
about the patient, particularly at his extremities, and wdien the temperature 
seems to be falling and the skin has a tendency to be relaxed and bedewed 
with sweat a hypodermic injection of yJ-Q- to yj-g- of a grain of atropine 
is advantageous. This injection should be into the trunk rather than into 
one of the extremities, since if the circulation is poor it will be absorbed 



CHOLERA 211 

more rapidly from the body than from an arm or the leg. Thirst is to be 
allayed by giving fluids to the patient in small quantities frequently, but 
large draughts of water are disadvantageous. Sometimes barley-water or 
soda-water is retained better than plain water. For the relief of the cramps 
gentle rubbing of the extremities with chloroform liniment, or ammonia 
liniment, may be employed, but the severity of this symptom is usually 
modified by the use of the camphor and the subcutaneous saline injections. 

To aid in the restoration of renal activity a hot compress may be placed 
under the loins. 

During the last outbreak of cholera in Europe salol was employed by a 
large number of physicians with excellent results, its employment being based 
upon the fact that if it is added to an alkaline solution of pancreatic juice 
it rapidly destroys the cholera bacillus. As an illustration of its value it may 
be stated that Hehir treated 88 cases with corrosive sublimate with a mor- 
tality of 44.7 per cent., and 11 cases with salol with no deaths; while Gon- 
zalez lost only 3 out of 53 patients when he employed salol. Similar statis- 
tics from other parts of the world might be quoted indicating its very great 
value. 

Under the leadership of Cantani the following treatment by injection 
has also become popular, it being necessary to give it in large quantities 
not only for the purpose of irrigating the large bowel, but if possible 
getting it into the small bowel as well; for it is in the small bowel that 
the micro-organism of the disease exists in largest number. The fluid 
employed by Cantani consists of infusion of chamomile flowers, 2000 
parts; tannic acid, 10 parts; gum arabic, 30 parts; and laudanum, 2 parts. 
The object in using tannic acid is not only to obtain its astringent influ- 
ence, but also because in the strength of 1 per cent, it inhibits the growth 
of intestinal micro-organisms, and, Cantani thinks, also neutralizes the 
poisons formed by these bodies. Lustig treated 117 cases of cholera in this 
way with 34 deaths and 193 cases by other methods with 146 deaths. Care 
must be employed in giving these injections that the fluid is introduced into 
the bowel slowly, the buttocks of the patient being slightly elevated and his 
body turned slightly to the left. Any tendency to bearing down on the part 
of the patient is to be avoided by diverting his attention from the injection 
and by momentarily stopping its flow when he feels the desire to expel the 
fluid. The fountain syringe containing the fluid should not be hung or held 
more than eighteen inches above the anus. If the fluid flows in under this 
gentle pressure, very large quantities may be retained, and Cantani asserts 
that it will find its way through the ileocecal valve and flush the smaller 
bowel. Such a passage through this valve in the healthy intestine is, I 
believe, impossible, but it is stated that in the relaxation of the muscular 
fibres produced by cholera its passage is by no means difficult. 

When collapse is threatened or present the fluid injected should be as hot 
as 105°, and the fluid in the bag may be at 110° or 115°, as it loses much 
heat in flowing slowly through the tube. If, on the other hand, hyper- 
pyrexia is present, cool water should be employed. 

As a rapidly acting diffusible stimulant in conditions of marked collapse 
Hoffmann's anodyne in the dose of a drachm every hour may ge given hypo- 



212 DISEASES DUE TO A SPECIFIC INFECTION 

dermically or by the mouth with shaved ice. A drachm of spirit of cam- 
phor may also be used with advantage for this purpose. Aromatic spirit of 
ammonia may also be given by the mouth, but is not so valuable. 



YELLOW FEVER. 

Definition. — Yellow fever is an acute infectious disease occurring chiefly 
in tropical or semi-tropical regions, and characterized by fever, yellow dis- 
coloration of the skin, black vomit in some cases, and a tendency to oozing 
hemorrhages from the mucous membranes. The early development of 
albuminuria is also a noteworthy symptom. 

History, Etiology, and Prevention.- — The earliest history of yellow fever 
records its occurrence among the followers of Columbus, and before that 
time it never attacked Europeans. It is, therefore, a disease indigenous to 
the Western Hemisphere. As early as 1648 the inhabitants of St. Kitts 
and in 1655 those of Jamaica were attacked by it. 

Since then yellow fever has devastated North and South America many 
times. It has extended its ravages all the way from Quebec to Montevideo, 
and on the western coast of the Western Hemisphere has been almost equally 
widely distributed. In the latter part of the eighteenth century it destroyed 
10 per cent, of the population of Philadelphia. On more than one occasion it 
has brought military expeditions to defeat by the frightful mortality which 
it has caused amongst the troops. During the French expedition to Hayti, 
in 1802, 22,000 out of 25,000 men died from it in one season, and the various 
attempts which were made by Spain to subjugate Cuba were practically 
frustrated by the mortality from yellow fever among the Spanish troops. 
Davidson states that out of a population of 9000 persons at Gibraltar in 
1800 only 28 escaped infection. In 1878 the financial loss in the Mississippi 
Valley produced by a single epidemic amounted to over $15,000,000. 

For one hundred and fifty years Havana was recognized as the focus 
in which yellow fever was practically constantly present, and from this focus 
many portions of the civilized world were again and again infected. It was 
not until the United States Army took possession of Havana and its medical 
officers instituted sanitary measures that any real attempt was made to dis- 
cover the means of propagation of yellow fever or to limit its development 
in that city. When the brave, skilful, and scientific labors of these officers 
were completed one of the most brilliant medical discoveries in the history 
of the world was announced. 

Under proper sanitary directions the death rate in Havana fell from 91 and 
a fraction, under Spanish rule in 1898, to 33 and a fraction in 1899 under 
American rule, to 24| in 1900, and to 22 and a fraction in 1901, but there 
was not a simultaneous diminution in the frequency or mortality of yellow 
fever. Indeed, at that period there was an actual increase in the disease 
notwithstanding the fact that all other maladies were decreasing. It was 
under these circumstances that a commission was appointed by the 
Surgeon-General of the United States Army for the purpose of studying 
yellow fever. The chairman of the commission was the late Dr. Walter 



YELLOW FEVER 213 

Reed, a major in the United States Army, and associated with him were 
acting assistant surgeons James Carroll, Jesse W. Lazear, and Aristides 
Agramonte. 

The medical profession should never cease to do honor to the members 
of this commission, which faced one of the most horrible and fatal diseases 
with the greatest bravery, and thereby have succeeded in saving the lives of 
hundreds of thousands of individuals. Dr. Lazear, who was one of the most 
enthusiastic members of the commission, allowed himself to be bitten by an 
infected mosquito. He was not infected by this bite, but several days after 
he was accidentally bitten, and lost his life from the consequent attack of 
yellow fever. Another member, Dr. Carroll, allowed himself to be bitten, 
was also attacked by the disease, and narrowly escaped death. 

The fact that Ross and others had proved that the transmission of malarial 
fever was by the mosquito, and that Dr. Carlos Finlay, a physician of 
Havana, a graduate of the Jefferson Medical College, of Philadelphia, had 
asserted as long ago as 1881 that certain species of mosquito in Havana 
was guilty of transmitting yellow fever from person to person, led the Army 
Board to direct their attention to the investigation of this question, and 
they soon found that if a female mosquito of the species Stegomyia jasciata 
were allowed to bite a yellow fever patient during the first three days of the 
disease, and then, from twelve to twenty days later, permitted to bite a non- 
immune, the latter almost invariably developed yellow fever. 

That the disease is never carried by fomites was also proved by these 
investigators, who had a number of young non-immunes sleep for twenty 
consecutive nights in a room which was hung with articles soiled by black 
vomit, bloody fecal discharges, and urine, from fatal and other cases of yellow 
fever. These persons also packed and unpacked these articles night and 
morning from boxes in which they were placed. Other non-immunes actually 
slept in garments and between sheets that had covered fatal cases of yellow 
fever, but in not a single instance was the disease contracted, although as 
soon as these non-immunes were exposed to mosquitoes several of them 
developed yellow fever. 

The practical result of proving that the mosquito is the cause of the 
transmission of the infection has been the complete clearance of Havana of 
yellow fever. All cases of yellow fever were protected by mosquito netting 
so that mosquitoes could not carry infection from them to others. All 
pools and gutters containing water upon which mosquitoes could breed 
were removed, and the destruction of mosquitoes was carried on actively, 
with the result that it was possible in a year to diminish the number of 
deposits of mosquito larvae in the city of Havana from 26,000 to 300. As 
a result, the death rate from malaria fell from 344 in 1900 to 151 in 1901, 
and up to July, 1902, it was only 47; while the diminution in the number 
of mosquitoes caused so great a decline in the prevalence of yellow fever 
that by September 28, 1901, new cases ceased to occur in Havana. Since 
that time, according to Dr. Gorgas, of the United States Army, from 
whose reports much of this information is taken, not a single case has 
originated in that city, until the latter part of 1905, when relaxed vigilance 
allowed the disease again to reappear. 



214 DISEASES DUE TO A SPECIFIC INFECTION 

The conclusions of the commission are so important that they are given 
verbatim : 

1. The mosquito — Stegomyia fasciata — serves as the intermediate host 
for the parasite of yellow fever. 

2. Yellow fever is transmitted to the non-immune individual by means 
of the bite of the mosquito that has previously fed on the blood of those 
sick with this disease. 

3. An interval of about twelve days or more after contamination appears 
to be necessary before the mosquito is capable of conveying the infection. 

4. The bite of the mosquito at an earlier period after contamination does 
not appear to confer any immunity against a subsequent attack. 

5. Yellow fever can also be experimentally produced by the subcutaneous 
injection of blood taken from the general circulation during the first and 
second days of this disease. 

6. An attack of yellow fever, produced by the bite of the mosquito con- 
fers immunity against a subsequent attack of the non-experimental form 
of this disease. 

7. The period of incubation in thirteen cases of experimental yellow 
fever has varied from forty-one hours to five days and seventeen hours. 

8. Yellow fever is not conveyed by fomites, and hence disinfection of 
clothing, bedding, or merchandise, supposedly contaminated by contact 
with those sick with this disease, is unnecessary. 

9. A house may be said to be infected with yellow fever only when there 
are present within its walls contaminated mosquitoes capable of conveying 
the parasite of this disease. 

10. The spread of yellow fever can be most effectually controlled by 
measures directed to the destruction of mosquitoes, and the protection of 
the sick against the bites of these insects. 

11. While the mode of propagation of yellow fever has now been defi- 
nitely determined, the specific cause of this disease remains to be discov- 
ered. 

Prophylaxis. — Attention has already been called to the fact that the infec- 
tious agent of yellow fever is conveyed by mosquitoes from patient to patient. 
It is therefore essential that all cases of yellow fever should be kept under 
mosquito netting so that they may not be bitten by mosquitoes, and it is 
also wise for those who are well to protect themselves at night from mos- 
quitoes by similar means. For screening those who are ill, a gauze of not 
less than twenty meshes to the inch should be used, otherwise the mosquito 
may pass through it. An active crusade against all mosquitoes and the 
destruction of their breeding-places should also be instituted. 

Pathology and Morbid Anatomy. — One of the most marked changes pro- 
duced in the body by the infection of yellow fever is that which takes place 
in the blood. Many of the red cells are crenated and some of the white 
cells are granular. Free haemoglobin, hsemin, and hsematin are found in it 
owing to the destruction of the red corpuscles. 

The heart is soft and flabby, and minute ecchymoses in its muscular tissue 
may be present. The pericardium may contain an excess of blood-stained 
fluid, and its membrane may be dotted with petechias. 



YELLOW FEVER 215 

The stomach shows changes with great constancy. It usually contains 
black fluid due to altered exuded blood; its mucous lining is congested in 
patches and is marked by ecchymosis or even softened. When placed 
under the microscope sections of the stomach show the bloodvessels engorged 
and their walls undergoing fatty degeneration. The intestinal canal also 
contains broken-down blood passed from the stomach, and its contents may 
be acid. Fatty degeneration of Peyer's patches and the glands of Lieber- 
kiihn is present. 

The liver is often pallid or yellow in hue, and its cells also may undergo 
fatty change. Councilman states that associated with these signs of fatty 
degeneration areas of necrosis can be demonstrated in every case that comes 
to autopsy. 

As in many acute and severe infections, the kidneys show signs of acute 
diffuse nephritis with fatty degeneration of the cells lining the tubules. 

Small hemorrhagic spots are sometimes found in the meninges of the 
brain and cord, and fatty degeneration of the cells of the solar plexus has 
been described. 

Symptoms. — A very noteworthy fact in connection with the symptom- 
atology of yellow fever is that in a majority of cases its onset is most abrupt. 
There may be, for a few hours before the well-defined symptoms show 
themselves, a sense of malaise and headache or vertigo. The first symptom 
of prominence is the appearance of a rigor, or rigors, which may be moderate 
or severe, but Bemiss states that chills are rare. In addition the patient 
suffers from severe lumbar and muscular pains, headache and eyeache, and 
marked pallor. There is often epigastric distress. In children the disease 
may be ushered in by convulsions. 

After the stage of onset the skin of the face becomes flushed and turgid ; 
the mind may wander, but as the disease develops it is usually remarkably 
clear and alert, so that the patient watches those about him with the same 
degree of attention as is often seen in acute peritonitis. The expression is 
anxious. The temperature rapidly rises so that it reaches its acme of from 
103° to 107° by the end of twenty-four or thirty-six hours. 

If the case is a very mild one the febrile movement may cease as early as 
the end of the first day or on the morning of the second day, but usually 
the acme of the temperature is maintained for from two to three days, 
during which time there may be slight morning and evening variations. 
In cases which are moderately severe the fever usually begins to fall after 
this time and reaches a point near the normal in from twenty-four to 
seventy-two hours. That is, the fall is by lysis. 

After the temperature has reached normal, that is when the stage of 
remission about to be described has become well marked, a secondary fever 
develops which, like that of the stage of onset, lasts from two to three days and 
falls by lysis. In cases which are likely to be fatal this fall may not occur. 

The respiration and pulse rate are at first increased in frequency and the 
individual pulse beat is increased in volume, but these circulatory condi- 
tions speedily undergo a marked change with the approach of the period of 
remission. On the second or third day, even if the temperature remains 
as high as before, the pulse rate begins to fall, or falls even while the tern- 



216 DISEASES DUE TO A SPECIFIC INFECTION 

perature is still rising, so that a pulse rate which early in the onset was 
as high as 110 may now be as low as 75. 

After the fever begins to fall owing to the beginning of convalescence the 
pulse, as in many cases of ordinary catarrhal jaundice, may fall still farther 
till it reaches 45 a minute. It is the slowing of the pulse in the stage of onset, 
while the temperature is still high, that is particularly worthy of note. 

The tongue is covered with a white fur save at its edges, which are 
red; the botvels are constipated, and there may be epigastric distress fol- 
lowed by the vomiting of acid mucus. 

The urine is scanty and it may be distinctly albuminous as early as the 
third day. This early albuminuria is considered by yellow-fever experts to 
be a very important aid to diagnosis. 

By the third day a very marked remission in the symptoms may occur. 
The pains and aches, the rapid pulse, the high temperature, and the flushing 
of the face all become modified. The gastric symptoms abate, but the con- 
junctivae may begin to be jaundiced and the skin of the body may also begin 
to show a yellow hue. This is the critical period of the disease, for the 
patient is now "at the parting of the ways." One path leads to rapid 
recovery with marked amelioration of all the symptoms; the other leads, 
after a remission of from twelve to forty-eight hours, to a recurrence of all 
the dangerous symptoms in an aggravated form. 

If the way is evil there is precordial and epigastric distress, persistent 
vomiting of clear liquid with flakes of brown reddish-looking material, which 
speedily increases in amount until the well-known black vomit presents 
itself. The urine is more scanty and more albuminous than ever, and the 
general state of the patient is that of profound illness. The temperature 
in some cases rises as it did in the stage of onset, but it may, and this sign 
is of grave import, fall below normal. Even yet it is possible for recovery 
to occur by a gradual amelioration of all the symptoms, but usually the 
symptoms continually get worse. The grave depression increases, the 
yellow skin develops a greater degree of yellowness, and petechiae are 
formed. The vomiting of black material is more severe and profuse, and 
hemorrhages may occur from other mucous membranes than that of the 
stomach. The scene closes with hiccough, profound asthenia, subsultus 
tendinum, the Hippocratic face, and in exhaustion and coma, due in part 
to the direct effect of the infection and in part to the uraemia produced 
by the intense renal lesions. 

While these may be considered the symptoms of yellow fever in many 
cases, in others they are very different. In the so-called apoplectiform type 
the patient is seized with vertigo, stupor, unconsciousness, and convidsive 
attacks. He speedily becomes more and more deeply depressed, his circula- 
tion fails, the bowels and bladder are involuntarily emptied, and with the 
development of multiple hemorrhagic extravasations he dies. 

In another severe type the symptoms are algid, the patient speedily pass- 
ing into profound collapse with a subnormal temperature and profuse hemor- 
rhages, death coming on in a few hours. In still another type the violent 
vomiting, purging, and collapse may cause the case to resemble one of 
cholera. 



YELLOW FEVER 217 

Diagnosis. — It is stated by all physicians of experience that in some cases 
it is almost impossible to make a diagnosis of yellow fever in its early stages, 
chiefly because it has few pathognomonic signs, and these are of value only 
when associated and not when they appear singly. Again, many cases of 
yellow fever pursue a very aberrant course, so that several days elapse before 
the diagnosis can be made. 

Yellow fever must be separated from dengue, pernicious malarial fever, 
from malarial hsemoglobinuric fever, and from relapsing fever. The dif- 
ferentiation of yellow fever from dengue has given rise to much bitter con- 
troversy, and even at the present time physicians of wide experience with 
both maladies are by no means agreed about the separation of these diseases 
in their early stages. 

Guiteras asserts that there are three notable symptoms of yellow fever 
which are of service in this connection. First, the facial expression of the 
yellow-fever patient is characteristic because in no other disease is it so 
flushed, the eyes so injected, nor the conjunctiva so icteroid after a few hours 
of illness. Second, the development of albuminuria as early as from the first 
to the third day, which may be transient and slight, or persistent and pro- 
fuse. The third differential point is the change in the pulse already noted 
as occurring on the second or third day of the disease during the continu- 
ance of fever. 

The jaundice of dengue rarely appears as early as the third day. 

The history of the patient as to exposure, the presence of the sestivo-autum- 
nal parasite in the blood, and the enlarged spleen of malarial infection point 
to pernicious malarial fever. A porter-colored urine, the blood infection, 
and the enlarged liver point to hremoglobinuric fever, while the discovery of the 
spirillum of Obermeier in the blood will demonstrate the presence of relap- 
sing fever. (See Relapsing Fever.) While all these facts may aid greatly in 
distinguishing yellow fever, it is not to be forgotten that the absence of some 
of them does not prove that the yellow fever is not present. Thus in some 
cases the albuminuria does not appear very early, in others the failure to dis- 
cover the sestivo-autumnal parasite may be due to the lack of skill of the 
observer or to the well-known difficulty of its discovery even by the most 
practised observers, i\gain, it is possible for the malarial parasite to be 
present when yellow fever is present, the two diseases existing simultaneously. 

Prognosis and Mortality. — In a disease which is so variable in its manifesta- 
tions, prognosis must always be guarded. If the febrile, gastric, and renal 
symptoms are mild in the stage of onset, the outlook is more favorable than 
if they are severe. If the period of remission is not well marked and hemor- 
rhagic tendencies are well developed, the prognosis is bad. 

The mortality varies very greatly in different epidemics, as already shown 
in tne discussion of the history of the disease. Sometimes it is as low 
as 15 per cent., again as high as 85 per cent. It is apt to be lower in 
private than in hospital practice. Some authors have made the interesting 
statement that the mortality is in inverse ratio to the morbidity. The average 
mortality may be stated at about 30 per cent. Thus, in 25,220 cases of 
yellow fever occurring in the West Indies, Central and South America, 
Mexico, and the United States, 8020 cases were fatal, a percentage of 31.8. 



21S DISEASES DUE TO A SPECIFIC INFECTION 

Treatment. — In the treatment of yellow fever it is essential that the patient 
shall have a plentiful supply of fresh air and sunshine, with absolute rest and 
proper sanitary surroundings. Bad hygienic surroundings always greatly 
increase the mortality of the disease. 

As soon as the patient is suspected to be suffering from yellow lever, he 
should be put to bed and required to remain there until convalescence 
has been completed, for physical and mental unrest distinctly predispose 
the patient to a fatal issue. During the whole period of the disease the 
patient should not be allowed to sit up in bed, since sudden cardiac failure 
may occur. All the food and medication should be given to the patient 
when in the recumbent position, and the contents of the bowels and 
bladder emptied into a bed-pan. The patient should be lightly covered, 
and the use of heavy blankets or quilts should be discouraged. 

Cleanliness of the mouth should be carefully maintained, since otherwise 
softening and ulceration of the gums not infrequently occur. 

Active medication for the treatment of the disease itself is unwise. The 
physician should give only remedies when they are very distinctly indicated, 
as for the relief of a failing heart, with the hope of increasing the activity of 
the kidneys and for the prevention of profound asthenia. In some portions 
of the world where yellow fever frequently occurs, it is customary to employ 
hot mustard foot-baths and even hot packs during the early stages of the 
disease, but they are unwise after the malady is once well developed. For 
the relief of the fever cool sponging with alcohol and water, or even with 
ice-water, may be employed, an ice-bag being applied to the head. The 
employment of the coal-tar products is never advisable, and they are particu- 
larly contraindicated when the depression is marked. Many practitioners 
have employed emetics in the early stages of yellow fever, but these are 
certainly not required unless it is known that the patient's stomach is 
overloaded with food, when 10 to 20 grains of ipecac may be given. 

Many years ago former Surgeon-General Sternberg advised the employ- 
ment of bicarbonate of soda, corrosive sublimate, and water in the treatment 
of yellow fever, but, although this method of treatment has been widely 
employed, it has now largely gone out of use, although large quantities of 
bicarbonate of soda are given freely by many practitioners as a matter of 
routine. 

As in most infectious diseases, the bowels, if constipated, should be moved 
by means of calomel, which in turn may be followed by one of the saline 
purges or by castor oil. Purgation may be resorted to every twenty- 
four or forty-eight hours, in order to keep the bowels thoroughly evacuated. 
To aid the purgatives and for the purpose of washing toxic materials from 
the large intestines, copious irrigations of the colon with normal salt solu- 
tion are advisable. The patient should be urged to drink freely of water 
in order to flush the kidneys, and alkaline mineral waters, such as Vichy, 
Apollinaris, or Seltzer, or plain water, to which bicarbonate of soda has 
been added in small quantities, may be used with advantage to neutralize 
the acidity of the gastric contents and to act as diuretics. 

For the arrest of excessive vomiting, cocaine has been highly recommended, 
but there is no reason to believe that it exercises any better anti-emetic prop- 



PLAGUE 219 

erties in this disease than in other diseases in which vomiting is present. One 
or 2 minims of creosote or carbolic acid are equally valuable. 

For the purpose of stimulating the heart and circulatory system, digitalis 
in the dose of 5 minims of the tincture, or strychnine in the dose of fa of 
a grain, or caffeine in the dose of 1 or 2 grains, may be given three or four 
times a day, and if collapse is threatened the strychnine may be given 
hypodermically with atropine, or Hoffmann's anodyne may be given by the 
mouth or by the hypodermic needle. Strong, black coffee may also be 
employed by the mouth or by the rectum, for the purpose of rallying the 
patient. 

For persistent hiccough, sipping very hot water is often advantageous. 

From the beginning to the end of the attack it is the duty of the physician 
to carefully watch the condition of the kidneys by making daily examinations 
of the urine, since uraemia is one of the greatest dangers which can beset the 
patient. After the kidneys have once become so inactive that the urine 
is exceedingly scanty it is often absolutely impossible to stimulate them to 
activity, whereas much can be done, if from the very first, renal activity is 
maintained. For this purpose calomel may be given as a diuretic in the dose 
of 2 or 3 grains every few hours for one or two days at a time, or one of the 
diuretic potassium salts, such as the citrate or acetate, in large amounts of 
water. Hypodermoclysis with normal salt solution may be employed. Renal 
congestion may be overcome by the application of mustard plasters and dry 
cups over the kidneys. 

During the acute stage of the illness the condition of the stomach is such 
that the administration of food is almost impossible, but milk diluted one- 
half with Vichy water or with water containing bicarbonate of sodium may 
be given. 

During convalescence the greatest possible care must be exercised that the 
patient does not take food in too large quantities. No solid food should be 
permitted before the end of a week, and, if the patient has been very ill, not 
for two weeks. In the mean time the diet should consist of partially pepton- 
ized milk, milk-toast, broths, and eggs. 

As in all exhausting diseases, the physician must insist upon the patient 
remaining in bed until the heart muscle has entirely recovered from the 
profound depression of the disease. Bitter tonics, such as iron, quinine, 
and strychnine, may be given. 



PLAGUE (BUBONIC PLAGUE). 

Definition. — Plague is an acute, specific, infectious, and contagious dis- 
ease caused by the Bacillus pestis. It occurs in widespread epidemics, is 
characterized by fever, inflammation of various glandular groups, and pro- 
found depression. The course of the disease is exceedingly rapid and the 
mortality extremely high. 

History and Distribution. — In ancient times plague occurred in pandemics, 
spreading over the whole known world. Most of the old world epidemics 
about the beginning of the Christian era have been described as plague on 



220 DISEASES DUE TO A SPECIFIC INFECTION 

wholly insufficient evidence. Hirsch dates the first recognizable epidemic in 
the second century B.C. Following this, historical descriptions do not satis- 
factorily identify the disease until the pandemic which persisted for nearly 
sixty years, during which time it ravaged the whole of Europe (a.d. 542). 
Following this epidemic, known in history as the plague of Justinian, the 
disease appeared from time to time, but only twice to so great a degree. 
The first of these two extensions was during the fourteenth century; the 
second, known as the Great Plague of London, began in 1664 and lasted 
until 1679. During the first year of this epidemic one-sixth of the total popu- 
lation of London perished. The advance of sanitary science since that time 
has gradually forced plague out of Europe and limited the area of its 
extension. During the last three decades it has lingered in Southeastern 
Europe. 

We are now in the presence of what must be considered a world-wide 
extension of the disease, limited only by effective preventive measures. 
The present epidemic began in Hong Kong in 1894. In 1896 it reached the 
Presidency of Bombay, and, in the ten years following, it has spread 
through nine British provinces and fifty-one native States, the cases increas- 
ing in spite of all restrictive efforts. It is estimated that to the middle of 
the year 1903 two million persons have perished in the Deccan since the 
beginning of the outbreak. In the city of Bombay over one hundred thou- 
sand persons have died, and in the Presidency of Bombay alone during 
January, 1903, the deaths averaged eight thousand weekly. Later, the 
disease appeared in Japan, Madagascar, and South Africa. It obtained 
a temporary foothold in Glasgow, Lisbon, and Oporto. In 1900 it reached 
Sydney, Australia. On the American continent it appeared in Brazil and 
the Argentine Republic. In 1899 it established a foothold in San Francisco, 
in which city rigorous measures have limited it to a very great degree. 
During the year 1902 the disease appeared in Peru, Mexico, and Alaska. 

Etiology. — Plague is caused by a specific micro-organism discovered by 
Kitasato and Yersin in 1894, during the epidemic in Hong Kong. This 
organism is a short, oval, non-motile, coccobacillus resembling the bacillus 
of chicken cholera. It occurs singly, joined in pairs, and occasionally in 
long chains. It is found in large numbers in the pus of plague buboes and 
in smaller numbers in the viscera and blood. It has been cultivated from 
all the accessible tissues of the body during life, and from all the excretions 
except the sweat. It has also been recovered from the floors and soil in the 
houses of patients sick with plague. 

The bacillus stains with all the ordinary staining reagents and is decolor- 
ized by Gram's method. It takes up the stain much more strongly at its 
poles. Sometimes a capsule is observed, but there is no spore formation. 
It grows best at the body temperature and on all the ordinary media. In 
fluid culture media, overlaid with a film of bland cocoanut oil, the bacillus 
grows in the form of long stalactites hanging from this oily layer that are 
considered characteristic of this organism. Its viability is rather low. If 
kept moist and cool, it may keep alive and virulent for months, but if dried 
at the room or body temperature it dies in from three to four days. Exposure 
to direct sunlight destroys it in a few hours. The bacillus is pathogenic for 



PLAGUE 221 

nearly all domestic animals. Indeed, most of them are subject to plague 
and aid in its dissemination. Sheep, calves, pigs, ducks, and fowls readily 
contract the disease, and the bacilli may be recovered from their viscera 
and excretions. The disease also occurs in bats, and the common rat is 
peculiarly susceptible to it. The great mortality among rats, preceding 
and often signalizing an epidemic of plague, is an observation that was 
well known to the ancients. 

The Chinese long ago recognized the association between the death of 
the rats in a house and the development of plague a few days later. Fin- 
ally, the fleas that infest rats and the flies in infected houses also serve to 
carry the contagion. 

The method of conveyance to man has been established with a fair degree 
of certainty. Inoculation experiments in man and animals have shown 
that when virulent bacilli are introduced into the tissues plague develops. 
Thus at Cairo in 1835 plague blood was used to inoculate two criminals, 
but though they developed the disease both recovered. The list, too, of 
physicians and laboratory workers, who have contracted the disease from 
accidental inoculation and dissection wounds, is a large one. Among them 
may be mentioned Whyte, who, in 1802, infected himself and perished, 
and Aoyama and his assistants who contracted plague from dissection 
wounds. 

In 1898 three deaths occurred in Vienna as a result of laboratory inocula- 
tions, one in 1899 in Lisbon, and one in 1902 in Berlin, while thirteen cases 
resulting from accidental inoculations in postmortem examinations have 
been collected in India. 

For a time it was believed that man was infected by inhalation of the 
germ, by swallowing it on infected food, and by direct inoculation. That 
infection takes place through air and food has not been substantiated. 
The disease enters through the skin, by direct infection through slight 
wounds or abrasions, or through the bite of suctorial insects. It has been 
shown that rats suffer more intensely perhaps than any other animal from 
plague. The rats are infested with fleas, which are also infected, and the 
disease is transmitted from rat to rat and finally from rat to man by the bite 
of these insects. There has been some conflict of opinion as to whether 
the fleas of plague-infected rats would bite man. To settle this question 
Tidswell examined the fleas from a number of rats and found five varieties, 
of which four were known to attack man. 

The possibility of infection taking place directly into wounds and abra- 
sions from infected soil must be admitted. Calvert reports an interesting 
case where the disease was acquired in sexual intercourse, and one case 
where the bite of an infected rat caused a fatal infection. Direct trans- 
mission from patient to patient, while always possible, occurs very rarely. 
This is borne out by the observations in Bombay, Hong Kong, and other 
places, that cases are extremely rare among the physicians, nurses, quar- 
antine guards, and disinfection laborers, who are constantly in intimate 
contact with plague cases. 

The disease principally attacks the poorer classes of the native popula- 
tion, those who live in the slums under poor hygienic surroundings. Lack 



222 DISEASES DUE TO A SPECIFIC INFECTION 

of personal cleanliness and deficient light and ventilation in living rooms 
are predisposing causes. 

Frequency. — Plague affects all ages and both sexes equally. Neither 
geographical location, character of soil, nor elevation have any influence on 
its spread. It prevails at all seasons of the year, although, generally speaking 
it is least active in the seasons of greatest heat or cold. 

Epidemics begin slowly. The common history is that in the beginning 
a few isolated cases develop, the epidemic slumbering along in this way for 
a year or more before rapid extension takes place. It declines in the same 
way. Not only do the number of cases grow less, but their virulence notably 
diminishes. It creeps slowly from town to town, following the routes of travel. 
Its extension from one country to another over sea is due to the presence of 
infected rats on the ships plying between them. Thus the epidemic in Peru 
was shown to have spread from the rats on a ship carrying grain from India. 

Symptoms. — Clinically plague may be divided into four varieties: 

1. Bubonic plague, pestis bubonica, malignant adenitis. 

2. Septicemic plague, pestis siderans. 

3. Pneumonic plague. 

4. Larval plague, pestis minor, pestis ambulans. 

Bubonic Plague. — This is by far the commonest type, averaging 80 per 
cent, of all cases. The incubation period varies from two to eight days, 
averaging four days. 

The attack begins with fever, lassitude, severe headache, and pain in the 
limbs. Rigors may or may not be present, but vomiting is usual in this 
stage. There is drowsiness, vertigo, and extreme anxiety. After lasting 
from twelve to twenty-four hours, fever begins and the temperature rises 
rather quickly to 103° to 107°. There is now hurried pulse and respira- 
tion. The face is heavy, swollen, and flushed; the tongue is coated with 
a heavy black fur; the teeth are covered with sordes. Vomiting is often 
persistent and diarrhoea may develop. The patient is most profoundly 
depressed, the depression being out of all proportion to the duration of the 
disease, and a low muttering delirium is present. Death may occur in this 
stage, accompanied by convulsions and collapse or by urcemic coma with 
total suppression of urine. 

In from twenty-four to seventy hours — that is, from the third to the 
fifth day of the disease — the characteristic glandular swellings develop. 
The glands involved are in the groin in 60 per cent, of the cases, the 
axilla in 35 per cent., and the neck and angle of the jaw in 5 per cent. 
The buboes are usually single and are much more common on the right 
side than on the left. Occasionally they are bilateral, rarely multiple. In 
size they vary from a pigeon 's egg to the size of a fist. They are frequently 
painful and always exquisitely tender. 

Coincident with the development of the buboes, small areas of gangrene 
of the skin, carbuncles, or generalized pustular skin lesions may develop. 

The buboes increase in size for three or four days and then become 
stationary. In a small proportion of cases gradual resolution takes place. 
In the larger proportion softening and suppuration occur and the bubo is 
opened or ruptured and discharges a foul-smelling pus. At this stage free 



PLAGUE 223 

suppuration is usually a good omen. If the pus continues scanty and 
sanious the disease remains virulent. 

In free suppuration the bacilli disappear from the pus in a very few days 
and convalescence is rapidly established. In the cases that terminate favor- 
ably a marked amelioration is observed with the development of the gland- 
ular swelling, and usually about the seventh day the temperature falls and 
the profound depression disappears. 

Septicemic Plague. — In this form the symptoms are much more severe 
and the stage of bubo formation is lacking. That is, there is no one gland 
or group of glands conspicuously involved, but the whole glandular system 
is engorged and swollen. The essential difference seems to lie in that the 
infection is more severe either quantitatively or qualitatively. There is 
a marked bacteriaemia. Clinically, these cases differ from the former in 
the more profound depression, more moderate fever (100° to 102°), and 
the greater tendency to hemorrhages. 

Pneumonic Plague. — This form begins suddenly with rigors and all the 
symptoms of acute pulmonary inflammation. Respiration is rapid and 
labored and there is a painful harassing cough. So far the symptoms 
resemble an ordinary lobar pneumonia. The sputum, instead of being 
scanty, tenacious, and of the usual prune-juice color, is copious, watery, 
and spotted and streaked with bright blood. Physical examination shows 
areas of consolidation scattered throughout the lungs. An entire lobe is 
rarely involved. This form of the disease is the most fatal of all, patients 
rarely surviving after the third day. In these cases, too, although it is not 
clinically apparent, postmortem examinations show- general involvement 
of the glandular system. Pneumonic plague is more common in children 
than in adults, and at the beginning of epidemics than at the end. 

Hemorrhages occur in all the various clinical types of plague, more com- 
monly perhaps in the septicemic. They appear in the skin as petechia* and 
ecchymoses. There may be epistaxis, hoem,aturia, and hemorrhage from 
the stomach or bowel. Haemoptysis is a very sinister symptom. 

The urine is diminished and commonly contains large quantities of albu- 
min with more or less kidney structure. Albuminuria is never absent in 
severe or fatal cases. 

The blood changes are not characteristic. There is a marked leuko- 
cytosis, varying from 20,000 to 50,000, with moderate reduction of the 
haemoglobin. 

Relapses occur in a small percentage of cases and are always grave. Con- 
valescence may be very much prolonged by indolent ulcers and burrowing 
sinuses at the seat of the buboes. 

Larval Plague, Pestis Minor. — Cases of this type occur in all epidemics 
and are very common toward their close. In larval plague the typical 
buboes develop with few prodromata. The constitutional reaction may be 
very mild, the fever is slight, and the patient is but little annoyed by the 
disease. Some epidemics are characterized by large proportions of such 
cases. 

Prophylaxis. — Personal prophylaxis should be directed in the first place 
to avoiding too close contact with plague cases. Nurses and physicians 



224 DISEASES DUE TO A SPECIFIC INFECTION 

should remain as short a time as possible in their immediate vicinity. 
Wounds, abrasions, and skin eruptions on the limbs should be carefully 
guarded, particularly against a germ-carrying finger-nail. Tight leggings 
or gaiters should be worn to prevent the bite of fleas. These measures 
combined with personal cleanliness, a good water supply, and abundant 
ventilation are efficient. 

The general measures to be taken for the prevention of plague are, first, 
strict attention to sewage, water, ventilation, and cleanliness of dwellings; 
second, the extermination of rats and mice. This has been tried on a large 
scale by trapping and poisoning. Quarantine has never been an effective 
check to this disease. 

The danger from contact is not very great. Exposed persons should be 
disinfected, given a prophylactic inoculation, have their clothing destroyed, 
and then be released. The quarters in which a plague patient has lain 
should be thoroughly scraped, disinfected, and repainted or whitewashed. 
Better still, when practical, they should be burned. The evacuations and 
bedding of the sick should be cremated. 

In spite of the most stringent prophylactic measures, plague is very diffi- 
cult to control. As a matter of fact, where it has once attained even a 
slight foothold it has not been successfully eradicated by any of these 
measures. Witness the cases in San Francisco, where after several years of 
effort the disease still persisted. It seems likely that the most we can expect 
with our present means is to hold the disease in check'. 

Protective Inoculation. — Haffkine introduced a prophylactic inocula- 
tion against plague. His method has been modified by Lustig and recently 
by Besredky. Briefly, these methods consist in injection of plague cultures 
killed by heat. Extensive experience has shown that these inoculations 
confer an immunity against plague, beginning in twenty-four hours and 
lasting from three to four months. Recent studies seem to show that, given 
during the period of incubation, they have the power to abort the disease 
in many cases. This system of protective inoculation was being tried on 
an extensive scale in the Punjab, when a very deplorable accident cut the 
experiment short. After more than 100,000 persons had been inoculated 
without untoward results, nineteen men received their injection from the 
same package, developed tetanus on the fifth day, and all died. This unfor- 
tunate affair practically stopped prophylactic work in India by greatly 
increasing the aversion the natives had always shown to it. 

Pathological Anatomy. — The visceral lesions of plague are constant 
and uniform. Punctate hemorrhages appear not only on the skin, but 
throughout the whole gastrointestinal tract. They are found on the peri- 
toneum, pleura, and pericardium, as well as in the capsules of the spleen, 
kidney, and liver. The cerebrospinal system is congested and there is an 
increase of its fluid. The liver and kidneys are hypersemic and the spleen 
very much enlarged. In pneumonic cases the bronchi are injected and 
swollen and there are small areas of consolidation scattered throughout 
the lung. The pleural cavities frequently contain moderate quantities of 
seropus. 

The glandular system shows constant involvement. In the bubonic form the 



PLAGUE 225 

glands appear on section as large, diffused masses, with extensive hemorrhages 
into their substance. This appearance is not confined to one group of 
glands, but extends along the lymphatic trunk and invades the glands in 
the immediate proximity to the main buboes. 

Microscopically, intense hyperemia with hyperplasia is found not only 
in the glandular but also in the periglandular structure. Before the glands 
break down the bacillus pestis is found alone; after suppuration is estab- 
lished other organisms are found with it. 

In the septicemic and pneumonic cases, or in those cases dying before 
marked bubo formation has taken place, the gross changes in the lymph- 
atic system are not so apparent, but there is always enlargement of one 
or more groups of glands or slight tumefaction and congestion of the 
entire lymphatic system. The pathological process is identical in all 
the types, only that in the bubonic form the intensity of the affection is 
expended on one gland or group of glands, while in the other form the 
adenitis and lymphangitis are diffuse. 

Diagnosis. — In the presence of plague in epidemic form the, rapid onset 
of the disease, the profound depression, the glandular swelling can hardly 
suggest anything else than this disease. The identification of the bacillus 
pestis in the blood, in fluid from the buboes, or in the sputum assures the 
diagnosis. Inoculations and culture experiments are important in the 
early stages of an epidemic with large numbers of atypical cases of plague. 
The best routine method of diagnosis is the microscopic examination of a 
drop or two of the fluid obtained from the buboes by means of a hypodermic 
syringe. The few drops of bloody lymph collected in this manner contain 
large numbers of bacilli. The diagnosis of the pneumonic form can only 
be made by demonstrating the micro-organism in the sputum. 

Prognosis. — Varying in different epidemics, the average mortality runs 
from 70 per cent, to 95 per cent. The variations depend on the stage of 
the epidemic, the proportion of pestis minor cases, and the race and hygienic 
conditions of the patients. In the Hong Kong epidemic the average mor- 
tality was 93 per cent, among the Chinese, 77 per cent, among the Indians, 
60 per cent, among the Japanese, and 18 per cent, among the Europeans. 
This gradation, as jVIanson has remarked, is "in general correspondence with 
the social and hygienic conditions with these different nationalities." 

The influence of the type of the disease on mortality is shown in the follow- 
ing figures from an analysis of 13,145 cases. In the bubonic cases the mortality 
was 77.25 per cent., in the pneumonic cases 96.69 per cent., and in the sep- 
ticemic cases 89.62 per cent. 

The number of the buboes and their location has no bearing on the mor- 
tality. Visceral hemorrhages are always unfavorable symptoms, while free 
suppuration of the buboes must be considered as a very favorable omen. 

Pregnancy complicating plague is also very unfavorable. Abortion 
invariably occurs and death is almost certain. 

Treatment. — Treatment of plague is wholly symptomatic. For the fever, 
headache, and delirium nothing is so effective as cold sponging. Cantlie 
recommends initial purging with calomel in large doses, followed by salines. 
This remedy frequently checks vomiting and permits nourishment to be taken. 



226 DISEASES DUE TO A SPECIFIC INFECTION 

For the pain and restlessness there is no remedy so effective as mor- 
phine, given hypodermicaliy, in small doses. In the profound depression 
and collapse, diffusible stimulants are indicated; ammonia to the nose, 
mustard to the skin, and ether or camphor subcutaneously. Alcohol should 
be given freely, particularly in a septicemic form. 

Suppuration of the buboes should be hastened by poultices and hot 
fomentations. When fluctuation occurs they should be opened freely and 
dressed antiseptically. 

Thomson reports excellent results in the epidemic in Hong Kong from the 
internal use of carbolic acid in large doses. He gave 144 grains daily in 
doses of 12 grains every two hours in a mixture of syrup of orange and 
chloroform-water. One patient took over 2500 grains of pure carbolic acid 
before his blood was free from plague bacilli. Beyond a few cases of car- 
boluria no toxic symptoms developed. He considers this the most hopeful 
method at our disposal. 

Yersin, Calmette, and Borrell have developed an antitoxic serum by the 
injection of ascending doses of cultures killed by heat into susceptible 
animals. Experimentally, plague in animals has been arrested by this 
means. Clinically the results with the antitoxic sera have been most con- 
tradictory. While they have not entirely fulfilled the hope that they first 
seemed to hold out, later experience in this direction is more encouraging. 
The antitoxin needs further study, and particularly needs standardization. 



CLIMATIC BUBO. 

Definition. — Climatic bubo, tropical bubo, tropical adenitis (non- venereal), 
is a subacute inflammation of the lymphatic glands of the groin, attended 
by a fever remitting in type and persisting from three to four weeks. The 
disease is widely distributed in tropical climates. It occurs on the coast of 
Africa and Asia, and is common enough in the Philippines, Japan, Malaya, 
the West Indies, and the Mediterranean. 

The disease commonly affects individuals living together under the same 
hygienic conditions, as sailors and soldiers, and occurs in small epidemic 
outbreaks. There is some evidence to show that its origin is due to the 
entrance of bacterial infection, either through minute wounds in the legs 
and genitals or the bites of insects. It has been described as due to tropical 
heat and to paludism, as a sequel to dysentery, and even as a form of bubonic 
plague (pestis minor). Bacterial evidence disposes of the last theory, but 
in the presence of epidemic plague these cases demand careful study. 

Symptoms. — They begin with moderate swelling, redness, and tenderness 
of the inguinal or crural glands of one or both sides. At the outset there 
is usually a chill, fever of a remitting type, headache, and backache. The 
buboes slowly increase until they attain the average size of a hen's egg, 
after which the fever gradually diminishes. After persisting from one to 
two months or longer they gradually disappear. In the large majority of 
cases the inflammation is limited to the gland structure proper. The peri- 
glandular tissues and skin are not involved and there is very little pain or 



DYSENTERY 227 

tenderness. In from 3 per cent, to 5 per cent, of all eases the inflammation 
spreads to the periglandular tissues. The skin becomes adherent over the 
glands and they finally suppurate. In these cases the constitutional symp- 
toms are intensified and the pain and tenderness are very great. The 
abscesses tend to burrow freely. After a period of free suppuration deep, 
sharp-edged, indolent, painful ulcers remain. The average duration of the 
suppurating cases is from two to three months. 

Treatment. — The febrile condition is not severe enough to demand special 
treatment. Iodine and ichthyol may be applied to the skin over the gland, 
and, after acute symptoms subside, mercurial ointment and elastic pressure 
should be used. 'When suppuration takes place the gland must be laid 
open. Rife advises calomel as a dusting-powder to control the severe pain 
in the chronic ulcers. 

DYSENTERY. 

Definition. — Dysentery is a condition characterized by diarrhoea, abdom- 
inal pain, and the presence, as a rule, of considerable quantities of mucus 
in the stools. When the condition becomes chronic it is often interrupted 
by periods in which constipation supplants the diarrhoea. Dysentery is to 
be separated from the diarrhoea due to indigestion and to catarrh of the 
small bowel by the facts that tenesmus is usually marked, the lesions are, 
primarily at least, in the large bowel, and the stools are, in the early part of 
the attack, rather scanty and consist of mucus and blood. 

It is, moreover, to be distinctly understood that dysentery is not a single 
disease, but that this term is applied to the conditions and symptoms which 
develop as the result of several distinct causes, although at present there is 
much confusion as to the causes of the various forms. Strictly speakirg,' 
amoebic dysentery should be classed among the diseases due to animal 
parasites, but it is best, from the clinical standpoint, to discuss it here. 

At the present time at least four well-defined types of dysentery are 
recognized, namely, that which is known as bacillary dysentery, which is 
due to infection with the specific bacillus of Shiga, or a bacillus nearly 
related to it. Second, amoebic dysentery, intestinal amoebicsis (Musgrove 
and Clegg), which is due to the Amoeba dysenterice. This form is 
found in all parts of the world, but is much more frequent in 
the tropics, from w^hence most of the cases seen in this country 
come. Strong, of the United States army, reports 561 cases of amoebic 
dysentery out of 1328 cases of dysentery in his service. Third, catarrhal 
dysentery, which is apparently not due to a definite infection, but to acute 
congestion of the mucous membrane of the colon; and finally, fourth, 
diphtheritic dysentery, which is not due to the Klebs-Loeffler bacillus, but 
is characterized by a yellowish exudate on the mucous folds of the bowel 
with areas of ulceration and necrosis. A form of catarrhal dysentery some- 
times also develops as the result of renal disease. 

History and Etiology. — Epidemics of dysentery have occurred since the 
earliest times, and Herodotus mentions one which ' attacked the army of 
Xerxes in the year 480 B.C. During the first part of the Christian era the 



228 DISEASES DUE TO A SPECIFIC INFECTION 

disease raged in France, Germany, and England. It has existed in Europe in 
pandemic form on at least two occasions, namely, in the years 1538 and 1779. 

In the year 1729 an epidemic, in which 5000 persons died, occurred 
in Holland, Friesland,, Guilders, and Liege. More than 2000 of 
Napoleon's soldiers died from it during the expedition to Egypt, and 
4000 cases occurred in the English army during the Crimean war. 
About one-fourth (288,000) of ail cases of sickness among the soldiers of the 
War of the Rebellion were said to be cases of dysentery. In the year 1890 an 
epidemic broke out in the province of Tuhuoka, Japan. This province 
had a population of 1,231,387, of which 25,272 were attacked. Of these 
25,272 cases 4742 proved fatal Smaller but equally fatal epidemics of the 
disease have repeatedly occurred on crowded ships and in periods of famine. 
Further than this it has long been recognized that this epidemic form of 
dysentery was distinctly infectious, and it can even be spread from one con- 
tinent to another by infected ships, as in the great outbreak in the United 
States from 1846 to 1856, when it was probably conveyed by emigrants 
from Ireland, where the disease was rampant. More recently an instance 
of ship conveyance of the disease has been reported from the New Hebrides. 
Davidson states that in the decade of 1841 to 1851 no less than 50,019 
persons died in the Irish workhouses from dysentery. 

Marshy lands seem to have a pronounced predisposing influence. Water 
which has been contaminated by those who are ill with the disease is an 
important factor in its spread. Milk and solid food may also carry the 
infection. 

Dysentery in its various forms is, in a large proportion of cases, the 
result of bad sanitation both as to surroundings and diet. It is much less 
frequent at present than in times past, and rarely ravages modern insti- 
tutions or armies as it did fifty years ago. 

Epidemic dysentery being exceedingly prevalent in Japan in 1897, Shiga, 
a Japanese investigator, became interested in its bacteriological study, and 
isolated from the stools of 36 patients suffering from this disease a slightly 
motile bacillus having rounded ends and decolorizing by Gram's method. 
When brought into contact with the blood serum of patients suffering 
with dysentery this bacillus usually agglutinates (as does the typhoid bacillus 
in the Widal test), although in a few mild cases the reaction fails to take 
place. Flexner, Strong, Kruse, Vedder and Duval, Vallard, Musgrave, 
Craig and Dopter, Spronck, Rosenthal, and other investigators have isolated 
in such cases organisms which they consider closely related to or identical 
with the one observed by Shiga, and which they believe to be the cause of 
acute epidemic, sporadic, and institutional dysentery, 

Recently (1902) Duval and Bassett have obtained a similar organism 
from the stools of children suffering from dysentery or the summer diarrhoea 
of infants. Still more recently (1903) Wolf stein, Park, Dunham, and Carey 
have not only confirmed these findings, but have shown that at least two 
bacilli are present in cases of cholera infantum and dysentery. One of 
these corresponds to Shiga's bacillus, but they believe that in all probability 
several closely allied pathogenic bacilli will be found responsible in different 
epidemics. The bacilli are found in numbers proportionate to the severity 



PLATE IV. 








#■> 




v%- 



^^ 








• ® 



, 





Amoebee from Cases of Dysentery and Enteritis. (Roemer.) 



DYSENTERY 229 

of the illness, but often are not demonstrable in the stools until the latter 
are typical of the disease, and usually only after the lapse of five to seven 
days of illness. Chantemesse and Widal assert that a bacillus which they 
found in the stools of five dysentery patients, and which they also recovered 
from the mesenteric glands and intestinal wall of a patient who died of 
dysentery, is identical with the Shiga bacillus, and as their observations 
were made in 1888, ten years before Shiga published the results of his work, 
they claim priority of discovery. In France and Italy it is generally con- 
ceded that they were the first to find a specific organism in cases of dysentery. 

Our recognition of the presence of amoebae in cases of dysentery dates 
from 1859, when Lambl first discovered an amoeba in the stools of this type 
of diarrhoea. Later the parasite was studied by Losch (1875) and Kartulis, 
but it was not until Osier (in 1890), Councilman, and Lafleur (1891) reported 
upon its presence in several cases of dysentery, and in the past decade, that 
it received the attention that it deserves. Leukart has placed the Amoeba 
dysenterice in the class of rhizopoda of the Protozoa. Schandinn calls it 
Entamoeba histologica or Entamoeba dysenterioe. 

The Amoeba dysenterioe is a spheroidal cell, four or eight times the size of 
the red blood cell. It consists of two parts, an internal part called the 
endosarc, or endoplasm, and an external part called the ectosarc, or ecto- 
plasm. These two parts cannot always be clearly recognized when the 
organism is at rest, but they are easily identified when motion is present. 
The endosarc makes up the greater part of the body and its granules may 
be fine or coarse. In this portion several vacuoles are not rarely found 
and a distinct nucleus is discernible when the organism is stained.- As in 
ordinary amoebae the Amoeba dysenterice often contains foreign bodies such 
as red blood cells, and even bacteria. The pseudopod, or arm, which is 
protruded from the amoeba when it is engaged in amoeboid movement, is 
of the hyaline ectosarc. (See Plate IV.) 

In addition to this particular amoeba other forms have been described 
by Quincke and Roos and other writers. One of these is much larger than 
that just described, called the Amoeba intestini vulgaris, which is not capable 
of producing dysentery in man. The other is the Amoeba coli mitis, which is 
pathogenic for man. It also is far larger than the amoeba coli of Losch — that 
is, the Amoeba dysenterice of Councilman and Lafleur. The latter parasite is 
found in the stools of acute and chronic dysentery, in the floors of the intes- 
tinal ulcers, and in the secondary abscesses which it is prone to produce. 

It is to be distinctly understood that two distinct types of infectious dysen- 
tery exist, one due to the bacillus of Shiga and one to the Amoeba dysenterice 
Indeed, a third division due to the Balantidium coli may be made. Savalier 
has collected 75 cases of this character and our own Strong has reported 
others. 

Amoebic dysentery may occur at any age from infancy to senility, but it 
is most common between twenty and thirty years of age., It is much more 
common in men than in women. Thus, in 119 cases reported by Futcher 108 
were males. 

Prevention. — Dysentery in all its forms is to be prevented by the use of 
boiled water and cooked foods, by the establishment of proper drainage, 



230 DISEASES DUE TO A SPECIFIC INFECTION 

and by the avoidance of cold and wet. Persons who are subject to catarrh 
of the colon and rectum should wear a flannel binder. When the disease 
develops, the stools of the patient should be thoroughly destroyed and the 
greatest care exercised that the food and drink of the healthy are not 
contaminated by his discharges. 

Frequency. — Until very recently it was generally supposed that amoebic 
dysentery was the type of the disease most commonly met with in the 
United States, but now that Shiga's bacillus has been found in many cases 
of sporadic and epidemic diarrhoea in this country it must be regarded as 
the less frequent form of the two. Indeed, it would seem probable that 
many of the cases hitherto regarded as catarrhal are due to this bacillus. 
(See also Cholera Infantum.) 

Pathology and Morbid Anatomy. — In bacillary dysentery, when death has 
occurred in the first week, the autopsy reveals the mucous membrane of 
the colon to be intensely corrugated and swollen, so that its natural rugosities 
are greatly emphasized, while over them is spread an easily detached layer 
of superficial epithelium, which has undergone necrotic changes. Numerous 
spots of ecchymosis, or hemorrhage, into the mucous membrane are often 
present, but ulcers are not found, although the necrotic process just named 
may be so severe that a superficial gangrene may be present. When the 
inflammation is very intense the whole thickness of the bowel wall may be 
indurated, and even the visceral peritoneum may be infected. In some 
instances an associated inflammation of the small bowel is present, some- 
what similar changes being present in its coats. 

Shiga described the morbid process of acute bacillary dysentery as a 
catarrhal inflammation proceeding to hemorrhagic, diphtheritic, or ulcerative 
inflammation. Kruse also observed diphtheritic membranes in eight cases 
which came to autopsy, and Flexner recognizes the tendency to their 
formation, although he did not find any in the cases which he examined 
postmortem in the Philippines. 

Craig has reviewed the morbid anatomy of chronic cases of infectious or 
bacillary dysentery, recognizing follicular, diphtheritic, and gangrenous stages. 
In the first the coats of the colon usually are thickened, and the follicles, par- 
ticularly of the caecum, ulcerated. The mucosa is of a gray-slate color, and 
shows patches of acute congestion ; the gut is narrowed, but there are areas 
of dilatation. The ulcers appear at the summit of the follicles as minute, 
ragged erosions. Later the necrotic areas extend, and their margins appear 
stamped out, but undermined. The ulcers measure J to J cm., but may 
attain diameters of 1.5 cm. and extend to the submucosa or muscular layer. 
Cicatrized and open ulcers may be found together. In the diphtheritic 
stage, which may be implanted on the follicular, the colon is grayish or 
greenish-blue, marked by red or dusky-brown areas and greatly thickened. 
The mucosa becomes necrotic, exfoliates in masses or irregular patches 
composed of granular detritus, leukocytes, and innumerable bacteria. Ulcer- 
ation practically always accompanies the formation of the membrane. The 
gangrenous stage seems but an intensification of the diphtheritic. The 
serosa is more affected, and matted adhesions are the rule. The necrotic 
colon is easily torn, greenish-black, and marked by inky-black areas. The 



DYSENTERY 231 

ileocecal region is sacculated, and the sigmoid flexure and rectum dark 
olive-green in color. Tumefied, purulent elevations show through the serous 
coat. Internally the mucosa shows an indescribable admixture of necrotic 
or gangrenous lesions, with purulent suffusion of all the coats of the colon. 
In each of the foregoing forms parts of the mucosa escape, and these manifest 
more or less catarrhal inflammation. The protean manifestations of bacillary 
dysentery, both acute and chronic, are so influenced by the pathogenicity of 
the infecting organism, the activity of mixed or associated infection, suscept- 
ibility of the patient, duration of the process and other factors that an exact 
description is impossible. 

The noteworthy difference between the lesions produced in children and 
adults by the Bacillus dysenterice is that in the former the solitary and agmin- 
ated lymphatic tissues are much more commonly and more severely affected 
than in adults. 

The lesions of amoebic dysentery are quite different from those of bacillary 
dysentery. In the first place the ulceration is confined almost entirely to 
the large intestine, although the lower part of the small intestine may be 
slightly affected. The submucous tissues become infiltrated and swollen 
in patches, which project above the level of the normal mucous membrane. 
These infiltrated areas undergo necrosis and slough away, leaving ulcers 
which may be superficial or deep, and which may extend as far as the 
peritoneal coat of the intestine, but perforation is rare. They are often 
very large and extend laterally as well as downward. The edge of the ulcer 
may be undermined and the floor honeycombed. Not rarely the extension 
laterally takes place under the mucosa or dissects the muscle coat so that 
there is only a small opening to a large area of necrotic tissue. Occasionally 
the submucosa is necrotic without evident superficial lesions. The amceho? 
are found in the ulcers in the neighboring lymph spaces and sometimes in 
the bloodvessels of the part, but there is an extraordinary lack of pus when 
the severity of the necrotic process is considered. 

When recovery takes place fibrous tissue covered by epithelium closes the 
spaces made by the ulcers, and as these scars contract strictures may 
develop. The colon becomes thickened and it may be adherent to the 
adjacent structures and uneven contractions form pockets in which the 
parasites may linger after apparent clinical recovery. The appendix may 
be involved. 

The changes in the liver in amoebic dysentery consist of two alterations. 
The first are multiple areas of local necrosis, and secondly abscess, either 
single or multiple. The single abscesses are usually large and in the con- 
vexity of the right lobe, or else in the concavity of the liver where it lies 
nearest the large bowel. Roux has collected 639 cases of amoebic abscess 
of the liver. Of these, 435, or 70.8 per cent., were in the right lobe; 85, or 
13.3 per cent., were in the left lobe, and 2, or 0.3 per cent., were in the 
lobus Spigelia. The multiple abscesses are usually small and widely scat- 
tered and often near the surface. It is noteworthy that these so-called 
abscesses do not contain true pus unless secondary infection with pus 
organisms has occurred. They are composed of a grumous material made 
up of a thick, coarse, irregular reticulum, in the meshes of which lie 



232 DISEASES DUE TO A SPECIFIC INFECTION 

the semi-fluid contents. As the area increases in size the fluid becomes red- 
dish, brownish, greenish-yellow, or chocolate color, and is mixed with pieces 
or shreds of broken-down hepatic tissue. Amoebae may be found in the 
contents of these cavities. 

Abscess of the liver due to the Amoeba dysenterice nearly always develops 
in the first few weeks of the disease. Occasionally one of the larger 
abscesses ruptures into the right lung. (See Complications.) Boston has 
collected statistics of 2340 cases of amoebic dysentery. Of these, 486, or 20 per 
cent., suffered from hepatic abscess. (See Hepatic Abscess.) The percentage 
varies from 60 per cent. (Kartulis) to 21 per cent. (Councilman and Lafleur.) 

A valuable contribution to the subject of the associated lesions of dysentery 
has been made by Craig, of the United States Army Medical Staff. Analyzing 
120 cases of dysentery, of which 60 were of the bacillary and 60 of the amcebic 
tvpe, he found that in nearly every instance the autopsy revealed an increase 
in the cerebrospinal fluid and oedema of the brain. In the amoebic cases an 
intense congestion of the cerebral vessels was also present, and in 50 per 
cent, minute capillary hemorrhages were present. In the bacillary cases, on 
the other hand, the brain seemed unduly anaemic. In the respiratory system 
bronchopneumonia is the most common lesion in the bacillary disease. Craig 
believes that fully 60 per cent, of the cases of dysentery seen in the San 
Francisco Military Hospital have coincident nephritis, and of the 120 cases 
already cited no less than 101 had this condition, usually of the parenchyma- 
tous type. More cases of nephritis occur in the amoebic than in the bacillary 
type. 

In the acute catarrhal form there is a free production of mucus which 
coats the surface of the lower bowel, chiefly in the sigmoid flexure and 
rectum. This mucus is filled with exfoliated epithelium, some of which has 
undergone fatty degeneration. Not infrequently blood cells are present in 
the mucus. When the inflammatory process is severe, marked congestion 
and infiltration of the mucous membrane and submucosa may be present, 
and even a purulent and superficial ulceration may occur. 

The diphtheritic type is characterized by congestion of the mucous mem- 
brane and the development upon its surface of a false membrane. The 
connective tissue under it, and between the glands, is infiltrated and filled 
with fibrin and pus. In cases in which the process is very active, the inflam- 
mation may reach not only the muscular coats, but even the peritoneal coat. 
The area covered by the false membrane varies greatly in different cases. 
In some only the rectal mucous membrane is affected, in others a con- 
tinuous exudate covers the entire colon, and in still others it appears in 
scattered patches. If the process is severe healing takes place by sloughing 
of the necrotic tissues, which may reach to the deeper layers of the bowel, 
leaving ulcers which gradually undergo cicatrization, or the ulcers remain 
granulating surfaces for months and only heal under direct treatment. 

Symptoms. — The symptoms of all the various forms of dysentery are 
closely similar. The onset is usually sudden, or it may develop in the course 
of a gradually increasing diarrhoea, which at first is thought to be an ordinary 
attack of looseness of the bowels. The patient suffers from wretchedness, 
which is thought to be the result of the intestinal disorder, and often has, 



DYSENTERY 233 

in the earliest stages, a considerable degree of griping pain. The initial 
diarrhoea soon sweeps the bowels clean of their normal contents, and as 
soon as this is accomplished the stools become scanty and consist largely 
of mucus which, not rarely, contains blood. The griping pain increases in 
violence, and there is marked tenesmus which often causes the patient to 
break out in a profuse sweat. The rectal irritation causes a constant desire 
to go to stool, which is not satisfied by the small evacuation that occurs. 
At first the constant irritation of the anus may cause spasm of the sphincters, 
but later when the disease is severe the sphincter ani may become relaxed, 
and even rectal prolapse may ensue. The centres in the spinal cord con- 
trolling the bladder become reflexly irritated and difficult urination may 
add to the suffering of the patient. 

It is manifest that such symptoms must speedily cause grave systemic 
disturbance by reason of the loss of nutritive material, the constant pain, 
the loss of sleep and straining, and so the pulse soon becomes rapid and 
feeble, and the patient rapidly emaciates not only because of the reasons 
just cited, but also because the local lesion in the bowels soon results in 
general systemic infection, either with the specific cause of the attack or 
with other micro-organisms which gain access to the general system through 
the diseased intestinal wall. 

The tongue is very foul and the secretions of the mouth scanty. 

If the disease persists the scanty mucous stools may be supplanted by 
more profuse serous discharges, which are often reddish in hue, and seem to 
contain small particles of flesh (probably bloody mucus and mucous mem- 
brane). This fluid is highly albuminous. The debility and emaciation of 
the patient speedily becomes profound, as the loss of fluid and albumin 
continues. Whether the stools are mucous or serous, they are fetid and have 
an odor which is quite characteristic. 

In that form of dysentery called bacillary the fever at first may rise as 
high as 103°, but in the .amebic form the temperature is usually not greatly 
disturbed unless secondary abscess develops. It rarely rises above 102°, 
and may be subnormal after the stage of onset. 

When the infection with Shiga's bacillus is very virulent, death from 
toxaemia and exhaustion may occur as early as the fourth day, but, on the 
other hand, the case may last for much longer periods before the fatal result 
ensues. There is sometimes met a subacute form, which lasts, in a modified 
type, for weeks or even months. 

Cases of amcebic dysentery may be divided into three types : (a) A mild 
form in which the general health remains good, although the number of 
stools may vary from two to six in a day. (b) A moderately severe form in 
which the general health is greatly impaired and there is much loss of 
flesh, with an evening rise of temperature and frequent stools, (c) A very 
severe type is met with in which the prostration and loss of weight are 
extreme, the stools are bloody and very frequent, and the extremities 
cold. In all these cases the patient may without any apparent cause pass 
to better or worse with extraordinary speed. 

Amoebic dysentery may cause death in a few days or last for weeks, and 
may cause death finally by the secondary abscesses in the liver. Free hem- 



234 DISEASES DUE TO A SPECIFIC INFECTION 

orrhages from the bowel may also occur in this form, and perforation from 
deep ulcers is recorded. A chronic form of amoebic dysentery also exists 
which lasts for months and has temporary periods of constipation. These 
periods of constipation, if abscess does not develop, give the patient an 
opportunity to be nourished, and so he may be able to retain strength 
and flesh. 

In the acute catarrhal form of dysentery there may be fever at onset and 
scybalous masses will often be found mixed with the mucus which is expelled. 
After an illness of from four to seven days the quantity of blood in the 
stools is decreased, and they become less frequent. Marked abdominal 
tenderness over the course of the large bowel is usually present in all cases. 

In the acute diphtheritic form the patient is usually extremely ill from 
the very first. The systemic depression is marked and profound adynamia 
is quickly developed. The belly is distended and painful upon pressure. 
Bloody mucus is not uncommonly absent from the stools. Just as in the 
other forms so in this, a subacute or chronic type is met with in which the 
abdominal signs are mild and the number of stools a day are as low as 
four or five. 

Complications and Sequelae. — Perforation of the bowel has already been 
named as a possible sequel of the amebic form of the disease. In other 
instances a localized peritonitis develops, and as the result of infection of 
the tissues about the colon a perityphlitis or periproctitis comes on. Rupture 
of an hepatic abscess is a very frequent occurrence. The pus finds its way 
through the diaphragm into the right lung or right pleural space. Rarely 
it has burst into the duodenum and even into the vena cava, or backward 
and downward along the psoas muscle, or into the kidney. Even the peri- 
cardium and the bladder may be perforated. Strong has called attention 
to the occurrence of profuse intestinal hemorrhage. 

In many epidemics of dysentery there is associated mild or severe malarial 
infection which renders the case difficult of treatment in that two infections 
have to be controlled simultaneously. Septic arthritis, pericarditis, and 
endocarditis sometimes occur as terminal infections. (See Pathology and 
Morbid Anatomy.) 

Diagnosis. — The diagnosis that the patient has acute inflammation of the 
large bowel, and is therefore suffering from dysentery in one of its forms, 
is easily made if the symptoms just described are present. It is not, 
of course, so easy to determine which of the several forms of dysentery is 
present. The bacillary form is separated from the amcebic variety by the 
presence of marked fever, which is usually absent in the latter disease; by 
the discovery of the specific bacillus in the stools, which discovery, however, 
requires special training in searching for it; and by the agglutination test 
of the bacillus with the patient's blood serum, which, as in the case of the 
Widal test of the blood in typhoid fever, gives us such valuable informa- 
tion. This reaction is uncertain in the first week, often positive after the 
sixth day, but in some cases it does not occur for two weeks. For this 
reason it does not possess great diagnostic importance in the early stages 
of the disease. To be of value it must take place in a dilution of 1 : 200. 
The percentage of positive reactions according to Rosenberger is 80.2 per cent. 



DYSENTERY 235 

The amoebic variety can only be recognized during life by finding the 
amoeba in the stools. This requires some practice and skill. The small pieces 
of blood-stained mucus are the parts in which the organism is to be sought for, 
first with a low-power and then with a high-power lens. (See Plate IV.) The 
light coming through the instrument should be stopped down by an appro- 
priate diaphragm. Several negative examinations do not exclude amoebic 
dysentery, and particularly in chronic cases it is necessary to make repeated 
examinations. In such cases acute exacerbations may afford stools relatively 
rich in amoebae even when intercurrent examinations have been negative 
several times. The stools should be as fresh as possible, unmixed with 
urine, and, if not warm, the slide examined should be warmed gently or 
placed on a warm stage so as to induce movements of the amoebae. If an 
organism which possesses active amoeboid movement is discovered and if 
it contains several red blood cells the diagnosis is practically assured. 

When examining the. stools it is essential to bear in mind that a multitude 
of intestinal bacteria are also present and that various parasites other than 
the specific amoeba may be present. Thus, the Trichomonas intestinalis and 
the Cercomonas intestinalis are often found. Thayer has recorded a case in 
which the Strong yloides intestinalis was present as an additional parasite. 

The diphtheritic form is to be suspected if from the first the patient 
seems profoundly adynamic. Typhoid fever is to be separated from dysen- 
tery by the fever, the rose rash, and the Widal test. 

Prognosis. — The prognosis in dysentery depends to some extent upon the 
variety of infection which is present, and upon the hygienic surroundings 
and vitality of the patient, for even the mildest types may be fatal if the 
patient receives bad food and is exposed to excessive heat or cold or wet. 
When the bacillus of Shiga is the cause the prognosis in acute cases must 
always be most guarded, both as to the recovery and the duration of the 
illness. The mortality varies greatly in different epidemics in different 
parts of the world. Thus in Japan, Shiga found it varied from 22 to 55 
per cent. In this country the mortality has been as low as 3 per cent. 
The general state of emaciation and depression must always be con- 
sidered. If the stools contain gangrenous sloughs, the outlook is of 
course very grave; and if hiccough, great nervous depression, and low 
delirium develop, the outlook is probably fatal. 

In the amoebic type the development of abscess in the liver of course 
adds very greatly to the gravity of the case ; but even when amoebic abscess is 
present and ruptures into the lung, it is possible for recovery to take place, 
if proper surgical measures of relief are undertaken. 

Even the most urgent cases may, when apparently near to death, recover, 
but convalescence is protracted. 

According to Duncan prognosis can be based, to some extent at least, on 
the character of the stools. He believes a good result can be foreshadowed 
in those cases in which are passed mucus with minute fecal lumps, stained 
or not with blood, and in which the blood and mucus disappear, after which 
the ordinary fecal characters will soon manifest themselves. 

The prognosis is of evil omen, according to Sir Joseph Fayrer: (a) 
in the cases in which pulpy stools without blood or mucus are passed; 



236 DISEASES DUE TO A SPECIFIC INFECTION 

(b) where fluid fecal matter is from time to time passed throughout the 
illness, the prognosis is unfavorable, inasmuch as these characters of the 
stools show the disease to be extensive, and affecting chiefly the upper part 
of the large as well as in some cases part of the small intestine; (c) where 
the stools in conjunction with the symptoms that are laid down as character- 
izing the true amoebic dysentery are present, the prognosis is again unfavor- 
able, on account of the high mortality that is said to attend this form of 
the disease; (d) the prognosis is of the worst possible character where the 
stools consist of blackish-red or blackish fluid with a horribly putrescent 
odor, and of bits of gangrenous tissue. Duncan has never seen a patient 
passing this character of stool recover. 

Treatment. — So far as diet is concerned it is self-evident that the food 
should consist of those substances which are readily digested and absorbed 
from the stomach and the duodenum, in order that as small a residue as 
possible may pass on downward into the large bowel. Milk, which is so 
universally resorted to in the treatment of all forms of diarrhoea, is not 
always as useful a form of nutriment as it is thought to be; for not uncom- 
monly it will be found that when milk is taken it remains undigested, or 
forms curds which are indigestible because of the feeble secretion of digestive 
juice. These curds pass through the bowels and afford pabulum for micro- 
organisms which, in turn, are injurious to the mucous membrane. If it 
is given, it should certainly be diluted freely with lime-water, barley-water, 
or Vichy water, or else it should be peptonized in order that its digestion 
may be readily performed; and it is of vital importance in this connection 
that it should be given in small quantities, frequently, rather than in large 
quantities. Solid food is, of course, contraindicated, but semi-solid foods 
like milk-toast, the digestion of which is aided by pancreatin or taka-diastase, 
and a very soft-boiled egg, will often prove a better diet than one which is 
more liquid, but less nourishing, since the physician, in the presence of 
dysentery, is faced by two opposing factors; on the one hand a feeble diges- 
tion, and on the other hand the necessity of supporting vitality to the 
highest possible point by the administration of proper foodstuffs. 

The treatment of the condition itself may be divided into three methods, 
and each one of these plans finds ardent advocates among those of the pro- 
fession who have had sufficient experience to make us feel that their opinions 
are of value. 

The ipecac plan may be considered among the first of these, and it cannot 
be doubted that physicians in tropical countries have found it of benefit in 
so large a number of cases that it is impossible to consider that they have 
been mistaken in their clinical observation. As Dr. Woodhull, late Assistant 
Surgeon- General of the U. S. Army, has said, the one remedy which, properly 
used, is as conspicuous in dysentery as quinine is in malaria is ipecacuanha. 
He gives the following directions for its use: 

"The stomach must be empty and the patient recumbent. About twenty 
minutes before giving the ipecac it is well to paint the epigastrium, not 
the whole abdomen, with tincture of iodine, or to apply a mild sinapism 
sufficiently to induce gentle counterirritation. This precaution, however, 
may sometimes be omitted, or may be deferred until the medicine has been 



DYSENTERY 237 

taken. Ten or 15 minims of laudanum may be given, always on an 
empty stomach, to be followed in ten or twelve minutes by from 15 to 30 or 
more grains of ipecac in pill form, or as a paste, with a very small quantity 
of water. No food or fluid should be taken for at least four hours, and 
recumbent rest should be strictly maintained. If the ipecac is administered 
in pill or capsule the laudanum may be mixed with it instead of given 
previously. One scruple of ipecac and 1 grain of opium can be made into 
four pills, or the laudanum can be put in the pills. When pills are used 
they should be freshly made. Or 20 grains of ipecac can be suspended 
in 2 fluid rachms of water with a few drops of an aromatic to disguise the 
taste. It is never advisable, on account of the popular idea associated with it, 
to disclose the name of the medicine, and the patient should be warned to 
resist any inclination to vomit. The size of the dose should be in proportion 
to the gravity of the case. Just as in severe colic very large doses of opium 
are tolerated, and in pernicious fever enormous quantities of quinine are 
indicated, so in dysentery surprisingly large doses of ipecac are well borne, 
although the magnitude of the dose should bear some relation to the severity 
of the disease. With a little experience, that relation will soon be deter- 
mined. Sixty grains is not a maximum dose for an adult, but w T ith ordinary 
acute dysentery from 15 to 25 grains at a time should suffice. If the first 
or any subsequent dose is rejected, which rarely happens if these rules are 
carefully followed, it is to be repeated after a short interval. The retching 
or vomiting of exhaustion or the restlessness of delirium is no bar, but 
rather an inducement to this treatment; and small children or delicate 
women can take it with impunity in proportionate amounts. 

"The common course in acute dysentery is, first, the relief of pain, next 
the subsidence of fever, and then the cessation of the bloody discharges. 
The usual sign that recovery is at hand is a painless, copious, semi-fluid 
evacuation, much the color of the ipecacuanha powder, not black as has 
been stated. The medicine then may be reduced or entirely suspended. 
In acute cases these results will follow very quickly. In chronic dysentery 
complete recovery may be delayed or, indeed, may fail of absolute attain- 
ment, but great amelioration may be confidently anticipated. That the 
powder should be pure and comparatively fresh is always essential." 

The second method of treatment is the purgative plan, which has come 
forward largely within the last few years, probably because of increasing 
experience on the part of American and English surgeons in the Philippines 
and in South Africa. Clinical evidence is rapidly accumulating which proves 
beyond all doubt that in a certain proportion of cases of acute dysentery 
the employment of sulphate of magnesium combined with aromatic sulphuric 
acid is a most advantageous method. The bowels are first thoroughly 
moved with Epsom salts or with Rochelle salts, and then aromatic sulphuric 
acid is given freely, so that it will exercise its well-known astringent or 
constipation influence. This plan is a more rational one than that which 
concerns the employment of ipecac, in that it is a well-known fact that the 
micro-organisms which are commonly found in the intestines in dysenteric 
cases are destroyed or rendered inert by an acid medium, and it has long 
been known by the profession that the administration of sulphuric acid is 



238 DISEASES DUE TO A SPECIFIC INFECTION 

apt to produce an acid reaction of the stools, so that its beneficial influence 
in dysentery does not rest alone upon its astringent effect, but upon its 
power to destroy the infecting micro-organisms, just as its use in Asiatic 
cholera meets the double indication of restraining diarrhoea and destroying 
the comma bacillus. 

The third plan of treatment consists in the administration of intestinal 
antiseptics, of which perhaps bismuth salicylate, benzonaphthol, and salol 
have been most commonly employed. Theoretically, it is easy to conceive 
that these substances may be advantageous, but practical experience has 
shown that they fail to exercise the degree of antiseptic influence with which 
they are credited, and they are not of sufficient importance to justify their 
employment to the exclusion of the ipecac or saline methods which have 
just been described. The employment of calomel and corrosive sublimate 
with good results in these cases rests upon the fact that they increase the 
activity of the liver, both in destroying toxic material and in secreting 
bile. 

Without doubt local treatment by high intestinal irrigations is of very 
great value. Copious clysters which will reach far up into the descending 
and transverse colon are necessary. In a number of instances the writer 
found that injections of sulphocarbolate of zinc, in the proportion of 20 
grains to the pint, have produced very satisfactory results, the zinc acting 
both as an astringent and antiseptic. Other practitioners have employed 
copious injections of weak solutions of nitrate of silver of the strength of 
1 drachm to 4 pints. The tenesmus which is frequently associated with 
the dysenteric condition, or on the introduction of the soft rectal tube, can 
sometimes be avoided by the use of a 10 grain iodoform suppository used 
half an hour before the injection is to be given. This suppository, by its 
local anaesthetic effect, is of service, and I have thought that the absorption 
of the iodine from it was also advantageous. 

The method of giving the intestinal lavage is of considerable importance. 
It should not be given with a Davidson or other pumping syringe, but 
always by means of a fountain syringe or surgical irrigator. The hydro- 
static pressure employed should never be greater than two or three feet, 
and it is much better that the injection should be gently given, so that it 
takes fifteen or twenty minutes to find its way up into the intestine, than 
that it should be delivered forcibly enough to produce angry contractions 
of the bowel, which will cause great agony and so much irritation that the 
treatment makes the patient worse. 

Where great irritability of the bowel exists it is probably better to employ 
two rubber catheters side by side, one being for the intake and the other 
for the outflow, since in this way great distention of the bowel is avoided. 
In instances in which cold-water injections seem inadvisable very hot water 
may be employed, but it is distinctly disadvantageous to employ tepid water, 
which has a relaxing and enervating effect, and does not possess the healthy 
stimulant effects of marked cold or high heat. Often it is best to employ 
normal saline solution, since by this means maceration of the intestinal 
mucous membrane is avoided. 

Specific treatment for bacillary dysentery promises much for the future. 



EPIDEMIC GANGRENOUS PROCTITIS 239 

Attempts to produce a protective and curative serum have been made, and 
Shiga maintains that he reduced the mortality of dysentery one-third by 
the use of such a substance. Up to November 1, 1899, he had treated 
156 cases with his serum, with a mortality of 8.5 per cent. During the same 
period 166 cases in Tokio and Honjo Hospitals under ordinary treatment 
gave a mortality of 37.9, and 398 at Komogone Hospital gave a mortality 
of 34.6. In private practice also mortality was high, 1119 cases giving a 
percentage of 28.5. Kitasato likewise obtained a low mortality rate by this 
plan of treatment. (See Cholera Infantum.) 

Another form of specific treatment is that which is directed to combating 
amoebic dysentery by means of injecting quinine bisulphate, in the strength 
of 1:5000, sufficiently high in the rectum for it to exercise its fatal effect 
upon the amoeba coli. Thymol 1 : 2500 may also be used in this way. 
(Thomas). Harris has highly recommended hydrogen peroxide given by 
injections as a parasiticide. 

Stimulants well diluted with water or with nutritive broths should be given 
if needed, and strychnine and quinine employed in convalescence as tonics. 

For the control of the diarrhoea when excessive, enemata of deodorized 
tincture of opium and starch-water are very useful. 



EPIDEMIC GANGRENOUS PROCTITIS. 

Definition. — Epidemic gangrenous proctitis is an acute contagious disease 
appearing as a rapidly spreading ulceration of the anus and rectum, with 
prolapse and gangrene of the ulcerated rectum and, in a large proportion 
of cases, death in coma or convulsions. 

This disease, originally believed to be limited to narrow areas in Central 
and South America, is now known to occur much more widely throughout 
the tropical zones. It is generally distributed in tropical South America 
and in Central America. It has been observed in the Philippines, the 
Celebes, and New Guinea. 

There is some question whether this affection should be regarded as a 
distinct disease entity or not. I (Kieffer) regard it as a localization of an 
intense dysenteric process unusually low in the colon, without hazarding 
any theory as to the cause of the localization. This idea is strengthened by 
the well-known liability in children to intussusception above the sigmoid 
in acute dysentery. It is quite fair to assume that the mechanism of the 
extrusion of the rectum in these cases is the same. 

Etiology. — Nothing is known of the direct cause of this curious condition. 
Ackers, of Curacao, states that it is the common belief of the natives in 
Venezuela that the disease is caused by eating unripe maize, of which the 
children are particularly fond. This seems hardly probable, although the 
symptoms of pellagra, which are assumed to be due to fermented maize, 
would indicate the possibility that unripe maize may account for the 
symptoms. The disease, however, has been observed in countries in 
which maize is practically an unknown food product. I (Kieffer) have 
reported one case in which the Bacillus pyocyaneus was undoubtedly the 



240 DISEASES DUE TO A SPECIFIC INFECTION 

active organism. A high degree of humidity seems an essential condition 
to the development of the disease. Ackers observed this disease in fowls 
and the smaller domestic animals, occasionally in calves. In Venezuela 
and New Guinea the disease is confined to children, particularly those of 
the poorer classes, and in the rest of the tropical world it also holds true 
that children are more frequently attacked than adults. 

Pathology. — The rectum and anus in early stages are affected by deep 
ulcers overlaid with a diphtheroid pseudomembrane. Two forms can usually 
be distinguished: the low form with limitation of the lesions to the rectum 
between the sphincters and the high form in which the disease extends well 
up to the sigmoid. 

Symptoms. — The disease begins with local symptoms referred to the anus 
and rectum. There is burning and intolerable itching followed by severe 
dysenteric symptoms. After twelve to twenty-four hours there is more or 
less constant and severe tenesmus. 

The evacuations, at first feculent, become mucoid and finally consist 
entirely of mucus and blood. The distress grows urgent, effort and pain 
become continuous, and there is a constant flow or bubbling out of slimy 
mucus stained with blood, or almost pure frothy blood. The evacuations 
are very fetid. As the disease progresses there is profound collapse. 
Nervous symptoms appear and the patients become either delirious or 
comatose. In children there may be convulsions. Emaciation is rapid 
and death usually occurs in convulsions or coma. If the patient sur- 
vives this stage the rectum is extruded and undergoes rapid necrosis and 
sloughing. 

In the early stages the diagnosis between epidemic gangrenous rectitis 
and dysenteric lesions in the descending colon can only be made by exami- 
nation of the rectum. In advanced cases the condition is self-evident. The 
mortality is very high, but even comatose patients need not be despaired 
of. Recovery occasionally occurs after prolapse and sloughing of the 
rectum. 

Treatment. — The Venezuelan treats this disease by introducing lemon- 
juice or diluted aguardiente into the rectum. When extrusion of the rectum 
occurs he keeps it dry by dusting with wood-ashes. Indications are for 
active antisepsis of the rectum with diluted creolin or hydrogen peroxide. 
Opium will be necessary for the control of pain, and is best applied directly 
to the diseased area. If prolapse occurs no effort should be made at first to 
replace it. The rectum should be dusted with an antiseptic powder or 
freshly made charcoal. If gangrene occurs the rectum must be extirpated. 



HILL DIARRHOEA. 

Definition.' — An acute morning diarrhoea with white stools and attended 
by marked flatulency. It is a disease of the acclimatized and not of the 
new-comer in the tropics. 

Etiology. — The etiological factors in the production of hill diarrhoea are, 
first, prolonged residence in hot countries with the establishment of acclima- 



HILL DIARRCEA 241 

tization, then an unaccustomed altitude, five to six thousand feet, with a 
high degree of humidity. Under these conditions the dweller in the low, 
hot plains who goes to the hills is very prone to fall a victim to this disease. 
It is consequently observed when business or relaxation takes the colonists 
into mountainous portions of the tropics. It is common in the hill sana- 
toria of tropical countries, particularly in India, where it was named Hill 
diarrhoea, Simla diarrhoea, etc. Hill diarrhoea bears a very close resemblance 
to sprue. The cardinal symptoms differ only in degree, but the tendency 
of hill diarrhoea is so constantly to recovery, and that of sprue so constantly 
downward, that they must be considered separately. 

Pathology. — Very little is known of the pathology of this peculiar con- 
dition. It seems to be clear that there is a temporary suspension of function 
of the liver and pancreas. This is probably the expression of exhaustion 
resulting from the extra strain on already overworked digestive organs 
seeking to adapt themselves to a further change of climatic conditions. 
Scheube thinks this condition depends on an atonic state of the colon which 
he believes to be a common sequel to long residence in hot countries, and 
that the diarrhoea is due to chilling of the abdomen in the unaccustomed 
cold and dampness of the early morning hours of the mountainous region 
of the tropics. 

The tendency in the vast majority of cases is to prompt readjustment 
and restoration within one or two weeks. A small proportion of cases 
persist and may end in typical sprue. Crombie reports cases in which cure 
has taken place only when the patients returned to the plains. In these 
cases every visit to the hills was followed by this diarrhoea. 

Symptoms. — Shortly after arrival in the mountains the patient is troubled 
with dyspeptic symptoms and a morning diarrhoea. On the succeeding 
days the diarrhoea becomes more troublesome until it reaches eight to ten 
movements daily. It comes on in the early morning, at or near dawn, with 
a sudden call to stool. It continues during the forenoon and ceases abruptly 
about mid-day. There is very little pain and that only as a vague, inde- 
terminate discomfort over the colon, and no tormina or tenesmus. The 
movements are large and frothy, they are devoid of coloring matter, and 
look like stirred mortar or whitewash. They have an unpleasant, mawkish 
odor. Dyspeptic symptoms are pronounced. There is distress after eating, 
particularly in the morning, and there may be marked tympanitic distention 
of the abdomen. 

Treatment. — Treatment is directed to the restoration of intestinal digestion 
and the maintenance of a relative degree of rest to the gastrointestinal tract 
by putting the patient on liquid or milk diet. Small doses of calomel to 
stimulate the hepatic function are of value. Similarly pilocarpine should be 
tried with the idea of increasing the flow of the pancreatic secretion. Judicious 
use of the digestive ferments should be made. These patients should be 
advised to keep to their beds during the morning hours. In persistent cases 
it may become necessary to send the patients down to, or near, the sea level. 



16 



242 DISEASES DUE TO A SPECIFIC INFECTION 



SPRUE (PSILOSIS). 

Definition. — Sprue (Atrophic Enteritis of the Tropics) is not a distinct 
morbid entity; it is but a terminal condition of many devitalizing and 
depressing factors. Sprue may be defined as a chronic catarrhal inflam- 
mation of the entire alimentary tract tending ultimately to most extensive 
atrophy of the gastrointestinal glandular structures, characterized clinically 
by three cardinal symptoms — sore mouth, flatulency, and diarrhoea. 

Sprue is a disease of the entire tropical world. The Malayan Archipelago, 
particularly the Philippine Islands, South China, Amoy, Ceylon, Java, and 
the Malayan Peninsula are the regions of its greatest development. 

It is not seen in subtropical or temperate zones, unless in imported cases, 
with the exception of Japan and northern China. It has been known by 
many names, all of them referring to one or another of the peculiar clinical 
manifestations of the disease. Thus, it has been called "diarrhoea alba," 
" aphtha? tropica?," " Ceylon sour mouth," and " white flux." The name 
sprue was given to it by the Dutch, who found it a veritable plague in their 
Javanese possession. Since the United States has acquired colonies in the 
sprue region, imported cases have become fairly numerous throughout this 
country, and their consideration is of great interest to the general practitioner. 

Etiology. — Extensive studies of the disease have failed to show any specific 
etiological factor. There is some argument whether sprue should be con- 
sidered a specific disease or whether it should be considered as a terminal 
state following other lesions. Sambon maintains the former. Extensive 
studies by army surgeons in Manila show that the latter view is the correct 
one. The disease commonly develops in the tropics, but may lie dormant 
for years after the return of the colonist to his home in the temperate zone. 

The conditions that predispose to the development of sprue are the 
following: The large majority of cases follow chronic amoebic dysentery and 
its sequela?, chronic ulceration of the colon and abscess of the liver, with 
prolonged suppuration. Following dysentery the intestinal parasites, and 
chief of these the uncinaria, are common antecedents of sprue. Next is 
the general deterioration in chronic malarial poisoning, and lastly syphilis 
is a cause. To these must be added the physical deterioration incident to 
prolonged residence in hot climates, even when no acute illness is suffered, 
and the following depressing conditions : childbirth and miscarriage, chronic 
disease of the kidneys, suppurating lesions anywhere, excessive fatigue, 
long marches, and prolonged campaigns. Some writers report the develop- 
ment of sprue as following the prolonged administration of iodides and 
mercury. Numerous organisms have been described as the cause of sprue 
and several parasites, particularly the strongyloides. Amoeba? are almost 
constantly found and various bacilli of the typho -colon group, but these 
must all be considered remnants of the preceding pathological condition 
rather than direct causes of the disease itself. 

Pathology. — Postmortem examination shows complete loss of subcutaneous 
and mesenteric fat. The tissues and cavities are extremely dry; the small 
intestine presents extreme thinning of its walls with atrophy of the mucosa 



SPRUE 243 

and, in some cases, entire destruction of the glandular structures. The 
serous coat is normal. Swelling and ulceration of Peyer's patches are seen 
and in many cases the colon presents the usual appearances of recent or 
present dysentery. Parenchymatous changes occur in the pancreas, liver 
and kidneys, and occasional areas of fatty degeneration are present. 

Symptoms. — Sprue is essentially a very chronic disease. The average 
duration is from one to two years, although cases lasting ten years or more 
are not by any means unusual. The patient is emaciated and anaemic. 
The complexion is muddy and sallow. There is great lassitude and weak- 
ness, and mental irritability with pronounced disinclination for physical and 
mental labor. The disease passes through numerous stages of ameliora- 
tion and numerous recrudescences, but its general tendency is always down- 
ward. The principal symptoms of sprue are sore mouth, diarrhoea, and 
flatulence. 

The mouth lesions of sprue are constant and striking. On examination 
the tongue is found unusually clean. The organ is small, pointed, and 
somewhat yellowish. Along the dorsum of the tongue, along its edges, and 
on the under side, particularly along the frsenum, there are numerous, fine, 
minute ulcers, with a thin, aphthous pellicle. These aphthous spots may also 
be present on the uvula and palate. Very commonly the tongue is covered 
with very superficial erosions from one-eighth to one-fourth of an inch in 
diameter, frequently coalescing and resulting in a serpiginous appearance. 
Where these marked lesions are temporarily absent, the tongue still has an 
unusually clean, dry, glazed appearance, and looks very much as though 
it had been recently varnished. The condition in older patients may be 
very much accentuated and extensive fissures may develop. The patient 
complains of soreness that may be limited only to the tongue, or may 
involve the palate or uvula, or the entire mouth. He particularly complains 
of burning or a stinging pain on taking salt or highly seasoned food. 
Occasionally the pain is also present on deglutition, and the progress of 
the food bolus on its way to the stomach is indicated by a burning and 
stinging pain in the gullet, showing that the oesophagus is in the same 
condition as the mouth. Nausea and vomiting are sometimes present in 
advanced cases : the vomiting coming on without reference to the time of 
taking food. Eructations and waterbrash are present; the appetite is very 
variable, sometimes being entirely absent, at other times ravenous. 

Flatulence is quite marked. The patient is swollen until the abdomen is 
tense and drum-like. In this condition the appearance of the very much 
emaciated figure, with extremely thin arms and legs, and large, inflated 
abdomen, is very characteristic. The flatulence is always aggravated by 
taking food and is accompanied by a constant sense of oppression and a 
gnawing and burning pain in the stomach. 

Diarrhoea is the most distinctive and constant symptom. There may be 
only one or two movements daily or there may be as many as ten or twelve. 
They are usually passed without pain; they vary very much in their 
character, but are nearly always liquid or semi-liquid. They are frothy, 
white, and have a fetid, mouse-like odor. Manson describes them as 
looking like recently stirred whitewash. They are usually remarkably large. 



244 DISEASES DUE TO A SPECIFIC INFECTION 

Their reaction is commonly acid. Microscopically they are found to contain 
bowel structure, a few red blood cells, and intestinal parasites, of which 
amoebae are the most frequent. 

As the disease advances emaciation and asthenia become extreme. The 
skin is dry and scurfy, the patient is unable to assimilate or retain food, 
and, in many instances, he involuntarily abstains from it on account of the 
severe pain in the mouth and throat. In all marked cases there is secondary 
anoemia, the red blood corpuscles being reduced as low as 1,000,000, with 
some degree of poikilocytosis and no leukocytosis. 

Diagnosis. — Diagnosis presents no difficulties, when the existence of such 
a disease as sprue is known and its cardinal symptoms are remembered. 
Incomplete cases in which one or the other symptom may predominate or 
be absent may give rise to some difficulties. 

Sprue in particular must not be confounded with chronic dysentery, 
although it is difficult, in cases where sprue develops from dysentery, to 
definitely mark the period where the one disease begins and the other ends. 

Prognosis. — If treatment is instituted before the atrophy of the bowel is 
too far advanced, cure is the rule. If, however, so much of the secreting 
surface of the bowel is destroyed as to make assimilation impossible, death 
is, of course, inevitable. 

Treatment. — Treatment consists in putting the patient on absolute milk 
diet. He should preferably be kept in bed and milk administered in small 
feedings. The quantity is increased as rapidly as possible, the mouth 
symptoms and the appearance of unchanged milk in the bowel movements 
being the index as to the quantity to be taken. If there be any increase 
in the amount of soreness of the mouth, the milk must be reduced for a time 
and later gradually increased, until the patient is taking from four to six 
quarts daily. This regimen must be persisted in from four to six weeks 
after the mouth symptoms disappear and the bowel movements become 
solid. Then soft diet should be resumed very carefully. Where milk 
cannot be taken, pure meat diet may be used or an exclusive diet of meat- 
juice. Success has also attended the exclusive use of a fruit diet. Recent 
observations have shown the value of fruit, particularly of berries, in the 
treatment of sprue as well as chronic dysentery. Manson reports the case 
of a man over fifty years of age, at which time of life the prognosis in cases 
of sprue is exceedingly grave. The patient was first treated, with little 
benefit, with milk diet and other special diets; finally the patient was put 
on a diet of strawberries. The stools at once improved and the patient was 
soon restored to health. This was not the only case in which recovery 
followed the use of strawberries. Manson considers this a decided advance 
in the treatment of sprue. Medicinally salol and Dover's powder may be 
given for control of the diarrhoea. For their tonic and reconstructive 
properties iron and arsenic should be used. These drugs have been shown 
to be of particular advantage in this disease when used by hypodermic 
injection. 



MALTA FEVER 245 



NASHA FEVER. 



Nasha, nasa, or nakra fever, first described by Fernandez and Mitra 
in 1894, is a specific fever confined to certain sections of India. It is pre- 
ceded by marked congestion of the nose and circumscribed swelling of the 
nasal septum. The disease begins with malaise, headache, and severe pain 
in the muscles of the neck, back, and shoulders. There may be a small, 
diffuse, rosy eruption. The fever is moderate and usually lasts from three 
to five days, gradually subsiding with the disappearance of the nasal symp- 
toms. In rare instances sudden diminution of the local symptoms has been 
followed by severe cerebral symptoms, coma, and death. 

The etiology is unknown. It occurs principally in adults, children and 
the aged being relatively immune, and it comes on usually in the summer 
months. Exposure, unhygienic surroundings, and poor food seem to be the 
predisposing factors. One attack does not confer immunity. 

There are some reasons for believing this to be an atypical form of malaria. 
It occurs in highly malarious localities, where, according to Bose, swelling 
of the nasal mucosa is a common symptom with fever. As against this 
theory, the malarial parasite has not been found in all cases and quinine 
is said not to be effective. 

Treatment is symptomatic. Puncture of the swollen septum is said to 
give great relief to the local and general symptoms. 



MALTA FEVER. 

Definition. — Malta fever, or, as it is sometimes called, "undularit fever," 
is a disease which is comparatively common in the island of Malta. The 
malady occurs not only in Malta, but along the shores of the Mediterranean 
Sea, and so is sometimes called " Mediterranean Fever." When it occurs at 
Gibraltar it is called " Gibraltar Fever " or "Rock Fever," and when in 
Italy, " Neapolitan Fever." The malady is due to an infection by the Micro- 
coccus melitensis. Its chief clinical characteristic is wave-like or undulant 
curves of febrile movement. There are also recurring exacerbations of fever 
with profuse sweats, pains in the limbs, swelling of the joints, and enlarge- 
ment of the spleen. 

History and Geographical Distribution. — Although the first accurate account 
of this disease was published in 1861 by J. A. Marston, who described it 
under the name of Mediterranean, remittent, or gastric remittent fever, it 
probably has been endemic in the islands and along the shores of the Mediter- 
ranean Sea for centuries. Hippocrates described cases of continued remittent 
fever which in their entire symptom-complex correspond with certain 
manifestations of undulant fever, and references to a protracted form of 
fever prevailing in Mediterranean countries were made by writers of the 
eighteenth century and by Sir William Burnett and Dr. Hennon early in the 
nineteenth century. While the disease is most common at Malta, Gibraltar, 
in the Balearic Islands, in Cyprus, in Crete, and along the southern coast 



246 DISEASES DUE TO A SPECIFIC INFECTION 

of Italy, evidence is constantly being produced to show that it has a wide 
distribution throughout tropical and subtropical regions. Cases of un- 
doubted authenticity have been reported from China, India, Porto Rico, and 
the Philippine Islands, and a fever occurring in Venezuela closely resembles 
it clinically, although no cases in which the specific organism has been 
obtained in cases in that country are on record. Recent investigations 
have revealed its presence in the United States, but all of the patients 
seem to have contracted the disease in some one of its endemic foci. The 
first case was reported in 1898 by Musser and Sailer, in Philadelphia, eight 
cases have been treated in the Army and Navy Hospital at Hot Springs, 
Arkansas, and another has recently been reported from Texas by Major C. 
F. Mason, of the U. S. Army. 

Etiology. — The pathogenic organism of Malta fever is the Micrococcus 
melitensis, which was discovered in 1887 by David Bruce, who isolated it in 
pure culture from the spleens of nine patients who died, and found it in 
two instances in blood drawn from the spleen during life. This microbe is 
a minute, round or oval coccus, staining readily with the aniline dyes, but 
not by Gram's method. It grows very slowly in bouillon, agar-agar, and 
gelatin, and agglutinates when placed in blood serum drawn from indi- 
viduals affected with the disease. A joint commission, appointed by the 
British Government, has proved it possesses great vitality, for the organism 
was found alive after sixty-nine days in dried, sterilized manured soil, 
after eighty days on dried fabrics, after seventy -two days in damp soil, and 
after thirty-seven days in sterilized water. When injected into monkeys it 
produces a malady similar to Malta fever, and its specific action in the 
human subject has been demonstrated by several cases of accidental inoc- 
ulation. Some investigators believe that this organism gains entrance to 
the body through the alimentary organs, others think that it enters through 
the respiratory tract, while still others are of the opinion that mosquitoes 
are the agents of its dissemination. Monkeys have been infected at the 
will of an experimenter, when forced to breathe an atmosphere laden with 
dust containing the specific organism. Horrocks has shown that in regions 
in which the disease is prevalent, milch goats are often infected and that 
they may excrete the micro-organism in their milk, so infecting human 
beings who partake of it. Malta fever is a disease of summer, being most 
prevalent in June and July. Persons of all ages are subject to it, although 
the period of its greatest incidence is said by Maltese physicians to be 
between the sixth and the thirtieth years. Sex appears to be without 
influence in its causation. One attack appears to confer immunity, at 
least for a number of years. 

Pathology. — The gross morbid changes observed after death vary some- 
what according to the stage of the disease in which death occurs. In those 
cases which die during the first four weeks of the attack, the spleen is invari- 
ably congested and enlarged and often is so soft that it resembles a large 
mass of clotted blood. The meninges, the liver, the stomach and intestines, 
and the kidneys are also frequently congested, and the lungs are always 
congested at their bases, while in some cases lobular consolidation takes 
place. The heart occasionally shows granular or fatty degeneration and 



MALTA FEVER 247 

in a few instances pericardial effusion occurs. In cases which die late in 
the disease there is evidence of a prolonged toxic action upon the tissues. 
The liver and spleen are larger than normal and of firm consistency, due to 
the formation of fibrous tissue, and the heart is usually pale, its walls are thin 
and its cavities dilated. The spleen is the only organ which shows charac- 
teristic microscopic changes, namely, an increase in lymphoid tissue and the 
presence of large numbers of the specific micro-organism. Sections of the 
liver and kidneys show granular or fatty degeneration. As to blood changes 
there is a reduction in the number of red cells, alterations in their size and 
shape, and a deficiency of haemoglobin. The white cells are often relatively 
increased, the basophiles being in excess. 

The incubation period is from three to twenty days, most commonly 
fifteen. 

Symptoms. — The onset of the typical or undulant form of the disease is 
gradual, and is attended by lassitude, anorexia, nausea, headache, insomnia, 
and slight evening elevation of temperature. As the morbific process advances 
the digestive and nervous symptoms become intensified, and the temperature 
rises slowly day by day, remitting somewhat each morning, until it reaches 
a level varying from 103° to 105°. Here it is maintained for a varying 
period of time, and then falls slowly with profuse sweating. The other 
symptoms abate simultaneously. Soon, however, the temperature rises 
again and a condition similar to the one just described supervenes, consti- 
tuting a relapse, of which several occur. The most noteworthy symptom of 
Malta fever is therefore the persistent recurrence of febrile movements which 
are wave-like in character, and which last from seven to twenty-one days. 
They are followed by a period of apyrexia or of very moderate fever, which 
lasts for a few days, when the febrile movement returns as before. In this 
manner the disease may persist for months, not being self-limited, as is the 
course of typhoid fever. The active fever, the profuse sweats, and the 
pain continuing for so long a period produce great exhaustion and emaciation. 
Sometimes cardiac or pulmonary complications arise which determine a 
fatal issue of the malady. 

In the majority of cases of this type, however, convalescence ensues, but 
it is slow and often attended by neuralgic and rheumatoid symptoms, and 
occasionally by orchitis. 

Variations from the typical form of the disease are not at all uncommon 
Some cases are characterized by rapid onset and the early development of 
severe constitutional symptoms, which usually end in death, while other 
cases run an extremely mild course with little constitutional disturbance 
other than general malaise and slow but progressive anaemia and emacia- 
tion. In this form the temperature is often intermittent, rising several 
degrees each afternoon and falling to normal or nearly normal the next 
morning. 

Diagnosis. — Accurate diagnosis of Malta fever depends upon the agglu- 
tinative serum test between the blood and the micrococcus, which should 
be made whenever possible. This reaction is almost always obtainable by 
the sixth day after the development of pyrexia and often as early as the 
fourth. F. J. A. Dalton, of the British navy, finds that trustworthy re- 



248 



DISEASES DUE TO A SPECIFIC INFECTION 







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suits are obtained by the use of a dilution of 
1 : 50, with a time limit of half an hour. 

Clinically, diagnosis presents many difficul- 
ties, for the different manifestations of the 
disease make it particularly liable to be con- 
founded with a variety of affections, such as 
typhoid fever, tuberculosis, chronic rheuma- 
tism, malaria, and malarial cachexia. Suspi- 
cion as to the nature of typical cases should 
be aroused by the presence of an undulating 
temperature curve and the characteristic fre- 
quent relapses. Additional aids to the differ- 
ential diagnosis may be named as follows: 

From malarial fever we can separate Malta 
fever by several factors which make differen- 
tiation possible. In the first place the absence 
of the plasmodium of malaria in the blood, 
and the presence of the Micrococcus melitensis 
in the spleen on puncture is of course a defi- 
nite means of separation. Again, the fever 
does not yield to quinine as does that of ma- 
laria, and the pyrexia is too persistent for the 
intermittent type of that disease, although at 
times the waves of fever may be abrupt enough 
to resemble it. Again, the marked arthritic 
symptoms and the neuralgic pains are not met 
with in malarial infection. 

The possibility of tuberculosis must be also 
considered. Careful physical examination of 
the thorax and abdomen will usually reveal 
signs of tuberculosis if it be present, and if 
need be the tuberculin test can be applied. 
Typhoid fever presents a temperature range 
after the first few days which does not re- 
semble that of Malta fever, and the absence 
of rose spots in Malta fever is also an impor- 
tant differential point. The presence of the 
Widal test will also aid in the differentiation. 

Duration and Prognosis. — The average dura- 
tion is from seventy to ninety days, although 
some cases last as long as six months. Prog- 
nosis as regards life is favorable, the mortality 
being about 2 per cent. From the evidence 
thus far accumulated it seems that the serum 
test may afford prognostic as well as diagnostic 
information, for it has been observed that those 
cases in which the agglutinating power of the 
blood serum is high during the early stages of 
the fever run a favorable course, while those in 
which the agglutinins remain low during the 



BERIBERI 



249 



entire course of the fever are subject to many relapses and a protracted con- 
valescence. A continuous rise with improving clinical symptoms indicates 
approaching convalescence (Bassett-Smith). 

Complications. — The principal complications are hyperpyrexia, cardiac 
failure, and pulmonary congestion. Pleural and pericardial effusions some- 
times occur, and persistent vomiting has been observed by Hughes, who 
regards it as a very dangerous complication. 

Fig. 42 




Temperature chart in the intermittent form of Malta fever. (Hughes.) 

Treatment. — Malta fever has to be treated solely on the expectant method, 
for there are no specific remedies. The diet should be nutritious and support- 
ing. Dalton, of the English navy, deprecates the practice of keeping Malta 
fever patients on liquid food. All his patients who do not have an evening 
temperature higher than 103° are put on solid food, such as eggs, bread, 
and rice, and in addition receive two or three pints of milk a day. If this 
diet is well borne, it is supplemented in the course of a few days by fish or 
meat. In severe cases with high temperature, foul tongue, and diarrhoea, 
nothing but liquid diet is given. Dalton also believes that patients whose 
temperature keeps below 102° are benefited by being allowed to sit up part 
of the time, it being necessary, of course, to have them avoid exertion and 
not remain up too long. The bowels should be carefully regulated. Cold 
spongings with friction should be used to reduce fever and the kidneys be 
kept active by mild diuretics. When the patient is strong enough to travel, 
he is greatly benefited by change of climate. During the early stages of 
convalescence he should receive inunctions of oils and cocoa-butter, get 
plenty of fresh air and sunshine, and receive aids to digestion, with iron to 
overcome his anaemia, which is always marked. 



BERIBERI. 

Definition. — Beriberi is sometimes called Endemic Multiple Neuritis, 
and is a specific infectious disease occurring in nearly all tropical and 
subtropical countries. The disease is endemic, is associated with marked 
evidences of peripheral neuritis, with sensory and motor palsies, and pro- 
found alteration of the motor mechanism of the heart. 

History. — The recognition of beriberi as a distinct morbid entity is almost 
as old as recorded medicine. The first mention of it was made by Strabo, 



250 DISEASES DUE TO A SPECIFIC INFECTION 

who describes the development of this disease in the Roman armies operating 
in Arabia (24 B.C.). It is also described in the medical writings of the 
Chinese of the second and seventh centuries. It has occupied an important 
place in the histories of all colonizing powers. Dutch and, later, British 
observers recognized its specific nature in the beginning of the nineteenth 
century. Our later knowledge of the disease, particularly the recognition 
of the specific pathological lesions, is due to the labors of the German 
teachers, Scheube and Baelz, in Japanese universities. 

Distribution. — Speaking generally, the centres of greatest intensity of 
beriberi are the Malayan countries. It devastates the coolie mining camps 
and the plantations of the Malayan peninsula. It has been a veritable 
scourge to the armies of England in India, and of Holland in Sumatra. It 
is always present in Japan, and in portions of the Philippine Islands it is 
very common and was the scourge of Aguinaldo's armies. It has occurred 
in widespread epidemics throughout the whole tropical and subtropical 
zones. It is found in the principal parts of the-world and has appeared 
as an asylum disease in many temperate regions. In the United States 
beriberi has been encountered with considerable frequency in the principal 
ports. It has been observed in asylums for the insane in Alabama and 
Arkansas. Birge and Putnam have encountered it among the fishermen on 
the Grand Banks. It seems very likely that beriberi occurs quite frequently 
in Louisiana. Within recent years it has been observed among Chinese 
fishermen from the Alaskan coast; by Currie and by Bailey in a settlement 
of Japanese at Cumberlands, British Columbia; in New Bedford whalers, 
and in several Dutch ships entering our ports. 

Etiology. — In studying the etiology of beriberi, the most striking fact is 
the part that the general hygienic surroundings play in the development of 
the disease. The chief factor is overcrowding. Where natives are crowded 
together, as in jails, ships, and barracks, particularly under poor hygienic 
surroundings, with an insufficient or poorly selected dietary, in the presence 
of considerable heat and moisture, the conditions are very favorable to the 
development of beriberi. 

The climatic conditions favoring the spread of beriberi are increased 
heat and increased humidity. Consequently, in tropical countries the 
greater number of cases are observed during the seasonal rains. In the 
Malayan peninsula Wright has observed the greatest number of cases during 
the prevalence of the southeast monsoon, during which season the relative 
humidity is at its highest. The disease is also observed with great frequency 
when these conditions are artificially maintained, as in the crowded, exces- 
sively heated and poorly ventilated forecastles of ships carrying Lascar or 
Coolie crews. Beriberi, as a rule, is a disease of lower levels and ceases 
abruptly at 3000 feet above the sea, although even in this important point 
exceptions have been noted. 

With regard to the specific etiology of beriberi much confusion has existed. 
Two principal views are held: The first, and the one to which all the later 
evidence points as the correct one, is that the disease is due to a specific 
germ infection, and, second, that the disease is a nutritional disorder con- 
sequent on either deteriorated or deficient food, or a nitrogen starvation. 



BERIBERI 251 

Gelpke, Miura, and Grimm have advanced the theory that in various ways 
fish were the infecting agents or carriers of the infection of beriberi, the 
various theories ranging from the latency of infected or spoiled fish to the 
specific statement that beriberi is due to eating raw fish, particularly a 
number of varieties of the scomboidse (Miura) or the infection of dried fish 
by a species of trichina (Gelpke). 

The recent exceedingly valuable studies by Wright have definitely excluded 
the fish theory, since his observations were made among a number of prisoners 
from whose dietary fish was totally excluded. Ross has recently suggested 
the idea that beriberi may be due to arsenical poisoning. In pursuing 
these studies he found arsenic in appreciable quantities in the hair of a 
number of cases from Penang. Manson has called attention to the very 
common adulteration of Chinese tobacco with arsenic in order to give a 
particularly desired garlic flavor. These cases must, however, be consid- 
ered accidental or coincidences in which laborers in arsenical ores, canned 
provisions, adulterated tobacco, etc., have added to the symptoms of beri- 
beri a chronic arsenical poisoning closely resembling beriberi. Competent 
observers have failed to find arsenic in the great majority of cases. 

The greatest conflict has always been waged over the theories connecting 
beriberi with rice and rice-eating. The disputants are divided into two 
classes, one of which considers the disease as a toxaemia due to a fungus 
poisoning of the rice, placing it in the category of diseases like chronic 
maize intoxication, or pellagra. The second class assumes that with rice 
as the bulk of an inadequate dietary the disease develops as the expression 
of nitrogen starvation. It is indeed curious to see how universal is the belief, 
in countries and among peoples where beriberi is endemic, that the disease 
is due to bad rice. In the Philippines the sailor or convict suffering from 
beriberi not only ascribes his condition to rice, but will confidently point 
out the particular rice which has brought him to his evil state. There is 
very much that is significant in the facts adduced in support of this theory. 
The disease is known to affect almost entirely the rice-eating peoples, and 
it is carried by these people into new regions. Perhaps the most suggestive 
of all facts in the etiology of beriberi is the extraordinary decrease in the 
cases occurring in the Japanese navy and army coincident with an improved 
dietary, in which a large part of the rice component of the nation was substi- 
tuted by bread and meat. But it must also be remembered that at the same 
time the most pronounced advances were made in Japan in general hygienic 
and sanitary reforms, and a large part of the good results must be ascribed 
to these. 

As against the theory that rice diet involving nitrogen deficiency is the 
cause of the disease we have a host of valuable observations. In the Dutch 
armies dietary changes produced no mitigation of the disease. Wright in his 
observations in Kwala Lumpor Jail, in the Federated Malay States, kept 
the prisoners on a dietary in which there was a decided preponderance of 
nitrogenous elements with the same incidence rate of the disease. Finally, 
in this country Ashmead in New York and Daland in Philadelphia have 
observed the disease in sugar ships that had no rice aboard. Nevertheless 
it must be conceded that nutritional disturbances which are very commonly 



252 DISEASES DUE TO A SPECIFIC INFECTION 

present in rice-eating peoples have a distinct predisposing influence to the 
development of the disease. With regard to the theory that smutted or 
infected rice is the cause of the disease, exhaustive examination of raw rice 
has revealed nothing but Aspergillus niger and Bacillus subtilis. In order to 
exclude this factor the rice has been boiled and prepared under two or three 
atmospheres of steam pressure, thus ensuring the destruction of any germ 
or toxin with entirely negative results as to the prevention or diminution of 
the disease. 

Other observers have connected the disease with various intestinal para- 
sites, uncinaria and strongyloides intestinalis, or with hsemic plasmodia 
(Glogner), but these have all been shown to be accidental complications, 
not causes, and due to the prevalence in given sections of either intestinal 
parasites or the malarial plasmodium along with the beriberi. 

There remains, then, the theory that the disease is due to a specific germ 
infection. The studies of Wright have given a very strong evidence in this 
direction. The statement of Wright's views is best given in his own words : 
"The theory of the causation of beriberi that fits the facts is that beriberi 
is due to a specific organism which gains entrance to the body via the mouth, 
that it develops and produces a toxin chiefly in the pyloric end of the stomach 
and duodenum, and that the toxin, being absorbed, acts atrophically in the 
peripheral terminations of the afferent and efferent neurons. Further, that 
the specific organism escapes in the feces and lodges in confined places 
through accident or careless personal habits of those affected by this dis- 
order, and that in the presence of congenial meteorological, climatic, and 
artificial conditions of close association from overcrowding, the organism 
becomes virulent and, gaining entrance to the healthy body in food, etc., 
contaminated by it, gives rise to an attack of the disease." 

This theory of the disease is also borne out by the peculiar epidemic 
extensions of beriberi and by the well-known infection of places, separate 
dwellings, particular ships, and certain wards or barracks in jails or camps. 
Wright has clinched his arguments by infecting monkeys, and also by pro- 
ducing typical beriberi in them by placing them in the cells with beriberi 
cases. I (Kieffer) have seen a typical case of beriberi in a monkey which 
was fed by a Filipino convalescent from beriberi, and have produced 
unmistakable beriberi in other monkeys in the same way. In support of 
the idea that the contamination is carried by the feces, the universal lack 
of any hygienic precautions in defecation or disposal of the fecal matters of 
the sick in tropical countries must be remembered. Also, that cleanliness 
of the anal region is very much neglected. When we finally remember 
that these peoples almost universally eat with their fingers, that the fingers 
are almost certainly contaminated with fecal matter, and that the custom 
is to eat out of a common bowl, these theories gain very much more weight. 
To complete the observations on the etiology of beriberi it must also be 
remembered how often beriberi has spread to the proportions of an 
epidemic in tropical countries following an epidemic of cholera. 

Frequency. — Beriberi is observed much more frequently in males than in 
females; not because there is any greater susceptibility in the male, but 
because women form a comparatively small number in Coolie camps, jails, 



BERIBERI 253 

prisons, and ships. Given an equal degree of exposure, there is no reason to 
believe one sex more resistant than the other. With respect to age, beriberi 
may be said to be a disease of early adolescence and adult life. Although 
it is true that cases have been observed in infants in the endemic areas, yet 
the occurrence of beriberi in children under ten years is very rare. The great 
majority of cases occur between the twentieth and fortieth year, although 
it must also be remembered that a large proportion of those exposed to the 
disease are young adults. 

Beriberi is chiefly a disease of the yellow races, occurring principally in 
emigrants. At the present day beriberi is very rarely observed in Europeans 
and North Americans. The white races enjoy a nearly complete immunity, 
due in part to the better hygienic conditions under which they live. 

The Prophylaxis of Beriberi. — When the disease breaks out in ships, jails, 
asylums, or barracks, these had, whenever possible, better be temporarily 
abandoned. They should then be thoroughly disinfected and whitewashed 
or repainted. Old woodwork should be scraped and painted or torn out. 
In ships the bilges should be cleaned. If dampness exists from deficient 
drainage it should be remedied. Ample ventilation must be provided. The 
dietary should be revised, and wherever possible beans or meal substituted for 
rice, and a sufficient amount of fresh animal food allowed. 

Pathology and Morbid Anatomy. — When death occurs rigor mortis is 
slight and of short duration. If the case be recent and acute, or if death 
be due to cardiac paralysis, the cadaver bears all the evidence of intense 
dyspnoea and cyanosis. The eyes are staring, the conjunctiva suffused 
with blood, the cervical veins tumid and full, the lips covered with bloody 
froth. In the atrophic cases there is very considerable wasting. In the 
dropsical cases the effusion is commonly associated with huge thoracic, 
pericardial, and abdominal dropsies and oedema of the lungs. In acute 
cases marked congestion of the pyloric end of the stomach and of the duo- 
denum with punctiform hemorrhages is found. The duodenal glands are 
swollen and congested. Wright considers this to be the specific lesion of 
the disease, and states that it is always found when the case ends fatally 
within three weeks of the beginning of the disease. 

The liver and kidneys are enlarged, hypersemic, and show cloudy swell- 
ing. The spleen is enlarged, but otherwise shows no characteristic changes. 
The heart is enlarged, the principal changes being found in the right 
side. The ventricle is both hypertrophied and dilated. Microscopically 
there is usually marked fatty degeneration of the myocardium. The 
intrinsic nerve cells of the heart show marked atrophic changes. The 
terminations of the vagus are also atrophied. The trunk of the vagus is 
not involved in early cases, but in later cases the trunk of this nerve as 
well as the splanchnics and phrenics are profoundly degenerated. The 
peripheral nerves show striking and constant changes. These begin with 
degeneration of the terminal branches of the nerves. Not only the mus- 
cular but also the cutaneous twigs, and in advanced cases the main 
nerve trunks, may be involved. The nerve changes are present in 
proportion to the extent and intensity of the paralysis during life. 

The voluntary muscles show similar changes in the distribution of the 



254 DISEASES DUE TO A SPECIFIC INFECTION 

degenerated nerves. The muscle fibres undergo fatty degeneration, the 
striations disappear, the nuclei are enlarged, and the interstitial connective 
tissue may be increased. The central nervous system shows in the brain 
and cord congestion of the meninges and brain substance, with increase 
in the cerebrospinal fluid. Degenerative changes can be found in the 
posterior ganglia, and sometimes atrophy of the posterior columns is present. 

Incubation. — The incubation period of beriberi has not been definitely 
determined. Pekelharing and Winkler have placed it as being a long one, 
possibly extending over months. In Wright's study of newly arrived emi- 
grants into infected regions, 78 cases developed within thirty days after 
arrival and no less than 12 of them within ten days; so that he has no 
hesitation in saying that the incubation of beriberi is between ten and 
twenty days. These observations need confirmation. 

Symptoms. — Clinically, several types of the disease are recognized. There 
are atrophic cases (paraplegic or dry beriberi), dropsical cases (wet beriberi), 
acute pernicious cases, and mild or rudimentary cases. These classes repre- 
sent not only variations of type, but variations of intensity. 

The disease is usually ushered in by marked prodromata. There is loss 
of appetite, with severe pain in the epigastrium and oppression in the chest. 
With these symptoms there is a slight febrile rise. In a few cases rigors, 
lassitude, mental disturbances, and head pains are observed. 

Atrophic Ca.ses. — After a few days or weeks the patient notices a slowly 
increasing weakness of the legs, with pain and tension in the calf muscles. 
There is next a loss of sensation in the soles of the feet. The patient does 
not "feel" the floor, or feels as though a soft insole had been placed between 
the foot and the shoe or sandal. This increases until the patient becomes 
bedridden. As a rule, the palsies are confined to the legs and trunk, some- 
times invading the arms, and very rarely affecting the head and neck. The 
paralyzed limbs rapidly atrophy and areas of anaesthesia and hyperesthesia 
develop. Examination shows the superficial reflexes preserved; the deep 
reflexes lost. The calf muscles and extensors of the legs are extensively 
wasted. The palsy is nearly always flaccid, may be quite profound, and is 
more marked in the extensors than in the flexors, resulting in drop-wrist 
and paralytic equinovarus. The electric muscle reactions are markedly 
altered. From the beginning there is marked diminution, going on to total, 
loss of reaction to both galvanic and faradic stimulation. 

The sensory symptoms closely parallel the distribution of the motor 
symptoms, and are even more constant. Spots of ancesthesia and paroesthesia 
are formed on the feet, calves, legs, trunk, and arms. Recovery from 
the condition is extremely tedious. Gradually the areas of hyperaesthesia 
disappear, sensation and motion return, and in the course of ten to twelve 
months the atrophied muscles regain their contour. 

Dropsical cases resemble the atrophic cases plus marked cardiac phe- 
nomena with dropsy. Sometimes the dropsical cases develop from the 
atrophic. The dropsy begins in the feet and legs and spreads until the whole 
body is affected. The face and lips are puffy and heavy. The arms, legs, and 
trunk are pudgy. With this there are marked evidences of cardiac distress. 
There are cyanosis of the lips and fingers, dyspnoea, and a marked sense of 



BERIBERI 255 

oppression in the pnecordium. Usually the patient is quite helpless, or, if 
he can walk, the slight exertion is attended by breathlessness and palpita- 
tion, these symptoms being very much increased by effusion into the 
serous cavities. The urine is greatly diminished, but contains no albumin. 
After persisting for weeks or months the dropsy may rapidly disappear, 
with an enormous increase in the urine. As a rule, these cases do not present 
the extreme grades of paralysis and atrophy that are found in the first type. 
Yet the absorption of the dropsical fluid will reveal marked wasting that may 
have been completely masked by the semi-solid appearance of the effusion. 

In both types of cases the cardiac changes are marked. The pulse rate is 
usually increased and slight exertion serves to further increase the rapidity 
to 120 to 140 beats per minute. The heart is enlarged, particularly on its 
right side. The carotids pulsate violently and in the severe cases pulsation 
is seen in the jugular veins. Systolic and diastolic murmurs are heard, the 
murmurs being propagated very widely, sometimes even into the bronchial 
and femoral arteries. Reduplication of the sounds is frequently heard, and 
there is equal spacing between the sounds. Despite the forcible cardiac beat 
and the violent pulsation in the vessels of the neck, the peripheral pulse is 
remarkably small and weak. All these cardiac phenomena are exceedingly 
fugitive. Even the most pronounced murmurs and evidences of dilatation 
come and go with rapidity. 

Acute Pernicious Beriberi. — This form attacks, as a rule, the more 
vigorous adults. It may appear as an acute type from the very beginning, 
or it may represent a sudden, fatal episode in mild or convalescent cases. 
Beginning in the ordinary way, the disease advances with great rapidity, 
so that the man becomes bedridden in a few days. The symptoms of car- 
diac involvement begin early and are marked. When this type develops 
from the milder forms the change is very sudden. Palpitation and dyspnwa 
become more and more severe. The patient gasps and struggles for breath. 
He complains of extreme pain in the prsecordium. He breathes with tremen- 
dous, laboring, gasps. The vessels of the neck pulsate violently. The eyes 
are suffused and staring. A blood-flecked foam collects on the lips; unless 
speedily relieved the patient dies a most dreadful death. In these cases the 
urine is notably diminished or even suppressed. Nausea and vomiting are 
common toward the end. 

Mild and rudimentary beriberi of all degrees are observed. These 
cases usually complain of pain and tension in the legs, with weakness and 
numbness. The anaesthetic areas may be very small and sharply marked. 
The patient usually develops some degree of cardiac irritability and palpita- 
tion. There may or may not be wdema of the legs. These cases are im- 
portant because here and there a very mild case may suddenly develop an 
acute pernicious cardiac attack. As a rule, however, they clear up com- 
pletely, rarely lasting over the cool season. 

Special mention should be made of the skin symptoms. Petechia? and 
herpes of the lips are very common in beriberi, as is also a diffuse or blotchy 
redness in the arms and legs. After the very beginning of the disease there 
is no fever. A marked rise of temperature means a reinfection or the 
development of some complication. 



256 DISEASES DUE TO A SPECIFIC INFECTION 

The blood shows no characteristic nor, indeed, any marked changes in 
beriberi. As a rule, there is a very moderate diminution of the red cells. 
In severe and long-continued cases the ansemia may become more marked, 
with some considerable loss of haemoglobin, the color index being minus. 
In the average cases there is no change in the white corpuscles. In severe 
cases a moderate leukocytosis is found. The bacteriological findings are 
negative. 

The urine shows very little change. The urea is diminished, and, as a rule, 
the specific gravity is also decreased. Sugar and albumin are not found. 
Indican is present in large amounts (Baelz). The urine is diminished in 
quantity in the pernicious cases, even to complete suppression. In the cases 
of wet beriberi the urine is greatly diminished. The secretion is re-established 
when the exudations begin to be absorbed. Under these circumstances 
an unusually large amount of urine may be passed, and this re-establish- 
ment of the renal function is a very favorable prognostic symptom. 

Diagnosis. — The occurrence of beriberi in its usual form in the endemic 
area, or in persons hailing from infected regions, offers no diagnostic diffi- 
culty. When the cases occur in groups, the symptoms of peripheral neuritis 
point to nothing else. In isolated cases, however, the diagnosis is not by 
any means easy, and the distinction between arsenical or alcoholic neuritis 
and beriberi may be difficult. The presence of oedema is significant of 
beriberi. The earlier and more decided alterations in the deep reflexes 
and the palpitating and irritable heart also point to beriberi. 

Prognosis. — The percentage mortality of beriberi depends on the per- 
nicious cases. The latter are almost always fatal and furnish certainly 90 
per cent, of the total mortality. In the remaining cases the mortality varies 
widely in different epidemics. Ten per cent, would be a very fair average 
mortality, although it may run as high as 40 per cent. There is no disease in 
which prognosis is so uncertain and hazardous. Again and again I (Kieffer) 
have seen cases I considered practically well, certainly out of all danger, die 
with rapidity in the appalling cardiac crisis of this disease. The prognosis 
is favorable, without regard to the extent of the paralytic lesions, in propor- 
tion to the integrity of the innervation of the heart. Increase of the urine 
is a favorable sign. So, too, are return of appetite and sexual desire. On 
the other hand, increasing irregularity of the heart; equal spacing of the 
cardiac intervals, the short and long pause becoming equal or nearly so; 
increasing cyanosis, paralysis of the diaphragm, and diminishing urine are 
very unfavorable signs. The presence of bronchitis, pneumonia, dysentery, 
alcoholism, and icterus are unfavorable. Vomiting is as sinister a symptom 
in beriberi as is black vomit in yellow fever. 

Treatment. — Baelz has recommended the use of salicylic acid or the salicy- 
late of sodium in 15 grain doses four times a day. Their value is prob- 
lematical. As much may be said for the plan of freely purging these patients. 
When constipation exists in beriberi a mild saline is indicated, otherwise it 
is not useful. In acute cases the dyspnoea, cardiac distress, and girdle pain 
are best controlled by morphine hypodermically. This remedy may allay 
the vomiting. 

For cardiac cases, particularly those with dropsy, digitalis is the best 



ANTHRAX 257 

remedy. It must be given freely in large doses. The cardiac attacks are 
best controlled by nitroglycerin or inhalations of the nitrite of amyl. These 
remedies should always be readily accessible in beriberi wards. If the 
symptoms of cardiac failure become severe, the patient should be bled. 
It will frequently be found impossible to bleed at the elbow, under which 
circumstances the patient should be bled from the jugulars. About 400 c.c. 
should be drawn. The relief from this measure is prompt but evanescent, 
but, as Manson says, "the patient is for the time being tided over an acute 
danger and given another chance." 

The patient should be put on a liberal diet scale in which nitrogenous 
foods and fats form a conspicuous part. He should be kept in a dry, sunny 
room, and whenever possible should be out of bed in the open air. The 
best remedy we have is removal of the sufferer from the endemic area. The 
extreme value of this measure is common knowledge to all tropical prac- 
titioners. If the patient cannot be removed from the town or province, 
removal to another house does a great deal of good, particularly if one on 
high and dry ground is chosen. 

The treatment of the residual palsies is the same as that of any other 
form of severe polyneuritis. 



ANTHRAX. 

Definition. — Anthrax is an infectious disease due to the presence of the 
Bacillus anthracis. It is much more common in Europe and in South America 
than in the United States and England, and affects animals far more fre- 
quently than man. While it is possible for one man to convey it to another 
by contact, the infection in the great majority of instances takes place directly 
from one of the lower animals. Among animals it is met with most fre- 
quently among herbivora, next among omnivora, and least frequently 
among carnivora. Anthrax is sometimes called malignant pustule, splenic 
fever, charbon, and carbuncle. The first synonym is unfortunate, for in many 
cases no pustule is found ; the second synonym is incorrect, as in man the 
spleen is not particularly affected, and the last is equally erroneous, as it is 
an entirely different state from ordinary carbuncle due to the staphylococcus. 

History. — Anthrax as it occurs in man has been recognized for over 2000 
years, and as long ago as the time of the Romans it was treated by the 
cautery. During the seventeenth and eighteenth centuries it was very 
prevalent. Barthelemy proved in 1823 that animals could be inoculated 
with it. In 1850 Heusinger published an accurate and exhaustive account 
of the disease. The bacillus was observed in the blood by Pollender in 1849 
and its relation to the disease was more fully worked out by Davaine in 
1863. Since then this discovery has been confirmed by many observers, 
the chief of whom are Pasteur and Koch. 

Etiology. — As already stated, anthrax is due to the entrance into the body 

of the anthrax bacillus. It usually occurs as a result of handling some part 

of an animal which has suffered from this malady. Of Legge's 211 cases 

72 were in workers in wool and 65 were handlers of hides. The infection 

17 



258 DISEASES DUE TO A SPECIFIC INFECTION 

takes place through some break in the skin, as a rule, and in the great 
majority of cases the site of inoculation is the hand or forearm, but it may 
appear on the face and chest. In Legge's series infection occurred in the 
neck in 84 cases, in the face and head in 77, forearm 16, and in but one 
case was the finger thought to be the point of infection. Sometimes more 
than one point of infection is present; but it occasionally happens that no 
external lesion is to be found, although general systemic infection is mani- 
fest. In such instances the bacillus gains access to the body by being inhaled 
in dust, or by being swallowed in milk or other food. Rarely infection 
of an external wound takes place by the transference of the bacillus by flies 
from an infected animal to the break in the skin of man or animal. 

Prevention. — The disease can be prevented in man by forbidding work- 
men to handle raw hides or infected animals if they have any superficial 
wounds, by the use of respirators designed to prevent the inhalation of dust 
laden with the bacillus of the disease, and by the disinfection of wool, hair, 
rags, and other articles of commerce which may convey the infection 

All animals suffering from anthrax should be killed and then destroyed 
by burning. Mere burial is insufficient, for it is claimed that earth-worms 
are capable of carrying the bacilli to the surface and so causing the reinfec- 
tion of healthy animals. When incineration is impossible burial in quick- 
lime may be resorted to. It is needless to add that the utmost care must 
be exercised by physicians and nurses in dressing cases of this disease when 
it occurs in man. 

Frequency. — In the United States anthrax is not a very common disease 
even among sheep and cattle, and is rarely met with in man. Inquiry 
among employers of men who handle raw hides in Philadelphia develops 
the fact that it is very seldom met with, and when it occurs is nearly always 
the result of handling imported hides. 

Pathology and Morbid Anatomy. — The changes in the skin produced by 
primary external anthrax will be described later under the head of Symp- 
toms. When systemic infection occurs as the result of either external or 
internal primary inoculations, very marked lesions of the viscera become 
apparent. The bronchial glands are generally swollen, and their increase 
in size may be quite remarkable. The pericardium may be dotted by 
petechial spots, and its cavity may contain a considerable quantity of gela- 
tinous material. The muscles, including the heart, are dark colored, soft, 
and flabby. The blood is fluid and dark in hue — sometimes almost black. 
Clots may be found in the pericardial space. Clear, straw-colored fluid 
may be present in the pleural cavity, and if the lungs are affected they are 
found engorged with dark-colored blood, the right lung being more affected 
than the left as a rule; the posterior portion is most congested and 
cedematous, particularly at the bases. Sometimes pulmonary infarctions 
are present. 

In the abdominal cavity numerous extravasations of the blood may be 
found in the mesentery. Petechial hemorrhages may be present in the 
stomach and intestines. The spleen is usually enlarged and contains a 
large amount of grumous blood. Microscopic examination of the tissues 
of the body, when general infection is present, discloses the bacillus usually 



ANTHRAX 259 

in large numbers. They are particularly numerous in the small blood- 
vessels and lymph glands which are near the site of the primary lesion. 

Symptoms. — Anthrax occurs in two forms, the external and internal. 
The external form manifests itself by the development at the point of infec- 
tion, about three to six days after contact with the source of the disease, of 
a small, itching papule, which is soon surrounded by an inflamed area. 
Usually this lesion is so insignificant that no attention is paid to it save the 
scratching or rubbing of it. There may be a history of an abrasion, scratch, 
or pimple through which infection has occurred. The papule speedily 
becomes red and angry-looking, and at its summit a vesicle develops which 
is filled with bloody serum. Around this centre of infection, on the reddened 
and cedematous zone or base, additional papules and vesicles appear and 
the inflammatory process spreads rapidly in all directions. The vesicles 
may become dry and crusty, and as they do so the tissues underneath undergo 
softening, the central part becoming black and necrotic. Curiously enough, 
this rapid process rarely causes much pain, but the neighboring lymphatic 
vessels become reddened and the nodes enlarged. By the end of forty- 
eight hours after the papule first appears the anthrax bacilli may be found 
in the blood, and in such a case the symptoms of systemic disturbance 
rapidly become very marked. 

The local lesion rapidly spreads up the arm if the hand be the part first 
attacked, and the part becomes intensely swollen and livid, the skin being 
dotted by blebs, but it is a noteworthy fact that the rapid spread of the 
surrounding inflammation is due largely to secondary infection by other 
organisms. In cases of pure anthrax infection the central papule is often 
surrounded by an area of induration, but no red areola even after the slough 
has formed. There is general wretchedness and rapidly increasing debility, 
followed by rigors, high fever, sweats, and diarrhcea, but after the early stages 
the fever falls and the temperature may be normal. Delirium rapidly ensues, 
and dyspnoea and cyanosis, with profound evidences of septic infection, close 
the scene in death. In some cases, however, the mind remains perfectly 
clear. 

When recovery takes place the local area is w T alled off by protective efforts 
on the part of the body, so that severe constitutional symptoms do not 
appear. The diseased tissues at the focus of infection undergo necrosis, are 
thrown off, and healing is finally accomplished. 

A second form of external anthrax infection is that which, because of its 
course, is called malignant anthrax cedema. This usually develops on the 
face or head and differs from the type just described in that no papule or 
similar local lesion is present, but in its stead an intense oedema of the tissues 
is produced. So active may be the local process that the parts may speedily 
slough or become gangrenous. Death usually comes rapidly to such cases. 

The internal form of anthrax manifests itself in the lungs or alimentary 
tract. In the first instance the anthrax bacilli enter the respiratory passages 
by inhalation in the dust arising from the handling of dried hides or wool. 
Hence it is called " wool-sorters' disease." The symptoms in these cases 
vary to an extraordinary degree in their severity. In some instances the 
patient feels wretched and miserable, and soon has a chill which is followed 



260 ~ DISEASES DUE TO A SPECIFIC INFECTION 

by fever and very marked thoracic distress. There may be pain in the 
side and labored, difficult breathing. Cough may or may not be present. 
The face becomes livid, marked cyanosis develops, and the patient dies in a 
few hours or days in asthenia and collapse. Pneumonia is rare, but areas 
of impaired resonance on percussion and bronchial breathing may be found 
as the result of enlargement of, and pressure by, the bronchial and mediastinal 
glands. In other cases the symptoms are so mild and indefinite as to possess 
no diagnostic value. A workman may feel only weak and feeble, his hands 
may be cold, and his breathing oppressed, yet he may die within twenty- 
four hours in collapse. Bell records several cases in which death came 
within twenty-four hours of what seemed to be perfect health. 

When the intestinal tract is infected, there are present diarrhoea, vomiting, 
great weakness, and failure of the circulation followed by collapse and death 
in from two to five days. 

Diagnosis. — In the external form of the disease the occupation of the 
patient and the presence of an itching papule should at once arouse the 
suspicion of anthrax infection, which will be strengthened by the rapid for- 
mation of the vesicle already described. The diagnosis can be confirmed by 
a microscopic examination of the fluid for the bacillus, or by inoculating a 
mouse with one drop of the fluid from a vesicle. This will cause the death 
of the mouse in about forty-eight hours, and in its organs the bacillus will 
be found in immense numbers, and from these cultures may be made. 

This condition is separated from carbuncle by the lack of pus and by 
the absence of its sloughing core. From erysipelas of the phlegmonous type, 
or from diffuse cellulitis, it is separated in the later stages by the absence of 
pain and fever. From malignant oedema it is distinguished by the absence 
of crepitation due to gas in the tissues. Agglutination tests based on the same 
principle as the Widal test in typhoid fever have not been generally 
adopted. 

Prognosis. — The prognosis of the external form depends upon the degree 
of general systemic infection, and therefore the size of the local lesion has 
not any great importance in determining the outlook It not rarely hap- 
pens that a small papule may be followed by the death of the patient in a 
few days, whereas a larger lesion may be recovered from. Thus, Bell states 
that a patient with so severe a lesion on the face as to have Targe bulla? and a 
free discharge of straw-colored fluid, with swelling of the entire head and the 
submaxillary glands, may recover. In other words, everything depends 
upon the degree of systemic infection. A rapid-running pulse is always an 
evil omen. 

Death may come as early as the first day of illness, but the majority of 
deaths occur on the fourth to seventh day. So far as mortality is concerned 
statistics vary very greatly, probably because of variations in the virulence of 
the infection. Thus, Woolmer states that out of 50 cases he lost only 2, and 
Muskett treated 50 cases with one death; whereas in England, even when 
the workmen have been taught to present themselves for treatment at once, 
the mortality has been 21 per cent., and in some collections of statistics it 
has reached 50 per cent. In Eppinger's epidemic among rag-pickers 78 
nut of 88 cases were fatal. 



HYDROPHOBIA 261 

In the internal form the prognosis is bad and death often comes, as already 
stated, as early as twenty-four hours after the primary symptoms. Cases 
in which recovery has taken place are, however, on record. 

Treatment. — The treatment of the external form consists in the destruction 
by actual cautery of the primary focus of the disease at the earliest possible 
moment. If this is not done it should be excised. Not only should the 
infected tissues be removed, but the surrounding tissues for at least an inch 
as well. As soon as this is done the part is to be swabbed with pure carbolic 
acid and then dressed, so that drainage into the dressings may occur. The 
patient's vitality should be maintained by good food and stimulants, and 
anthrax antitoxin should be given. 

'Within the last few years an anti-anthrax serum has been employed with 
success. Legge states the following facts as to its use: (1) In very large 
doses it is innocuous; (2) it can be well borne even when introduced into 
the veins; (3) no case taken in an early stage, or of moderate severity, is 
fatal if treated with serum; (4) with the serum some cases are saved when 
the condition is most critical and prognosis almost hopeless ; (5) when in- 
jected into the veins the serum quickly arrests the extension of the cede- 
matous process so as to reduce notably the danger from suffocation which 
exists in many of the cases where the pustule is situated on the face or 
neck; (6) the serum, if used early enough, reduces to a minimum the de- 
struction of tissue; (7) in some situations of the pustule, as the eyelid, 
serum must be used in preference to any other treatment; (8) persons 
attacked, when treated with the serum, appear to become convalescent in 
the course of a few hours; to these I may add (9) that in internal anthrax 
if it is administered intravenously it is the only treatment which can hold out 
any hope. 

In almost all cases injection of the serum is followed by a rise in 
temperature often to over 105°, and with this there is an improvement 
in the general condition of the patient. The prognosis where there is this 
rise Sclavo regards as favorable. In the same way the necrotic process 
itself is to be regarded as a sign that the organism is making effort to re- 
sist the anthrax infection. 



HYDROPHOBIA. 

Definition. — Hydrophobia is an acute infectious disease of animals com- 
municable to man, the specific cause of which has not as yet been isolated. 
It is characterized by great restlessness and delirium, by an apparent dread 
of water in some instances, and by delirium and paralysis in its later stages. 
It is often called " rabies " or " lyssa." 

History. — Hydrophobia was well described as long ago as nearly 500 
B.C. by Democritus, but not until about 200 years B.C. was it described 
in man. Since then it has been discussed by many ancient and modern 
writers, of whom Griiner, in 1813, found that the saliva was the vehicle of 
infection. 

Trousseau wrote its best description in modern times in 1850. In 1882 



262 DISEASES DUE TO A SPECIFIC INFECTION 

Pasteur first clearly discussed the cause of the disease and devised a plan 
of rational treatment. 

Distribution. — No less an authority than Virchow believed that hydrophobia 
was not to be met with in Greenland, Denmark, Africa, and parts of Asia 
and South America, and with others claimed that it is peculiar to temperate 
zones; but in 1860 an epidemic occurred in Greenland among animals when 
the temperature was 25° below zero. Boulanger is probably correct in stating 
that no part of the world is free from it. The idea that it is more prevalent 
in summer than in winter is erroneous. Suzor has reported twice as many 
cases in animals in March, April, and May as in the summer months. Two- 
fifths of all cases in human beings are under fifteen years of age. The 
disease, affects dogs, skunks, foxes, and wolves more commonly than other 
animals, but all animals are apparently susceptible to it. Cows may develop 
it from dog-bites or from bites of other infected cows, and in 1888 I saw 
a number of deer from the royal herd in Richmond Park, near London, 
which suffered from this disease and which were studied at the Brown 
Institution. 

Etiology. — As already stated, the cause of this disease has not been deter- 
mined with certainty, although recently Negri claims to have established 
that it is due to a protozoal organism. It is known that its cause has a 
special affinity for the nervous system, and is found in the saliva, but not in 
the urine or the blood. The disease can be passed from animal to animal, 
from an animal to man, and from man to an animal, and it can be passed 
on from one to another without rapidly losing its virulence. The transfer 
is always made through some solution of continuity, usually a bite, but it 
has occurred through a pimple, and it is said to have been transferred by 
the milk of a nursing mother. 

In the dog it has been proved that the saliva may be virulent as long as 
three days before any symptoms of the disease appears. 

Prevention. — The only efficient measures of prevention are the universal 
muzzling of dogs, particularly when a mad dog is known to have been in the 
neighborhood, and the killing of all animals found suffering from the disease. 
In London the muzzling of dogs decreased the disease from 176 cases in 
dogs in 1889 to 3 in 1892, but on relaxation in enforcing the law the number 
of cases in dogs and man rose again to about the original number. (For 
preventive inoculation see Treatment.) 

Frequency. — Hydrophobia is not a common malady in animals, and is rare, 
comparatively speaking, in man. Sporadic cases are met with in animals 
in every large city during the year. (For statistics see Salmon's article in 
the Year Book of the U. S. Department of Agriculture, 1901.) Woodhead 
states that only about 16 per cent, of those bitten by rabid animals become 
victims of the disease. 

Pathology and Morbid Anatomy. — It has been generally stated that there is 
nothing pathognomonic in the morbid anatomy of rabies, but recent studies 
controvert this view. Examined microscopically the medulla and spinal cord 
show small hemorrhages and large numbers of small round cells in the peri- 
vascular lymph spaces and around the motor ganglia cells, and progressive 
degenerative changes in the spinal nerve cells appear, consisting in chroma- 



HYDROPHOBIA 263 

tolysis and overgrowth of the nucleolus. These changes are, however, by no 
means pathognomonic, as they may be found in other diseases. 

Van Gehuchten and Nelis have, however, discovered changes in the 
peripheral, cerebral, and sympathetic ganglia, in the intervertebral ganglia, 
and in the plexiform ganglia of the pneumogastric nerve, which they consider 
to be diagnostic of rabies. These changes consist in the destruction of the 
nerve cells by newly formed cells from the capsule. Ravenel and McCarthy 
have studied (1901) 28 cases of rabies occurring in dogs, rabbits, and other 
animals, and found these changes in all but one case. The plexiform ganglia 
were affected in all in which positive results as to the presence of the rabies 
were obtained. In 21 cases the bulb was examined for the rabic tubercle 
of Babe's, and positive results were obtained in 19, although in 2 no distinct 
tubercle formation was observed, chromatolysis only being present. The 
rabic tubercle of Babe's is an accumulation of embryonal cells around the 
nerve cells. , The cells of the bulbar nuclei undergo degeneration and mani- 
fest various stages of chromatolysis. 

As a result of their studies Ravenel and McCarthy conclude that these 
changes, taken in connection with the clinical symptoms, afford a rapid and 
trustworthy means of diagnosis of hydrophobia, but that their absence does 
not imply that the disease is not present. They also believe that the rabic 
tubercle of Babes is present often enough to afford diagnostic evidence in 
cases where the central nervous system only is obtainable without any 
ganglia. 

Symptoms in Animals . — The symptoms of rabies in animals vary greatly. In 
the dog we find that he is at first stupid and heavy and often cross and rest- 
less. When he stands up he may sway slightly and stagger when he runs. 
At this time he is easily frightened and his reflexes are acutely increased. He 
usually refuses food and drink, but will often gulp down all sorts of substances 
not food, such as rags, manure, and pieces of wood. Even at this time he 
may be obedient, and may not bite his master, although he will snap at a 
stranger. The bark is muffled and peculiar, and may be a series of yelps 
or howls, the lower jaw never completely closing as in health. Thirst may 
be manifest, but though the animal may lap the water, spasm of the throat 
prevents swallowing. The idea that a mad dog has a peculiar dread of 
water is erroneous. Any repulsion he may have to it is due to the spasm of 
the gullet. 

He next becomes delirious and maniacal, galloping or swiftly trotting, with 
a slouching demeanor, as if shrinking from some enemy. The jaws are 
usually open, and the saliva may flow freely from the mouth. Some 
amblyopia may develop so that he is prone to run into objects which should 
be easily avoided. This may, however, be due to stupidity or muscular 
inco-ordination. Sometimes he seems to see imaginary objects and snaps at 
them. Rapid emaciation is a noteworthy symptom. Finally, the animal 
becomes more feeble and paralyzed. The paralysis is gradual in onset. 
The hind legs are at first moved with difficulty and finally the animal sinks 
on his haunches, there being a simultaneous loss of power in the fore- 
legs, upon which, however, he can occasionally raise himself. During this 
period convulsions may ensue. Death occurs on the fifth or sixth day as a 



264 DISEASES DUE TO A SPECIFIC INFECTION 

rule, but life may be prolonged until the eighth day, but never longer than 
the tenth day. 

In some cases, probably in those which are very severe, the paralysis may 
develop almost at once. 

Animals sometimes manifest symptoms of what is known as "dumb 
rabies," which is to be distinguished from the maniacal form. In this con- 
dition the lower jaw is dropped and the animal is unable to close the mouth. 
The tongue hangs out and the saliva dribbles. As the jaw is paralyzed the 
dog is unable to bite, and does not attempt to do so. This form usually 
causes death in about two to four days. It is important that these mani- 
festations of dumb rabies be remembered. Dr. Gill, a veterinary surgeon of 
New York, asserts that this is a very common form of the disease, which 
frequently misleads persons into thinking that the dog has a bone in its 
throat. They are still further deceived by the fact that the animal has no 
hydrophobia and not infrequently actually plunges his head into water, or 
will even swim a river. He adds as additional advice: "Beware of a dog 
when it becomes dull and hides away, appears restless, is always on the 
move and prowling, whose countenance is sombre and sullen, and w T hich 
walks with his head down like a bear. Beware of one which barks at nothing 
when all is still. Beware of the dog that barks incessantly and tears up 
things. Look out for the dog which has become too fond of you and is con- 
tinually licking your hand and face; and beware, above all, of the dog which 
has difficulty in swallowing, which appears to have a bone in its throat, 
and of one which has wandered away from home and returns covered with 
dirt, exhausted and miserable. " 

These symptoms in the dog have been described in detail because a correct 
diagnosis of the malady in the dog is of vital importance in determining 
whether a patient is to be a victim of rabies and if he should be given 
Pasteur's treatment. 

Symptoms in Man. — When a human being is infected by rabies the stage 
of incubation may last from fourteen days to eighteen months, although 
if the animal produces a punctured wound and is in the active stage of the 
disease the shorter period is more common. It is usually shorter in young 
children than in adults. At the end of the period of incubation the part 
infected begins to itch and tingle and then to burn. The skin in its neigh- 
borhood may develop vesicles, and the old wound may open. 

The primary systemic symptoms in man are apprehension, restlessness, and 
finally marked anxiety. This is followed by thirst, but when the water is 
brought near the patient he seems to have great fear of it — hydrophobia. 
This fear is chiefly due to the pharyngeal spasm, which is produced at the 
sight of water, which, if the patient tries to swallow, becomes exaggerated. 
This spasm is the most pathognomonic symptom of rabies in man. 

Often the site of the inoculation is red and inflamed and there may be 
local irritation or pain. This stage lasts about five days and is followed by 
the stage of excitement, with labored respirations and spasm of the laryngeal 
and pharyngeal muscles. The reflexes are greatly exaggerated and delirium 
or mania may come on. Occasionally the jaws may be snapped together, 
although snapping is said to be characteristic of false rabies. Very commonly 



HYDROPHOBIA 265 

the curious symptom of spitting develops, the patient ejecting small quan- 
tities of spittal upon surrounding objects. 

Occasionally paralytic rabies occurs in man, but it is very rare. 

Diagnosis. — It is only in the early stage of the disease in either the animal 
or man that any difficulty can exist as to its diagnosis. As the saliva of a 
dog for several days before it seems very ill is virulent, all sick dogs, ill of 
unknown causes, should be regarded with suspicion or caution. In man the 
history of having been bitten will usually be obtainable. 

Occasionally a hysterical person, after reading or hearing a description of 
rabies, develops symptoms which resemble it. The fact that the patient is 
of this type, and that threats, or inhalations of amyl nitrite, speedily 
cure the ailment will permit a differentiation. This state is called pseudo- 
hydrophobia or lyssaphobia. It is important to remember that symptoms of 
pseudohydrophobia or hysteria simulating the true disease often develop as 
early as twenty-four or forty-eight hours after exposure ; whereas true hydro- 
phobia rarely develops in less than fourteen days. Again, the hysterical 
patient often presents the symptoms of the second convulsive stage, with- 
out having shown any primary symptoms. He is apt to show a disposition 
to bite, which is very rare in true human hydrophobia, and if he barks, 
growls, or snaps it is an imitation and not the true disease. Finally, should 
the patient survive for a period of active symptoms longer than ten days the 
case is probably hysteria. 

True hydrophobia is to be differentiated from tetanus by the presence of 
marked lock-jaw in the latter disease, and by the fact that in tetanus there is 
no dribbling of saliva and no expression of terror. The convulsions in true 
hydrophobia are rarely as tonic as in tetanus. The paralytic form of rabies 
may resemble Landry's paralysis. 

Prognosis. — It may be possible for true hydrophobia to permit of recovery 
in man, but, if it is, no case of recovery has ever been reported in which 
there was undeniable evidence that the diagnosis was correct. 

Treatment. — The treatment of hydrophobia is entirely in the line of pre- 
ventive medicine, for, once the disease is developed, curative measures are 
not possible. As soon as the bite is received the wound, if a punctured one, 
should be washed and then sucked and the spittle expectorated. If the part 
injured be an extremity a tourniquet should be used until this is done. The 
punctured wound should be converted into an incised wound, and the opening 
should not be closed, but given free drainage and kept open, well protected 
from other infection, for several weeks. Where possible, without great 
mutilation, the part should be excised as is now recommended for the pre- 
vention of tetanus. The value of caustics depends on the one employed. 
Nitric acid is the best. If the wound is incised, well washed with normal 
saline or with bichloride of mercury, real tissue destroyers may be set 
aside. 

The specific and rational method of treatment is that proposed and 
instituted by Pasteur by means of attenuated virus. This investigator found 
that if the virus of hydrophobia is propagated, through the inoculation of a 
series of rabbits, it increases in virulence, and the spinal cords of the rabbits 
of the last series of inoculations contain the poison in a very active state. 



266 DISEASES DUE TO A SPECIFIC INFECTION 

If these spinal cords are preserved under certain conditions this degree of 
virulence progressively diminishes. If an emulsion be made from the 
attenuated cords and a dog inoculated with it in small amount the animal 
survives, and if successively inoculated with virus of increasing virulence 
gradually becomes immune as larger doses are given, until he is able to 
stand inoculation with the most virulent matter obtained from the cords 
of rabbits. This same process is now employed for the treatment of a 
man who has been bitten, the endeavor being made to produce an artificial 
immunity before the stage of incubation following the bite is completed. 

Two methods of producing immunity to hydrophobia are now employed. 
One is known as the "simple" and the other as the "intensive." In both 
methods spinal cords of infected animals are employed in gradually increas- 
ing strength until finally what is known as a three-day cord — that is, one 
which has been kept three days — is administered subcutaneously. In 
the "simple" method nineteen injections are given in fourteen days. 

In those cases which have severe lacerated wounds of the face, in which 
not only infection has taken place, but the tissues have been devitalized by 
traumatism, the "intensive" method is used. This consists in the admin- 
istration of twenty-eight injections in twenty-one days. During the first 
three days as many injections are given in the "intensive" method as are 
given in five days by the simple method. 

Out of 17,395 cases treated at the Pasteur Institute in Paris in this manner 
between 1886 and 1895 there were 139 deaths from rabies. If the average 
mortality after inoculation is in the neighborhood of 20 per cent., as already 
stated, it is evident that instead of there being 139 deaths there would have 
been approximately 3476 deaths, which shows the great value of the plan. 
As the treatment is absolutely harmless if properly employed, the value of 
Pasteur's method cannot be doubted. It is, of course, useless after the 
malady is well developed. 

After the disease is established care must be taken that the patient does 
not wound his attendants. His sufferings should be relieved by morphine 
or chloral in sufficient doses to spare him from much misery. Nutrient 
enemata may be used to help support nutrition if food cannot be swal- 
lowed. 

Efforts have been made from time to time to provide an antirabic serum. 
Babes and Lepp, in 1889, Tizzoni and Schwarz, and later Tizzoni and 
Centanni have all endeavored to reach this much-desired product. They 
have used virus which has been attenuated by digestion with gastric juice, 
and their serum is of such a strength that in the proportion of 25000 per kilo- 
gram weight of rabbit it will protect against one infection unit of virus 
if administered subcutaneously twenty-four hours before the subdural injec- 
tion of virus is given to an animal. An infection unit of the virus is the 
greatest dilution of any virus which will surely kill, without prolongation of 
the incubation period, when 0.012 c.c. per kilogram of animal is admin- 
istered under the dura. These investigators believe that the antirabic 
virus should be injected subdurally, as it is far more efficacious in this 
way than when it is given by the hypodermic needle, and they claim that 
the subdural dose is 12,000 times as efficacious as the subcutaneous dose. 



TETANUS 267 

Unfortunately, these investigations only give promise of good for human 
beings. Sufficient statistics as to their value have not as yet been forth- 



TETANUS. 

Definition. — Tetanus is an acute infectious disease due to the entrance 
and development in the body of a specific organism, the bacillus of tetanus. 
It is characterized by the development of rigidity of the muscles so that the 
limbs are fixed and the jaw locked. 

History. — Tetanus has been known for many centuries as a disease that 
occasionally follows small wounds, but it was not until 1884 that Carle and 
Rattone discovered that when an animal showed symptoms of tetanus it was 
possible to produce similar symptoms in healthy animals by injecting virus 
obtained from the first. In 1885 Nicolaier obtained from the pus of infected 
animals, bacteria which,when inoculated into healthy animals, caused tetanus, 
but he was unable to isolate the organism absolutely, although he described 
it as a small, slender bacillus. In 1886 Rosenbaeh confirmed Nicolaier's 
discovery, but he also did not get a pure culture of the bacillus of the dis- 
ease. In 1889 Kitasato, Tizzoni, and Cattani succeeded in its complete 
isolation. Faber also proved that he could obtain from a culture of this 
bacillus a toxin which, when injected into animals, caused symptoms iden- 
tical with those met with in human beings suffering from this malady. 

Distribution. — Tetanus is met with everywhere in tropical and temperate 
zones. Its bacillus is particularly prevalent in garden soil and about stables 
and dungheaps. In the United States it is most prevalent in Louisiana, 
New York, Pennsylvania, Texas, and Ohio in the order named. Wells 
has shown that the curve of deaths in this disease starts in May, reaches its 
highest point in July, and then declines to October. 

Etiology and Frequency. — The specific organism, the Bacillus tetani, is 
4/i to bfi in length and about 0.4/i wide; during sporulation one end enlarges 
giving the organism a drumstick appearance. This bacillus is an anaerobic, 
slightly motile, flagellated rod, possessing unusually resistant spores and the 
faculty of producing a highly poisonous toxin. It is frequently demonstrated 
in discharges from wounds in cases of tetanus, and has been found on the 
object producing the wound and in freshly made wounds. 

The chief causative factor in tetanus is the presence of a wound through 
which the specific germ may enter the body. This wound may be so insig- 
nificant as to be overlooked. In other cases the infection takes place through 
a break in the mucous membrane of the mouth. Accidents of this type 
probably account for the cases of so-called idiopathic tetanus. Small, 
punctured wounds are much more apt to result in the development of the 
disease than large ones with free drainage, for the accumulated necrotic 
tissues of punctured wounds afford approximately ideal conditions for the 
development of the anaerobic bacillus. Within the last few years several 
outbreaks of tetanus have followed the use of contaminated vaccine. 

Tetanus is not a very common disease, but nearly every large hos- 
pital service has presented to it occasionally an isolated instance. It has 



268 DISEASES DUE TO A SPECIFIC INFECTION 

been epidemic in many hospitals and camps; it has also been epidemic 
among newborn infants, infection taking place through the umbilicus 
and causing a frightful mortality, particularly in the West Indies, where 
at times more than 60 per cent, of all children born died within eight days 
after birth from its ravages. In this country it is seen in hostlers, gardeners, 
agricultural laborers, men employed about stables, and in children who run 
about with bare feet. By far the most common incidence of the disease 
occurs in children who suffer from wounds produced by toy pistols and 
fire-crackers. As many as 466 cases of this disease were due to these causes 
in the celebration of the Fourth of July in 1903 in the United States; but it 
is interesting to note that owing to the warning issued by medical men 
against the use of these explosives the number of deaths due to this cause 
was only 105 in 1904. 

Prevention. — Tetanus is to be prevented by the excision or conversion 
of all punctured wounds into incised wounds with free drainage, by the use 
of tetanus antitoxin as soon as the wound is received, and, if the disease 
develops in a hospital or camp, by the careful isolation of those who are ill 
with it. 

The measures taken to destroy the bacillus and its spores outside the 
body, as in dressings and clothing, must be very radical, because the spores 
are extraordinarily resistant to those measures usually employed to destroy 
pathogenic germs. Thus, the spores can survive two hours' exposure to 
corrosive sublimate 1 : 1000, and even survive exposure to boiling water if 
the exposure is brief. So, too, fifteen hours' treatment with 1 : 20 of carbolic 
acid is necessary to destroy their vitality. Drying does not kill the bacillus. 
Miguel has produced the disease from infected soil kept for eighteen years. 

Pathology and Morbid Anatomy. — A most important fact to be remem- 
bered in regard to tetanus is that the specific organism primarily does not 
spread through the body, but develops at the site of infection, and from this 
focus the toxin which produces the symptoms of the malady is dissemi- 
nated. It has been proved by Meyer and Ransom that the poison passes 
to the central nervous system through or along the nerve trunks. Another 
fact of importance is that the toxin combines with the cells of the nervous 
system with remarkable celerity, and having done so forms so firm a com- 
bination that it cannot be dislodged, and in consequence the subsequent use 
of antitoxin often fails. 

The tetanic convulsions are not due to any influence of the poison on the 
nerves or muscles, but upon the spinal cord and brain. 

In cases of death from tetanus there are no characteristic changes in the 
tissues of the nervous system. 

Symptoms. — The symptoms of tetanus are so characteristic that they can 
hardly be mistaken for any other disease save hysteria and strychnine 
poisoning. The dominant symptom is the state of rigidity of the voluntary 
muscles, which, when the disease is well developed, are practically constantly 
contracted, although at intervals they relax and contract spasmodically, 
causing the well-developed convulsions of the disease. It is a curious fact 
that the earliest symptoms often emanate from the muscles nearest the focus 
of infection, but very commonly they originate in the muscles of the jaw 



TETANUS 269 

and neck, producing the symptom called "lock-jaw," that is, a state in 
which, by reason of the spasm in the masseter muscles, the lower maxilla 
is firmly pressed against the upper jaw. 

The contraction of the facial muscles in the spasm gives the face a 
peculiar expression of painful mirth, or risus sardonicus, and it is a note- 
worthy fact that this expression may be the first warning of an oncoming 
attack of the disease, for as the patient attempts to show his tongue to the 
physician who is inquiring as to his general health, the physician is startled 
to see the facial muscles produce this strange expression. 

The muscles of the back and abdominal wall are rigid to the touch, and 
pain and oppression due to spasm of the diaphragm may be present when 
the disease is well developed. The muscles of the hand are the least affected 
of all the voluntary muscles, as a rule. 

If the more powerful muscles contract forcibly the patient's body is arched, 
resting on his heels and the occiput; this is called opisthotonos. If the 
muscles of the anterior part of the body are the more powerfully contracted 
he may be arched forward — emprosthotonos. 

Pain in the affected muscle is not severe as a rule, but is rather the 
aching due to prolonged strain and weariness. Sometimes, however, it is 
severe. There may be alarming spasm of the glottis or fixation of the 
respiratory muscles endangering life, and, indeed, in severe cases, this is 
the cause of death, particularly when, by reason of exhaustion, the patient 
is unable to withstand asphyxia for any length of time. 

The mind usually remains clear till the time of death. The temperature 
is moderate if the convulsions are moderate, and high if they are severe, 
ranging from 100° to 106°. The pulse varies in speed, becoming rapid 
during a seizure. Finally it becomes feeble from exhaustion. 

Diagnosis. — Tetanus rarely is as sudden in onset as is strychnine poison- 
ing, and it very rarely causes death so rapidly. It affects the muscles of 
the face primarily, which strychnine very rarely does. There is usually a 
history of punctured wound in one case or of the ingestion of poison in the 
other. In strychnine poisoning the convulsions are followed by periods of 
complete relaxation, whereas in tetanus constant spasm with exacerbations 
are present. 

In hysteria the ecstatic facies of the patient, the presence of clonic move- 
ments, the fact that the patient is a woman of a neurotic type, and that 
laughing and crying are often present, aid greatly in the diagnosis. Further 
areas of anaesthesia are often present in hysteria and inhalations of nitrite 
of amyl may cause relaxation followed by sobs and tears as the spasm is 
relieved by the drug. 

Tetany rarely presents such severe contractions, but it may do so. The 
spasms are often localized, and if they occur in children signs of rickets or 
gastric dilatation may be present. Tetany practically never causes death, 
and it affects chiefly the hands and feet, which tetanus does not. 

Prognosis. — The prognosis in tetanus depends very greatly upon the 
severity of the paroxysms and upon the virulence of the infection. In virulent 
infections death comes as early as the second day and usually by the sixth. 
It is essential that two forms of the disease be recalled in studying this ques- 



270 DISEASES DUE TO A SPECIFIC INFECTION 

tion. There is an acute form with a very high mortality of 80 per cent., 
and a chronic form in which recovery takes place in a large percentage, 
about 50 per cent. The mortality is very high in children in all cases. 

Treatment. — Before everything else in the treatment of tetanus must be 
considered the use of tetanus antitoxin. Its value, however, is chiefly 
limited to those cases in which it can be administered as soon as the inocu- 
lating wound occurs, or within a short time after this. Its failure to be of 
value when employed after the symptoms are well developed is not due to 
any lack of power on the part of the tetanus antitoxin, *but to the fact that 
the tetanus toxin so rapidly and firmly combines with the nervous proto- 
plasm of the brain and spinal cord that it is impossible for it to be disasso- 
ciated from this protoplasm, and therefore the antitoxin cannot combine 
with it and prevent it from damaging the central nervous system. 

When children are wounded by means of toy pistols tetanus antitoxin 
should be injected at once, since the proportion of cases in which tetanus 
develops from this injury is very large, and by the prompt administration 
of the remedy the disease may be prevented from producing its character- 
istic symptoms. Thus in 1903, out of 56 cases of so-called Fourth of July 
tetanus treated without antitoxin 16 died, whereas in 1904, out of 36 cases 
treated with antitoxin none died. In 1216 cases of tetanus treated by 
antitoxin, Packard and Wilson found that the mortality was 42.2 per cent., 
and Moschowitz in 461 cases treated in this way found a mortality of 40.3 
per cent. As the death rate of acute tetanus is about 80 per cent, and of 
chronic tetanus about 50 per cent., it is evident that antitoxin saves many 
lives. Even after tetanic symptoms have developed tetanus antitoxin 
should still be used, as it may be of some value. 

A suggestion has been made that in severe cases the patient be trephined 
and the antitoxin injected by the hypodermic needle between the mem- 
branes of the brain or into a cerebral ventricle. It does not seem that this 
measure offers sufficient promise of usefulness to justify so serious a method 
of treatment. If the symptoms are very severe, and doubt exists as to the 
rapidity with which the antitoxin can be absorbed from the subcutaneous 
tissues, it may be advisable to inject it into the cerebrospinal fluid, inserting 
the needle between the fourth and the fifth lumbar vertebrae. In this way 
it will reach the spinal centres quite rapidly without exposing the patient to 
a surgical operation. The needle should be introduced according to the 
directions given in the section on Cerebrospinal Meningitis, and proof that 
it has entered the membranes of the cord assured by the discovery that a 
few drops of cerebrospinal fluid drip from its external orifice. The syringe 
containing the tetanus antitoxin is then attached to the needle and the injec- 
tion is made. According to Luckett it is best to withdraw a considerable 
quantity of cerebrospinal fluid before injecting the antitoxin. 

Still more recently the use of antitoxin injected into the nerve trunks 
supplying the part of the body through which the infection has taken place 
has been tried with satisfactory results, the idea being that the infection 
spreads along the nerve. 

The wound, by means of which tetanus infection has possibly taken place, 
should, if small, be excised, or if it is large it must be thoroughly cleansed 



GLANDERS 271 

first with normal salt solution or some antiseptic liquid, care being taken, 
if an antiseptic is employed, that it is not used in sufficient strength to in 
any way interfere with the vitality of the tissues with which it comes in 
contact, since it is probable that the vitality of these tissues is of greater 
value in protecting the individual against infection than are the ordinary 
antiseptic drugs. If the wound is a punctured wound, it should be con- 
verted into an incised wound in order that the tetanus bacillus may be 
thoroughly washed out of it and that free drainage may be provided. This 
is exceedingly important. Nothing aids in the production of tetanus so 
certainly as the closure of such a wound in its early stages. Wounds should 
be allowed to heal by granulation, as this is the surest way to prevent the 
development of the disease. 

After the disease is developed the patient must be fed with nutritious 
and easily digested foods in order that his nutrition may be maintained. 
In the rapid type of tetanus death usually comes so soon that great emacia- 
tion does not occur. But in the more chronic form the question of nutrition 
must be constantly kept in mind. 

If the jaws are so locked that food cannot be introduced into the mouth, one 
or more teeth should be removed in order that a stomach tube may be passed, 
or a rubber tube may be passed by way of the nostril, as in feeding insane 
patients who refuse to take nourishment. Humphrey has gone so far as to 
recommend in these cases that a gastrostomy be performed, the tube intro- 
duced, and the patient nourished through the operative wound. This seems, 
however, an unnecessarily heroic method when the tube can be used. 

The severity of the tetanic seizures can be to some extent modified by the 
administration of full doses of chloral and the bromides, which act as seda- 
tives to the motor and sensory portions of the spinal cord. These remedies 
are, however, in no way curative, but simply symptomatic in that they 
diminish to some extent the force of the convulsions without in any way 
influencing the deleterious influence of the poison upon the system. 

Care should be taken that the activity of the kidneys is maintained by the 
administration of mild diuretics and by providing the patient with plenty of 
water. The state of the bladder should also be watched, as retention of 
urine is not uncommon. To prevent this, repeated catheterization should 
be resorted to. 

Under the name of " Kopf -tetanus," or head tetanus, a modified form of 
the disease sometimes occurs. It is said to be particularly apt to take place 
after injuries to the face. In these instances the spasm is chiefly confined 
to the muscles of the neck and face, but often extends to the abdominal 
muscles, and there, is frequently spasm or paralysis of the glottis, which not 
rarely becomes a most serious symptom. In some instances the disease 
gradually spreads until it becomes like an ordinary case of tetanus. It is 
to be treated by the employment of antitoxin and other antitetanic measures. 

GLANDERS. 

Definition. — Glanders is a disease which is usually met with in the horse, 
but it may also affect man. It is due to the presence of the Bacillus 



272 DISEASES DUE TO A SPECIFIC INFECTION 

mallei. When it appears as nodular masses in the nostrils of the horse it 
is called " glanders, " but when these nodules are in the skin it is called 
" farcy/' Analogous types occur in man. 

Etiology. — The Bacillus mallei is usually conveyed to man while caring 
for a horse suffering from glanders, and enters his body through some 
break in the skin. It may also find its way into the system by way of the 
nasal mucous membrane. Rarely one person is infected by another by 
contact and through a wound. The bacillus is a slender organism, somewhat 
thicker in proportion to its length than the bacillus tuberculosis, with 
rounded ends. It is easily stained with aniline dyes, but is equally readily 
decolorized by feeble acids or alcohol. It can be readily cultivated outside 
the body. 

Fig. 43 




Character of the cutaneous eruption in human glanders. The variation in size and general lack of 
umbilication are noteworthy points in differentiating it from that of smallpox. On account of shrink- 
age the skin and pustules appear more wrinkled than they did before removal from the body. (Pho- 
tograph, natural size, by Roman Mercado, assistant photographer of the Bureau of Animal Indus- 
try, TJ. S.) 

Pathology and Morbid Anatomy. — The Bacillus mallei produces a circum- 
scribed infiltration of the tissues with accumulations of leukocytes and 
connective-tissue cells, which resemble macroscopically small miliary 
tubercles, but, as Baumgarten has shown, these nodules histologically 
occupy a position midway between tubercles and miliary abscesses. The 
surrounding tissues are infiltrated with blood or show many, or few, petechial 
extravasations. After a short time they undergo necrotic changes, and 
as they break down abscesses are formed, which by necrosis of the over- 
lying tissues are changed into ulcers, which may be superficial or deep. 
Like tuberculosis, the infection tends to spread along the lymphatics and 
eventually the bacilli may reach the blood and be distributed in the viscera, 
causing nodules in various organs. Such nodules occur in the testicles, 
lungs, spleen, liver, and kidneys, and sometimes the bones are affected, 
causing an osteomyelitis. 



ACTINOMYCOSIS 273 

When the nodules break down secondary infections perpetuate the sup- 
puration, the specific bacilli become much diminished, and it may be 
impossible to discover them by staining, because at this period they lose 
their property of being readily stained. 

Symptoms. — Acute glanders develops, in about four days after inoculation, 
with general wretchedness, some fever, and the appearance at the site of 
infection of a circumscribed red swelling. This is followed in a few days 
by breaking down of the granulomatous mass, in ulceration of the nasal 
mucous membrane, and the discharge of muco-piis from the anterior nares. 
Secondary infection of the lymph glands in the neck may occur, and if the 
process is severe the nose may become necrotic. Cough and dysphagia may 
be present. Upon the face and about the joints there develops an array 
of papides which as they become pustules may very closely resemble the 
eruption of smallpox. A septic pneumonia often comes on. 

Death comes to such cases almost invariably by the end of a week or 
ten days. 

In rare instances the process becomes subacute or chronic, and the nasal 
discharge, unless accompanied by the severe symptoms described, may make 
a diagnosis difficult, if not impossible, by the ordinary methods of observation. 

When the inoculation is by the skin, producing farcy, the same acute 
localized swelling takes place and the neighboring lymphatics become 
inflamed and swollen. Not only does this occur as it does in most acute 
local infections which are severe, but small nodules are found scattered 
along the neighboring lymphatics forming the so-called " farcy buds." 
These undergo necrosis, and sloughs form. A septic arthritis may develop. 
The nasal passages escape, as a rule, in farcy. Death takes place in the 
majority of these cases in from ten to twelve days. 

Chronic farcy lasts, like chronic glanders, for a longer period of time than 
the acute disease, sometimes for years. It presents the picture of multiple 
abscesses and sloughs, associated with more or less general septicaemia, 
death taking place from this cause. Very rarely recovery occurs. 

Diagnosis. — Glanders — that is, infection of the nasal mucous membrane 
by the Bacillus mallei — can scarcely be mistaken for any other disease. 
Farcy must be separated from multiple abscesses and carbuncles. This is 
done by the history of exposure, the distribution of the "farcy buds," and, 
finally, by the injection of mallein, which produces a reaction as does 
tuberculin in the tuberculous. 

Treatment. — The swellings should be promptly opened and free drainage 
provided. If possible the local focus should be well removed by excision 
or by the cautery." A nutritious diet should be given and stimulants used 
if needed. Mallein has been used as a curative agent, but nearly all acute 
cases die, do what we will. 

ACTINOMYCOSIS. 

Definition. — This is a chronic infectious disorder produced by the Strepto- 
thrix actinomyces, sometimes called the "ray fungus." It is far more 
common in cattle than in man, and in cattle it usually affects the lower jaw, 
18 



274 DISEASES DUE TO A SPECIFIC INFECTION 

producing a tumor or growth which gives the disease the popular name 
" lumpy jaw." In other cases the tongue is involved, producing the so-called 
" wooden tongue." 

Etiology. — The actinomycotic infection may be conveyed from cattle to 
man by the hands of the individual, or by straws used for picking the teeth, 
whereby infection of the jaw occurs. Direct transmission from man to man, 
or beast to beast, or beast to man does not appear to be of very frequent 
occurrence; apparently both are infected independently by some common 
route or source, the exact character of which often cannot be determined. 
Grain which has been soiled by the slobber of an infected animal may infect 
other cattle. Cereals are thought by some to be the most frequent carriers 
of the disease to man and beast. 

The organism appears, in the discharges from the areas of infection, as a 
minute, rounded mass so tiny as to be microscopic in some instances, but in 
others as aggregated masses, called granules, which are as large as a pin's 
head. These masses are yellowish-white, resembling particles of sulphur 
or iodoform, grayish or drab in hue, and even with slight magnification 
often appear in groups or clumps of radiating filaments, which have caused 
the organism to be called the "ray fungus." Each terminal filament in 
some stage of its evolution develops a bulbous end. 

Pathology and Morbid Anatomy. — In the lower animals the disease produces 
a slow, suppurative, and proliferative process, which results in the develop- 
ment of large fungous growths, which may in part become calcareous. From 
these growths, which are usually situated primarily in the jaw, secondary 
extensions occur, so that the fungus is found in the tissues of the tongue and 
pharynx, and even in the lungs, the intestines, and in the nearly related 
glands and skin. When the disease affects man it does not so commonly 
involve the jaw, but results in the development of abscesses which often 
change into ulcers or form fistulse. These may lead to the deeper tissues, 
although the disease is usually superficial. 

Histologically the new tissue may closely resemble sarcoma, for which 
it is often mistaken, but its richness in pus cells and resemblance to gran- 
ulation tissue, combined with the presence of the fungus, should prevent 
this error. 

The lower jaw is more frequently attacked than the upper; cutaneous or 
subcutaneous forms occur and invasion of the alimentary and respiratory 
organs, both primarily and as a secondary process, is not uncommon. A 
chronic bronchitis actinomycotica and cerebral actinomycosis are among 
the rarer manifestations of the disease. 

Symptoms. — The symptoms of actinomycosis in man depend to a great 
extent upon the part of the body which is affected. When the infection 
takes place through a carious tooth or by ulcer of the gum the jaw is invaded, 
and the tissues covering it become swollen. To such an extent may this 
swelling increase that the neck and face may be involved. In these tissues 
suppuration ensues and pus is discharged from chronic and somewhat 
puckered sinuses, which heal in one place only to break out elsewhere. 
Rarely the disease may spread to the fauces and to the tongue. 

By the swallowing of the fungus it may infect the intestines and even 



MYCETOMA 27.") 

the liver, and in all these organs it often causes the formation of abscesses. 
It has been found in the stools in these cases. 

Actinomycosis affects the lungs even more frequently than the alimentary 
tract, and produces symptoms of subacute bronchitis or bronchiectasis or 
even those of pulmonary abscess. The patient suffers from cough and 
from fever, and expectorates purulent material in which the micro-organism 
is often found. The pulmonary lesions are not very acute in their course, 
but rather chronic, life usually being prolonged in these cases for a year 
or even longer than this. Rare cases of brain abscess have been recorded 
as the result of the organism reaching this organ. Howard has been able 
to find only four primary cases beside his own, and thirteen secondary 
cases. Such cases must not be confused with those equally rare instances 
of streptothrix infection which Musser has recently reported. 

Diagnosis. — The disease, when the jaw is affected, must be separated from 
ordinary necrosis and from sarcoma. In the first the swelling is not so 
widespread and the sinuses not so numerous. In the second condition there 
is no suppuration, the growth is usually more rapid, and the surface is not 
so fluctuating. An examination of the pus in those cases in which it escapes 
will decide the diagnosis by revealing the ray fungus. It is to be remembered 
that secondary pyogenic infection and extensive necrosis may render the 
detection of the specific fungus difficult if not impossible, and undoubted 
cases are on record in which for relatively long periods the characteristic 
organism was absent. Search for the germ is most likely to be rewarded 
during recrudescence in old lesions and in newly formed nodules or 
extensions, when they are freshly opened. 

Treatment. — This is largely surgical when the growth is so placed as to 
permit of its being attacked by this means. The mass and the surrounding 
tissues should be excised and all dead bone and infected tissue removed, 
after which drainage should be maintained and the sinuses irrigated with 
weak solutions of odine or of iodoform in oil. When the pleura is involved 
iodoform injections are particularly useful. Iodide of potassium is also an 
effective drug when given internally in doses of from 20 to 60 grains a day, 
it being thought that in its liberation of iodine it acts as a specific against 
the ray fungus. 

Periods of marked improvement and even apparent cure should not 
cause relaxation in treatment, nor do they justify a too hopeful prognosis, 
as a recrudescence of lesions long obsolescent is of frequent occurrence. 

MYCETOMA (MADURA FOOT, FUNGUS FOOT OF INDIA). 

This is a mycotic disease, usually invading one or both feet and rarely 
appearing in other parts of the body. It is most commonly observed in 
India. Sporadic cases occur in other parts of Asia, in Europe, and in South 
America. A number of cases have been reported in the United States. 
Two varieties of the disease are recognized: the melanoid, or mycetoma 
with black granules, and the ochroid, with white or yellow granules. They 
are due to distinct varieties of streptothrix {Streptothrix maduroe and Strepto- 
thrix mycetomce). The disease is closely related to actinomycosis; indeed, 



276 DISEASES DUE TO A SPECIFIC INFECTION 

some of the cases reported in the United States as mycetoma are undoubted 
cases of actinomycotic feet. 

The disease commonly attacks one foot; beginning as a firm, hard nodule 
on the sole, which gradually softens and discharges an oily, fetid pus con- 
taining the black or yellow granules. The sinus thus formed persists. 
Other nodules appear and go through the same course. The foot gradually 
enlarges and the sole is greatly thickened. The disease attacks the deeper 
tissues until eventually all structures, including the bones, are converted 
into a greasy, yellowish mass. The appearance of the fungus foot, with the 
thickened sole, the toes strongly extended upward, and the plantar and dorsal 
surfaces covered with the button-like orifices of the sinuses, is character- 
istic. Occasionally, the disease shows some tendency to the formation of 
secondary deposits, spreading along the lymphatic vessels. The diagnosis 
between mycetoma and actinomycosis rests on the microscopic character 
of the organisms. 

Treatment. — The treatment consists of conservative resection in early 
cases and amputation in older cases. 



SYPHILIS. 

Definition. — Syphilis is a contagious disease, the cause of which is as yet 
undiscovered. It is sometimes called " Lues" " Pox," or " Lues Venerea." 
It occurs in two forms, the acquired and the hereditary, and is characterized 
in the different stages of its progress by a greater number of pathological 
changes in the tissues of the body than any other known malady. It has 
been said that he who knows the whole pathology of syphilis and tubercu- 
losis knows all pathology. This is, of course, an exaggerated statement, but 
it emphasizes the fact that the disease presents lesions in many different 
tissues. 

The acquired form is usually divided into three stages, called the primary, 
secondary, and tertiary, and to these Fournier has added a fourth group of 
affections, apparently quite separate from any of the foregoing, which he 
calls the parasyphilitic or metasyphilitic affections. 

The primary stage is characterized by the development of a chancre or 
hard sore, also called the " initial lesion"; the secondary stage by the appear- 
ance of eruptions and lymphatic swellings, and by ulceration of the mucous 
membranes. The third stage consists in the growth of tumor-like masses, 
called gummata, and pathological changes in the bones and in the nervous 
and vascular systems. In the parasyphilitic forms there is atrophy of the 
cells of the part involved and overgrowth of connective tissue. 

History. — The history of syphilis is not definite. Certain investigators 
believe that it is one of the most ancient maladies, but it was not clearly 
recognized as a separate affection in Europe until 1494. Those who wish 
to look into this question should consult Syphilis in Ancient and Prehistoric 
Times, by Buret, translated by Ohmann-Dumesnil. 

Distribution. — Syphilis is found all over the world, and in its frequency 
and virulence is not modified materially by climate or geographical con- 



SYPHILIS 277 

ditions, but it is worthy of note that the disease is unknown among savage 
peoples who have not come in contact with civilized communities. 

Etiology. — No one seems to doubt the micro-organismal nature of syphilis, 
although a demonstrated etiological agent is wanting. A great number of 
organisms have at various times been regarded as the cause of syphilis, 
among them being the bacteria described by Lustgarten, Van Niessen, 
Lisle and Jullien, and the parasites studied by Dohle and by Schuller. 
None has been proved an etiologic factor. Siegel describes a small body, 
the cytoryctes luis, which he finds in the blood of syphilitics and regards 
as the cause of the disease. His findings lack confirmation. A distinct ad- 
vance in the investigation of the disease was made in 1903, when Metschni- 
koff and Roux succeeded in producing characteristic lesions in the higher 
apes by inoculating syphilitic virus from human beings; this has since been 
many times repeated. Early in 1905 Schaudinn and Hoffmann described a 
small spiral organism which they found constantly in primary and secondary 
syphilitic lesions and which, because of its indifferent staining qualities, 
they termed the Spirochceta pallida. Recently they have given it the name 
Treponema pallidum. Their findings have since been confirmed by hun- 
dreds of observers in all parts of the world. No authentic instance of the 
organism in tertiary lesions is on record. It is found in the artificially 
produced lesions in apes and highly important is its presence in the blood 
and tissues of infants dead from hereditary syphilis. Levaditi has made 
extensive studies of these cases and finds the organism in greatest numbers 
in the liver, lung, and suprarenal glands respectively. It exhibits a prefer- 
ence for the perivascular tissues rather than for the blood stream and is 
found in and without the vessel walls in enormous numbers. Many are 
intracellular, especially in epithelial cells. The organism is 4 to 14// long 
does not exceed 0.5/^ in thickness and possesses numerous pronounced 
spirals. It is actively motile, but flagella have not been positively demon- 
strated. The specificity of this parasite is regarded by MetschnikorT and 
many others as being abundantly proven and they accept it as the un- 
doubted cause of syphilis. Some investigators as yet hold more conserva- 
tive views. It may at least be said that evidence in favor of the specificity 
of the organism is constantly accumulating. 

In the vast majority of cases syphilis is acquired by sexual intercourse, 
although a large number of cases of acquired syphilis, due to non-sexual 
contact with syphilitic persons or their garments w T hen infected by dis- 
charges, have been recorded. (See Bulkley on Syphilis Insontium.) Obstet- 
ricians, mid wives, and nurses have often contracted the disease through a 
break in the skin of the finger. Wet-nurses have been infected through the 
nipples by syphilitic infants, and drinking utensils, knives, forks, spoonsj 
pipes, and dental instruments have conveyed the poison to the mouths of 
innocent persons. The disease can be transmitted by kissing and by the 
drinking cup. Primary lesions of syphilis have also been produced in the 
mouth by perverted sexual practices. 

The virus of the disease is active in the transmission of the malady through- 
out the primary and secondary stages, and during this time all secretions 
from the lesions of these stages are capable of producing the disease in 



278 DISEASES DUE TO A SPECIFIC INFECTION 

another person, provided that they be brought in contact with a solution 
of continuity in the skin or mucous membrane. Infection does not take 
place through healthy skin or mucous membrane, but the break in the 
surface may be so slight as to be overlooked. The blood of the patient 
during the secondary stage is capable of spreading the disease by inoculation, 
but notwithstanding this fact it is noteworthy that the secretions of the 
various glands do not contain the poison unless they are contaminated by 
discharges from local syphilitic lesions. 

The acquired disease is not conveyed by the discharges from syphilitic 
sores, or by the blood of a syphilitic, if five years have elapsed since the date 
of primary infection; indeed, in most cases the virus ceases to be capable of 
inoculating another person at the end of two years after infection. This rule 
holds true, even although the patient may be suffering from syphilitic sores or 
other active lesions at the time of contact. On the other hand, the spermato- 
zoids may indirectly transfer the poison from the man to woman by the fetus. 

A person who is suffering, or has suffered, from acquired syphilis is protected 
against a second infection in the vast majority of instances, although a few 
cases have been recorded which seem to throw doubt upon the statement 
of some syphilographers that the protection is absolute. This immunity 
is developed at once after primary infection, as early as the development 
of the primary lesion or chancre, and in some cases even earlier than this. 
In the case of a person who has inherited syphilis from one or both parents 
the protection against acquired infection is absolute, even if no signs of the 
hereditary disease be present. 

Hereditary syphilis may come to a child through one or both parents. 
When the father only is syphilitic, the term " sperm inheritance" is employed, 
and when the mother only is syphilitic it is called "germ inheritance." A 
syphilitic male may transmit syphilis to his offspring without manifesting at 
the time of intercourse any symptoms of syphilis and without producing in 
the mother any signs of the disease. It is also possible for him to have a 
healthy child; that is, he may fail to transmit the infection. This depends 
largely upon the stage of the malady, its virulence and activity, and the 
value of any antisyphilitic treatment that may have been instituted for the 
father's benefit before conception, and for the benefit of the mother and 
child after conception. 

A woman suffering from syphilis may or may not bear a syphilitic child, 
and if active antisyphilitic treatment during pregnancy is maintained, the 
child is likely to escape. It is also possible for a mother who contracts 
syphilis during her pregnancy to give birth to a non-syphilitic child, but it 
is also possible for the child to contract primary syphilis from a mucous 
patch as it passes through the birth canal. It is interesting to note, however, 
that while the syphilitic mother is not always able to confer immunity to 
primary infection upon her child, so that it cannot be infected by the disease 
before or after birth, it is possible for the syphilitic foetus in utero to confer 
immunity upon its mother, or, to express it differently, given a child in 
utero by a syphilitic father, that child may be syphilitic at birth, but its 
mother may not have been infected during pregnancy, and is protected 
against syphilitic infection subsequently. This is known as Colles' law. 



SYPHILIS 279 

That immunity to syphilis can be so acquired is proved by the fact that if 
a syphilitic baby nurses at its mother's breast she will not contract syphilis, 
even if its mouth be filled by mucous patches, but if that infant is nursed 
by an innocent wet-nurse it can produce syphilis in that nurse. 

From what has been said so far it is evident that a syphilitic father or 
syphilitic mother may be the parent of a syphilitic or non-syphilitic child. 
If both parents are syphilitic, the probability of the child being infected is 
twice as great as if one parent is affected. 

Prevention. — The prevention of syphilis is one of the great social questions 
of the age that has not been solved. In many cities prostitution has been 
licensed in order that, by governmental and medical control, prostitutes 
suffering from syphilis might be treated and prevented from plying their 
vocation while capable of transmitting the disease. This plan when insti- 
tuted has not checked the dissemination of syphilis, since it continues to 
spread through illicit intercourse carried out with unlicensed women who 
will not be classed as registered prostitutes. 

Syphilis may also be prevented by forbidding intercourse on the part of 
persons suffering from the disease, and by instructing the non-syphilitic to 
avoid intercourse while any break exists in the mucous membrane or skin 
of the external genitals. Careful regard to cleanliness after intercourse is 
of some protective value. 

Frequency. — It is almost impossible to determine the prevalence of syphilis, 
since the living keep its presence secret and the physician rarely returns a 
death as due to it, but to some indirect result of it. 

In 1874 Dr. F. R. Sturgis estimated that, out of a population of 942,292 
in New York City, 50,450 were suffering from syphilis. 

In an appendix to Sanger's History of Prostitution, 1892, it was estimated 
that 100,000 persons out of a population of 1,800,000 had syphilis. 

At the present time the population of Greater New York is about 3,560,000, 
and assuming that the rate of increase of the disease has kept pace with 
the increase in population there would be nearly 200,000 syphilitics in that 
city. These estimates are not made, however, on a statistical basis. 

A committee appointed by the Medical Society of the County of New 
York for the study of measures for preventing venereal diseases, addressed 
a circular letter to all the physicians in Greater New York asking them to 
report the number of cases of gonorrhoea and syphilis which they had treated 
from May 1, 1900, to May 1, 1901. Of the 4750 physicians to whom the 
letter was sent, 678 forwarded statistics of their cases. The total number 
of cases of syphilis reported was 7200. Assuming that as many cases occurred 
in the practice of the physicians who sent no reports as in the practice of 
those who forwarded statistics, calculations would show that 50,400 cases 
of syphilis were under treatment in private practice during the period of 
time which the investigation covered. As many patients go from one phy- 
sician to another, it is not improbable that some of the reported cases may 
have figured twice in the statistics; but the committee believed that the 
number which did so was more than offset by the large class of patients who 
take treatment from advertising quacks. 

Of forty-five dispensaries and charitable institutions visited by the com- 



280 DISEASES DUE TO A SPECIFIC INFECTION 

mittee nine refused to give any information. An inspection of the records 
of the remaining thirty-six showed that 7607 cases of syphilis had been 
treated during the year. 

Burre shows by statistics that the morbidity of syphilis among the inmates 
of the licensed houses of prostitution in Paris has fallen from 30 per cent, 
in 1873 to 0.25 in 1902. On the 1st of January, 1873, 1126 public women 
were registered, and during the year 338 cases of syphilis were recorded 
from among the number. On the 1st of January, 1902, 429 public women 
were registered, and only 1 case of syphilis was observed among them dur- 
ing the year. Burre attributes this decrease in syphilis to the more general 
dissemination of knowledge concerning the infectious nature of the disease 
and to the adoption of hygienic measures for its prevention, which at 
present are largely practised by all the licensed prostitutes. He also lays 
some stress upon the matter of obligatory elementary education, believing 
that it may have served to make the prostitutes more intelligent as a class 
than they were thirty years ago. His statistics illustrate very w T ell the fallacy 
of collecting cases and drawing conclusions from them without due care. 
Surely no one supposes that the number of prostitutes in Paris has dimin- 
ished in the proportion of nearly 75 per cent. 

R. W. Taylor states that most of the cases of syphilis which he has seen 
in hospitals are from tenement houses and have not contracted the disease 
from regular prostitutes, which illustrates the difficulty of preventing its 
spread by licensing women of the town. 

Pathology and Morbid Anatomy. — As already stated, syphilis may in its 
various stages of development affect almost every tissue of the body. Some 
of these manifestations are not distinguishable from lesions resulting from 
other causes, and hence their syphilitic character can only be established, 
if at all, by the exclusion of other factors and the associated presence of 
recognizable luetic phenomena. 

The primary lesion of syphilis, called the chancre, develops at the point 
of infection, and is usually characterized by an obliterative endarteritis with 
spheroidal cell infiltration of the surrounding connective tissue, and by the 
formation of connective-tissue cells which are particularly numerous about 
the bloodvessels. As a result of the vascular changes and associated lessened 
nutrition and possibly the action of the syphilitic poison, with or without 
added infection, superficial and usually central necrosis occurs and an ulcer 
results. 

Soon after the formation of the chancre, just described, the secondary 
stage develops. The lymph nodes all over the body, but notably those 
adjacent to the initial lesion, become enlarged and inflamed, and inflam- 
matory and degenerative or necrotic processes develop in the skin, in the 
mucous membranes, and in the bones and viscera. 

Following this so-called secondary period of the disease there develops 
the tertiary stage, in which the periosteum and the internal viscera suffer 
from peculiar growths of newly formed tissue. A most constant lesion is 
characterized by the formation of a new tissue consisting of spheroidal and 
polyhedral cells and scattered giant cells, w T hich are commonly abnormal, 
poorly supplied with bloodvessels, and having a marked tendency to necrosis, 



SYPHILIS 281 

especially coagulation necrosis, and hyaline degeneration in their earlier 
stages, and later caseation closelv resembling that seen in tuberculosis. The 
growth of this new tissue is usually in circumscribed nodes, and it is in these 
masses that the necrotic and degenerative processes just named occur most 
markedly or are most evident. These " gummata " may grow to consider- 
able size. They appear as dirty-white, firm masses which, on section, often 
are found to be caseous at the centre, where the new tissue has undergone 
necrotic change. 

Syphilis produces grave changes in the bloodvessels, and no other patho- 
logical process impairs the general vascular system so markedly, except it 
be renal disease. A syphilitic arteritis develops with diffuse overgrowth 
of fibrous tissue in the adventitia, and even gummata may form along the 
vessels. The arteritis also involves the middle coat and even the endothelial 
lining of the vessels, and so narrows or occludes them. This of course 
diminishes the blood supply to the various organs and increases the labor 
of the heart. The heart muscle also suffers from a myocarditis characterized 
by overgrowth of its connective tissues, and the pericardium and endocar- 
dium may be thickened for a like reason, but gumma of the heart is very 
rarely produced. The changes in the heart are, therefore, almost entirely 
due to the effects of the disease on the vessels which supply it, and upon the 
changes which occur in the aorta and the peripheral vessels. In other words, 
while arteritis may result in myomalacia cordis the conspicuous change is a 
fibrosis of the heart muscle. The aortitis and general arteritis result in 
increased cardiac and vascular stress. 

In the secondary stage of syphilis an acute syphilitic nephritis has been 
described. Later on a destructive overgrowth of connective tissue develops 
in association with the vascular changes just described, and gummatous 
growths occur in the kidneys. 

The liver is very commonly affected by the formation of gummata or by 
connective-tissue proliferation, which produce grave interference with its 
function. These changes take place in both the acquired and in the heredi- 
tary form of the disease. This overgrowth of connective tissue occurs in 
two types. It is developed between the lobules constituting an interlobular 
or perilobular cirrhosis, and between the cellular columns forming an intra- 
lobular cirrhosis. In some instances these connective-tissue formations 
consist in large, firm bands which run in various directions through the liver 
and, in contracting, draw in the capsule of Glisson and so cause great 
distortion of its surface. (See Fig. 44.) Not rarely gummata are 
enclosed by these bands. In the earlier stages and milder forms of syphilitic 
hepatic cirrhosis the changes cannot be considered pathognomonic, but in 
the exaggerated form, just described, typical syphilitic changes occur. As 
secondary lesions of the liver amyloid disease and atrophy of its paren- 
chyma are occasionally observed. (See Cirrhosis of the Liver.) 

The lesions in the lungs consist in gummata which are often surrounded 
by exudative material, as in pneumonia. These gummata may contain a 
cheesy area as in tuberculosis and, by pressure, may cause secondary altera- 
tions. A second change is overgrowth of fibrous tissue around the bronchi 
which, associated with catarrhal processes involving their mucosa, distorts 



282 



DISEASES DUE TO A SPECIFIC INFECTION 



these tubes, causing narrowing at some points and at others bronchiectases. 
Infarctions may occur because of the obliterative changes in the bloodvessels. 
A true syphilitic phthisis presenting symptoms resembling tuberculous pul- 
monary phthisis, but in which tubercle bacilli are not present, may occur, 
but it is exceedingly rare. It is true that cases have been reported in 
which gummata in the lungs have, like tubercles, undergone softening of a 
caseous type, and Wilks has recorded an instance in which this process had 
gone on to the development of a cavity. Virchow and Fowler have recorded 

Fig. 44 




Nodular syphilis of the liver. (Kast and Rumpler.) 

similar cases. These cases, however, although they may produce physical 
signs of cavity do not present the characteristics of pulmonary phthisis in the 
sense of pulmonary tuberculosis, nor do those instances in which bronchi- 
ectatic cavities develop as the result of syphilitic fibroid changes in the 
lungs do so, even though the physical signs may be similar. The main 
pathological difference in the two states is this — viz., that in tuberculosis 
there is not only a destruction of the tubercle by softening, but the inter- 
vening tissue is infiltrated with exudate which soon becomes tuberculous 



SYPHILIS 283 

and proceeds to necrosis. This does not occur in syphilis. In rare cases 
syphilis of the lung and tuberculosis may be coincident. 

In the hereditary syphilis of infancy a lobar or bronchopneumonia in 
which the pulmonary tissues show red, gray, and white exudates, according 
to the stage of the local disease, is sometimes met. 

The lymph nodes in cases of syphilis are always affected by an over- 
growth of connective tissue after the primary infection. In the third stage 
gummatous masses may develop in them. 

Next to changes produced in the organs of circulation syphilis manifests 
its gravest changes in the central nervous system. The meninges may be 
the seat of gummata with or without the presence of chronic, indurative 
overgrowth of connective tissue. 

In the brain it causes gummata manifesting the symptoms of brain tumor; 
it also produces a syphilitic inflammation which is associated with the forma- 
tion of a gelatinous tissue, and finally and most frequently it gives rise to 
serious degenerative changes in the arteries which interfere with the nutri- 
tion, and later by rupturing bring about cerebral hemorrhage. It also causes 
gumma of the cord and its membranes, which usually have their origin in 
the tissues of a bloodvessel or in the pia arachnoid. Rarely it affects the 
peripheral nerves, through pressure, as they emerge from the cerebrospinal 
sheaths. In the spinal cord it causes degenerative changes of cells and 
fibres and overgrowth of the sustentacular tissue. 

The parasyphilitic affections, paresis, meningoencephalitis, locomotor 
ataxia, etc., will be discussed with diseases of the nervous system. 

Symptoms. — The symptoms of acquired syphilis are best described as 
they appear in the three stages of the disease. 

First Stage. — In from twelve to twenty-one days after exposure and 
infection the patient develops at the site of original contact with the virus a 
small papule or pimple which has an area of indurated tissue about its 
base, the so-called primary lesion or hard chancre. Further examination 
of the patient w T ill reveal the fact that the inguinal glands are slightly 
enlarged. 

This period of primary syphilis lasts from three to ten days or two w T eeks, 
and is followed by the development of the secondary stage. 

Second Stage. — In the secondary stage we find fever as an early 
symptom, which varies in its degree very greatly in different patients. In 
some instances it is so mild as to be overlooked; in others it may rise to a 
point as high as 104° or even 105°. The more common febrile movement 
is one in which the temperature for some days stays in the neighborhood of 
101°. When the fever intermits, being fairly high at one period and then 
breaking sharply, it may mislead the physician into a diagnosis of malarial 
infection or acute sepsis. I have seen several cases in which a diagnosis of 
typhoid fever, malarial fever, or tuberculosis w r as made when in reality the 
disease w T as early secondary syphilis. 

The skin eruptions of the secondary stage consist chiefly of the roseola, the 
development of which often marks the onset of the secondary stage. This 
roseolous rash may occur in limited areas or be widely distributed over the 
body and even involve the face. On one occasion a woman with a well- 



284 DISEASES DUE TO A SPECIFIC INFECTION 

developed syphilitic roseola presented so scarlet a visage that, although she 
was veiled, she caused the other patients to leave my waiting-room in 
alarm, they thinking that she had scarlet fever. As a rule, however, the 
rash is not so marked on the face. 

In other cases, in place of roseola there develops a macular syphilide, 
characterized by the appearance of reddish-brown or copper-like macules 
scattered over the trunk. 

As the secondary stage advances the eruption may be papular and 
finally pustular, and at this time it may closely resemble that of true 
variola. In still other cases a squamous or scaly eruption appears which 
differs from psoriasis in that it is not chiefly on the extensor surfaces as is 
ordinary psoriasis, and in addition it is frequently copper-colored. 

At the point of junction between the mucous membrane and the skin, as at 
the anus or at the angles of the mouth, "mucous patches," or ulcers, develop, 
and upon the skin in the neighborhood of these lesions warty growths of a 
flat character, the so-called syphilitic condylomata, appear. Mucous patches 
on the buccal mucous membrane and tongue also appear. 

There is nearly always some falling of the hair in secondary syphilis. 
Sometimes this falling is well distributed; in other cases it is in patches — 
syphilitic alopecia. 

A serious, oftentimes painful complication at this stage is syphilitic iritis. 
If the treatment is not active sight may be lost. 

A rapid development of anxmia, which often becomes quite marked, not 
as to haemoglobin, but as to the number of the red cells present, is often 
observed. 

The secondary stage lasts from twelve to eighteen months, and is usually 
followed by a period during which the symptoms are modified or entirely 
disappear, the virulence of the disease seeming to have spent itself, but 
even if no syphilitic symptoms are present a child begotten at this time will 
usually suffer from hereditary syphilis. 

Third Stage. — In the great majority of untreated cases the malady pro- 
ceeds to the so-called tertiary stage. This is characterized by the presence of 
skin lesions, which are more severe than those of the secondary period, such as 
tuberculous and ulcerous formations of a subacute or chronic character. There 
is an overgrowth of connective tissue in different parts of the body, as in 
the secondary period, and multiple gummata are often present in numbers, 
developing in the skin, in the subcutaneous tissues, in the muscles, and in 
the internal viscera, particularly in the liver. When in the skin they often 
slough and produce ulcers, and in the internal organs they become filled with 
fibrous tissue and undergo contraction in the manner already described. 

Last, but by no means least, of the changes due to syphilis in its tertiary 
stage, we meet with lesions of the nervous system. These changes, as a 
rule, are late manifestations of the disease, occurring some years after the 
infection. Rarely they may appear as early as within the first six months, 
usually within the first ten years, seldom as late as twenty years. 

Syphilis in certain cases may seem to possess great virulence and become 
destructive in its course, almost from the onset. The chancre may rapidly 
ulcerate and spread, the fever may be marked, and the anaemia severe. The 



SYPHILIS 285 

skin lesions become pustular, even in the secondary stage, and form deep 
ulcers, which, in turn, cause scars as they heal. Destructive changes rapidly 
develop in the bones and viscera. The patient may die within a few months 
of the infection. In these cases there is usually a lowered vital resistance 
which permits the disease to progress unopposed. 

In other cases the symptoms are remarkably mild. The chancre is so 
small that it is overlooked, the patient truthfully stating years afterward that 
he has never had a primary lesion. The rose rash may not occur, or be so 
faint and fleeting as not to attract notice, and the primary anaemia may be 
entirely absent. Syphilis may end in complete recovery at the close of the 
secondary stage, but such a fortunate result is rare, unless active treatment 
has been instituted. 

It is a fact worthy of note that nervous lesions seem to occur more 
frequently in cases which have presented mild secondary symptoms than in 
those who have had severe secondary and tertiary lesions of internal viscera. 

Three intracranial conditions due to syphilis may produce violent head- 
ache, namely, arteritis, meningitis, and gumma. When arteritis is the cause, 
giddiness, weakness of groups of muscles, difficulty of speech, and, it may 
be, signs of general paresis develop. On the other hand, when the ocular 
muscles are affected and an optic neuritis is present, meningitis is the more 
likely condition, particularly if there is spasmodic contraction of certain 
cranial muscles and fever. Neuroretinitis is present in meningitis and in 
gumma, but is not commonly present in arteritis. (See Meningitis.) 

The symptoms of syphilis of the brain depend very largely upon the site 
of the lesion, for, as already stated in the section on the Morbid Anatomy 
of Syphilis, these lesions may be at the base, on the convexity, or in the 
membranes. By far the most common symptom of cerebral syphilis is 
headache, which is usually diffuse and constant, but if the meninges are 
involved, or a gumma is causing pressure, it may be exceedingly severe and 
characterized by what are known as "crashing pains." Patients with cere- 
bral syphilis are often unduly somnolent. (See Diagnosis.) 

When gummatous growths form at the base of the brain the symptoms 
are those due to interference with the cranial nerves, such as squint, optic 
atrophy, and facial paralysis. When the convexity of the brain is affected 
the symptoms are those of localized or Jacksonian epilepsy, or of petit mal. 
Sometimes the epileptic seizure is general. Fournier laid down as a law 
that epilepsy beginning in adult years is, nine times out of ten, syphilitic. 
A third form of cerebral syphilis is that in which there are psychical disorders, 
such as melancholia or delusions of grandeur. (See Paresis.) 

Spinal syphilis manifests itself as the result of the presence of guminata or 
of connective-tissue changes in the cord. W 7 hen the lesion is a gumma 
the symptoms are those of pressure on the cord. When connective-tissue 
changes occur the signs are those of spastic paralysis of the lower limbs, with 
markedly exaggerated reflexes, low muscle tension, and vesical disturbances. 
Often the disorder of the functions of the bladder is the first sign of spinal 
difficulty. The bladder may lose its expulsive power or incontinence may 
occur. As a parasyphilitic affection locomotor ataxia is the most common 
nervous disease. (See Locomotor Ataxia.) 



286 DISEASES DUE TO A SPECIFIC INFECTION 

Diagnosis. — The diagnosis of acquired syphilis is readily made if the 
patient presents the well-developed symptoms. In many cases, however, 
these are not manifested. The indurated base of the chancre is an invalu- 
able sign if the chancre has not been cauterized, and the presence of enlarge- 
ment of the lymph nodes in the groin and in the great chain of nodes in 
the neck is also a useful diagnostic point. The presence of secondary 
syphilitic roseola, and fever with sore throat, and mucous patches are diag- 
nostic. In some cases, however, the secondary symptoms never develop or 
are so mild as to be overlooked, yet well-marked tertiary signs develop later. 
The employment of mercury or iodide of potassium, followed by the dis- 
appearance of the symptoms, is a therapeutic test, but such a result is not 
a pathognomonic sign of syphilis. 

Prognosis. — The outlook in acquired syphilis as to severity of attack and 
ultimate recovery depends largely upon the state of the general health, and 
the promptness with which specific treatment is instituted. Much depends 
also upon the faithfulness of the patient in carrying out the treatment for a 
sufficient length of time. In the great majority of cases active and skilful 
treatment permits a favorable prognosis as to complete cure, and even as to 
the safety of future marriage. In the malignant cases, or those in which 
tertiary lesions have already formed, we can only hope to modify the progress 
of the malady, or perhaps arrest it without being able to remove all signs 
of its invasion. Gummatous growths may, however, be removed by treat- 
ment, even in the tertiary stage. 

Hereditary Syphilis. — The symptoms of hereditary syphilis may be present 
at birth, the skin being already the site of syphilitic eruptions, of which pem- 
phigus neonatorum — that is, a bleb-like eruption about the wrists and ankles 
— is typical. The liver and spleen are usually enlarged, and the child may 
be wasted and poorly nourished. In other instances the child manifests no 
lesions at birth, but within its first six months of life develops syphilitic 
rhinitis, or, as it is called, "snuffles." This is accompanied or followed 
by cutaneous lesions, of which the most frequent is mucous patches about 
the anus and in the mouth. It may waste away from so-called syphilitic 
marasmus, developing a syphilitic rosary at its costocartilaginous junctures, 
as in rickets. The ends of the long bones are the victims of syphilitic 
epiphysitis. If the child lives to reach the period of second dentition its 
teeth may be notched — the so-called "Hutchinson" or "peg" teeth. This 
malformation does not appear in the milk teeth. In many cases of heredi- 
tary syphilis in infancy the child looks like an old man, whereas in hereditary 
syphilis of early adult life the patient often looks very immature — "syphilitic 
infantilism." Children having hereditary syphilis are prone to suffer from 
syphilitic keratitis, from deafness, and from bone lesions which develop 
after several years of life. The periosteum is thickened and even nodular 
in its appearance, particularly on the tibia. 

Another lesion is deformity of the fingers, in which they become thickened 
at the base and taper rapidly to the tip, being somewhat pear-shaped or 
top-shaped — the so-called syphilitic dactylitis. 

Treatment. — -Divergent views have existed in regard to the proper treat- 
ment of syphilis in its early stages. A certain number of practitioners of 



SYPHILIS 287 

experience have insisted that it is unwise to administer mercury to a patient 
suffering from a suspicious primary lesion until, by the development of 
secondary symptoms, the diagnosis of syphilis is absolutely confirmed; since 
if we do not wait for these symptoms, the possibility exists that a patient who 
has not really acquired syphilis may be condemned to the belief that he has 
been inoculated, and this may cause him great mental suffering during the 
rest of his life. 

Another group of practitioners have strongly urged a view directly opposed 
to this, claiming that we have no right to permit the disease to become thor- 
oughly engrafted upon the patient's system without instituting measures 
for its relief, or at least for the diminution of the severity of the infection. 
The leaders in this line of thought have advocated the excision of the 
chancre in the belief that by so doing the primary focus of infection was 
removed. It must be remembered, however, that the primary lesion does 
not develop until two or three weeks after the actual inoculation, and, there- 
fore, although it appears at the site of inoculation, there is good reason to 
believe that it is not a source from which still further infection takes place, 
but rather a localized manifestation that inoculation has been accomplished. 
Nearly always there can be found in the adjacent lymphatics evidence that 
they are affected as early as the chancre appears. The question as to whether 
the chancre should be excised must, therefore, be left to the judgment of the 
individual physician, with the statement that it is possible, but not probable, 
for the excision to have some influence for good. 

It is with those who believe in the immediate administration of anti- 
syphilitic treatment as soon as the chancre is developed that I agree. It does 
not seem to me rational to permit the disease to run on uncontrolled until 
he who runs may read that infection has taken place. While it is true that 
the chancre at times is not sufficiently characteristic to enable us to make 
a positive diagnosis that it is true syphilis, we are justified in such a case 
in considering that it is such and proceeding at once to the relief of the 
patient. 

The main treatment during the primary and secondary stage of syphilis 
must consist in the administration of full doses of the protiodide of mercury, 
which should be given in the form of uncompressed tablet triturates in the 
dose of \ of a grain three times a day, increased by one or two quarters 
each day, until the patient manifests distinct evidences of the full systemic 
effect of the drug, as evidenced by some looseness of the bowels or by the 
development of tenderness of the teeth and slight salivation. It is impor- 
tant when this drug is given that tablet triturates, and not compressed tablets, 
are employed, as the compressed tablets are often unabsorbed, because of 
their hardness, and frequently cause irritation of the stomach, whereas, the 
properly made tablet triturate rarely does. 

As soon as the patient manifests any of the symptoms, mentioned as indic- 
ative of the fact that he is using all of this drug which he can well bear, it is 
proper to diminish the dose one-half, and keep it at this point, provided that 
this dose seems competent to prevent the development of further syphilitic 
manifestations. If, however, this half dose is not sufficient for this purpose, 
the drug must be given in ascending doses the second time, and if the 



288 DISEASES DUE TO A SPECIFIC INFECTION 

syphilitic manifestations are at all malignant it may be necessary to continue 
it, even if opium or bismuth have to be given to control diarrhoea. 

It is essential in the use of the protiodide of mercury in syphilis, first, 
that the stomach shall not be disordered, because it is of vital importance 
that the patient should be able to take full quantities of highly nutritious 
food, in order that by maintaining his vitality his own vital processes may 
aid him to combat the infection. 

It is also essential that great care be taken against the development of mer- 
curial stomatitis. If this condition once develops, it is often difficult to cure 
it while the mercury is continued, and it frequently will prevent the patient 
from taking sufficient doses of the drug to favorably influence his syphilitic 
infection. If the patient is directed to take the greatest possible care as to 
cleanliness of his mouth, to use a tooth-brush and some antiseptic dentifrice 
after each meal, to keep particles of food from between the teeth by the 
use of floss silk, and, finally, if he also be given a prescription calling for 10 
grains of chlorate of potassium and 10 drops of tincture of myrrh in an ounce 
of elixir of calisaya, which is to be diluted one-half with water, and used 
as a mouth-wash night and morning, it will be found that he will be able to 
take much larger doses of mercury than if these measures are delayed until 
some evidences of mercurial sore mouth present themselves. 

Should the manifestations of syphilis be virulent, then it is necessary to give 
the drug to the patient not only in the form of the protiodide by the mouth, 
but to use blue ointment rubbed into the skin at least once a day, in the dose 
of about 1 drachm, choosing a different spot each time for the rubbing, and 
exercising great care that the rubbing is continued long enough to actually 
cause the absorption of the mercury. Usually a hot Turkish bath or, if this 
is impossible, an ordinary hot-water bath should be taken before the mercurial 
ointment is used, in order that the skin may be rendered pliable and put in 
such a state that the mercury can be readily taken up by the tissues beneath 
it. The entrance of mercurial ointment into the body may also be aided by 
smearing it on a flannel binder and placing this about the patient's waist. 

In other instances, in addition to the internal and external use of mercury, or 
in place of one of them, hypodermic injections of mercury may be employed. 
For this purpose one of the best preparations is corrosive sublimate dissolved 
in normal salt solution and given in the dose of -J- of a grain, injected deeply, 
but gently, into the loose cellular tissues of the buttocks or back, or, better 
still, into the body of the greater muscles, such as the gluteus. Great care 
must be exercised that antisepsis is complete, since otherwise the irritant 
drug, although antiseptic in itself, may cause abscess. This injection should 
not be given oftener than every two or three days. In other instances 
gray oil may be used, prepared by rubbing 2 drachms of lanolin with a 
sufficient quantity of chloroform to form an emulsion, continuing the rubbing 
until most of the chloroform is evaporated, then adding metallic mercury to 
the extent of 4 drachms, and rubbing again until the mixture is complete. 
This strong gray ointment, diluted still further by the addition of equal parts 
of olive oil, may be injected in the dose of 1 or 2 minims every second or third 
day in the same manner as corrosive sublimate. 

Still another way of getting mercury into the body is by means of the sub- 



SYPHILIS 289 

limation of calomel. The patient, being stripped of all clothing, is wrapped 
in a blanket and placed upon a chair with a wooden seat. Under this chair 
is placed an alcohol lamp and over it a disk of metal upon a small iron 
stand, on which 20 grains of calomel is laid. Upon this stand is also placed 
a tincupful of water. The heat of the lamp vaporizes the water and sub- 
limes the calomel, and the mercury, being deposited upon the skin of the 
patient, is absorbed. This method of treatment is useful for the relief not 
only of the systemic symptoms, but also for the syphilitic eruption of the 
skin. A similar plan of sublimation can be carried out with inhalations, the 
patient holding his face eighteen inches away from the pan and inhaling the 
fumes. If this is done mucous patches in the mouth are very frequently 
rapidly healed, but after each employment of sublimation and inhalation, 
the mouth should be well rinsed with water, in order that an excess of mer- 
cury may not remain there and produce stomatitis. In many cases the best 
results are produced by a plan of treatment in which both the iodide of 
potassium and protiodide of mercury are given together or alternately. 

The treatment of the tertiary stage of syphilis consists chiefly in the admin- 
istration of iodide of potassium or iodide of sodium or iodide of strontium, 
in as full doses as the patient can well bear, but should evidences of gum- 
matous growth in the brain present themselves the iodide is not sufficiently 
active in its action, and mercury should be given with it. 

The dose of the iodides varies greatly with the susceptibility of different 
individuals. As a rule, tertiary syphilis is not benefited by giving less than 
100 grains a day. I have had a patient under my care who would take 800 
grains a day with great benefit, with no other disagreeable symptoms than 
the development of an intense acne. But we rarely meet with instances 
where these enormous doses must be taken. 

The proper way to administer the drug is to order a saturated solution of 
iodide of sodium dissolved in the strength of 1 grain to the minim of water, 
and direct that 10 minims of this be given in a dessertspoonful of the com- 
pound syrup of sarsaparilla three times a day an hour after meals, being 
increased each day from 1 to 5 minims at a dose. If careful attention is paid 
to the diet and to the condition of the bowels, patients who would not be 
able to take large doses at first soon become fairly immune so far as untoward 
effects are concerned, and can take effective quantities within a brief period 
of time. 

Hereditary syphilis is to be treated by the active employment of mercury. 
In babies suffering from syphilis, gray powder may be given in the dose of 2 
grains two or three times a day, and mercurial ointment may be rubbed into 
the abdomen and on the inside of the thighs and smeared upon the abdom- 
inal binder of the child. This will prove a most advantageous plan of treat- 
ment. The change in the nutrition and appearance of the infant under these 
circumstances is little less than marvellous. 

The diet should be carefully regulated, and, if the digestion will stand 
it, cod-liver oil should be given internally. The employment of the mer- 
curial ointment produces an active systemic influence without disordering 
digestion, and is, therefore, particularly advantageous when hereditary 
syphilis is being treated in infants. 
19 



290 DISEASES DUE TO A SPECIFIC INFECTION 



TUBERCULOSIS. 

Definition. — Tuberculosis is an infectious disease caused by the presence 
in the body of the Bacillus tuberculosis. It is characterized by a local 
inflammatory process followed by the development of areas of necrosis. 
While the lesions produced by the disease are varied, the typical manifes- 
tation is the formation of small nodules which appear as gray, or white, or 
sometimes yellowish bodies called tubercles. It is because of these tubercles 
that the name "tuberculosis" is applied to the malady. 

Etiology. — The chief etiological factors in this disease are the specific 
bacillus and the presence of a favorable state in the tissues of the individual 
for the growth of the germ. As the disease is constantly present all over the 
world, except in a few scattered areas, the specific germ is always at hand, 
and as a large number of causes produce a condition of the tissues which 
is favorable to their development the disease is only too prevalent. 

The bacillus of tuberculosis appears as a straight, slightly curved or bent 
rod with rounded ends, devoid of motility, and reproducing itself by fission; 
the often expressed belief that it is a spore-bearing organism is not 
unequivocally established. It stains with the ordinary aniline dyes and by 
Gram's method. (See Pathology.) 

The Bacillus tuberculosis enters the body by several pathways, of which 
the most common is undoubtedly the respiratory passages. It also gains 
access by way of the alimentary canal with the food, and occasionally by 
accidental inoculation. Recent studies have shown that the tonsils and 
lymphoid tissues of the pharynx are portals through which the tubercle 
bacillus frequently enters. The position of the tonsils exposes them 
to both air-borne and food-borne infection, and their crypts and lymphatic 
communications afford favorable opportunities for the entrance and dis- 
semination of the micro-organism. Very rarely true hereditary transmission 
takes place by the passage of the bacillus through the placenta or possibly by 
the infection of the ovum by this organism. Such instances are, however, 
so rare that they are curiosities in medicine. 

When the infection takes place by inhalation it usually occurs by the bacilli 
being dissipated through the air in the form of dust, or by their expulsion in 
small masses of sputum which, falling on pillows, bedding, or clothing, are 
easily taken into the respiratory passages when the sputum dries. Flugge 
has shown that when a patient coughs with his mouth open the ejected air 
may contain droplets holding the bacillus, thereby rendering the immediate 
neighborhood of the sufferer especially dangerous. There can be no doubt 
of these facts, for they are proved by the very great frequency of the disease 
in the lungs, particularly when opportunity exists for infection by dust, 
and by the fact that susceptible animals can be infected by this disease if 
forced to breathe dust which has been contaminated by dried tuberculous 
sputum. 

Kingsford found in analysis of 339 cases that 216, or 63.7 per cent., 
occurred by inhalation, 65, or 19.1 per cent., by ingestion, and 17 per cent, 
were of doubtful origin. 



TUBERCULOSIS 291 

That tuberculous infection by way of the alimentary tract occurs very 
commonly as the result of drinking milk from tuberculous cows, or milk that 
has been contaminated by the sputum from tuberculous human beings has 
long been held. The infection of milk by coughing or sneezing by persons 
suffering from this disease occurs quite frequently. The milk of a tuber- 
culous cow will convey the infection even if local tuberculous lesions are 
not present in the udder, and the bacillus may be found in butter made 
from such milk. The fact that tuberculosis is so frequently found in the 
mesenteric glands of young children is significant in this connection. Infec- 
tion by the meat of a tuberculous animal can only occur if the meat actually 
contains the bacilli and is eaten uncooked. This form of infection is 
probably very rare except when sausages made from what are known as 
Bologna cows 1 are eaten in a raw or half-cooked state. 

Medical publications have teemed during the last few years with rather 
heated debates as to the communicability of bovine tuberculosis to man. 
In the minds of some bacteriologists, in Germany in particular, this question 
is still sub judice, but the majority of those best qualified to judge now agree 
that no doubt can exist of its transference, particularly from the udders of 
tuberculous cows to the mesenteric glands of children who drink the milk 
from these animals. 

Raw, Theobald Smith, and others have maintained that man is subject to 
two forms of tuberculosis, one derived from members of his own zoological 
group and another due to infection by the bovine bacillus. The wide 
distribution of tuberculosis in the animal kingdom, the morphological, 
cultural, and pathogenic differences in the bacillus found under different 
conditions, and the generally admitted possibility of ranging these organisms 
in a scale, or at least in closely allied groups, explain, at least in part, the 
different phenomena as seen in man. 

The mere presence, however, of the tubercle bacillus is not the only requi- 
site for the development of tuberculosis, for as already stated the tissues must 
be in a favorable state for its growth. This favorable state is produced by 
any cause which impairs vital resistance and prevents the body from destroy- 
ing invading micro-organisms soon after they enter it. Of these causes, 
aside from diseases which impair the general health, we find the most 
potent are bad air, particularly that due to poor ventilation when large 
numbers of persons are crowded together; lack of exercise, so that all parts 
of the lungs are not thoroughly expanded; and, lastly, those conditions of 
air and soil which are associated with excessive humidity, particularly if 
there be much dust in the atmosphere, as in large cities. 

In addition to these causes, which increase the susceptibility of all persons, 
we also find that certain individuals inherit conditions which undoubtedly pre- 
dispose them to this disease. They belong to two classes : those who by inheri- 
tance possess faulty thoracic development, or bad chest configuration, so that 
the apices of the lungs never expand properly, and those who seem to inherit 
a condition of the tissues which is unable to cope with the infection when it 
takes place. Both these causes are often present in one case. Such persons 

1 A Bologna cow is an animal so feeble and wasted that it cannot be used for milking, breeding, or for 
the providing of ordinary butchers' meat. It is killed and used 10 make sausage. 



292 DISEASES DUE TO A SPECIFIC INFECTION 

are usually lightly built and have small bones and delicate features, with a 
thin skin and superficial veins about the temples. It is a mistake, however, 
to think that this configuration is always present, for another type exists in 
which the bony structures are large and the muscles powerful, the so-called 
"lanky" type, in which tuberculosis is very apt to run a rapid course. Every 
clinician of experience has been astonished to find active tuberculosis of the 
lungs in heavy and powerfully built men, and has seen more than one 
generation of the same family, though strongly built, succumb to this 
malady, although promising in early life to escape all danger from it. In 
these instances the vital resistance to infection is poor, although the physique 
may seem excellent. 

The influence of age upon the development of the disease is distinct, but 
it is not sufficiently powerful to confer immunity upon any period of life. 
In the first ten years of life tuberculosis is quite common, affecting the 
lymphatic system most frequently, the bones being also commonly involved, 
and more rarely the membranes covering the brain. After puberty the 
pulmonary tissues are the parts which are affected in the majority of cases, 
and this predisposition of the lungs to the disease persists throughout the 
rest of life, although after the thirty-fifth year the frequency of pulmonary 
tuberculosis rapidly decreases, so that in persons over fifty years of age it 
is really very uncommon as a new ailment, unless they have been specially 
exposed by occupation to infection by the malady. The only cases I have 
seen of primary pulmonary tuberculosis which bego.n in persons of over 
fifty years of age were miners and grinders. 

The sexes are about equally affected by tuberculosis. 

Of the races, negroes and North American Indians are very susceptible, 
and half-breed negroes and half-breed Indians are peculiarly prone to the 
malady. I have had opportunities of studying the frequency of tuberculosis 
among both of these classes and have been impressed by this well-recognized 
fact. Perhaps this susceptibility is due to the fact that the white father is 
usually a degenerate, or one whose vitality is impaired by alcohol and abuse. 

Of the occupations which favor the development of tuberculosis may be 
named knife-grinding, mining, weaving, and other pursuits which cause 
large quantities of dust to enter the lungs. (See Pneumonoconiosis.) 

All the infectious diseases which diminish the vitality of the patient pre- 
dispose him to infection by this bacillus. Thus, pneumonia, particularly that 
of the catarrhal type, not rarely causes pulmonary tuberculosis to develop, 
and influenza renders the patient especially prone to its development. In 
many cases the catarrhal process provides the centre in which a new, or 
an old and slumbering, infection can become active. Among the acute 
infections, measles and whooping-cough are active predisposing factors, 
causing catarrhal pneumonia or exhaustion and diminished vitality. Dia- 
betes mellitus very commonly ends in a rapid and fatal tuberculosis. 

A very important point is the relation of injury to the development of 
tuberculous lesions. There can be no doubt that trauma to the chest wall 
may be followed by an outbreak of pleural or pulmonary tuberculosis, that 
injuries to the joints, even if seemingly trivial, may cause tuberculous arthritis, 
and blows on the abdomen may incite tuberculous peritonitis or tuberculosis 



TUBERCULOSIS 293 

of the retroperitoneal or mesenteric glands* (See also article on Pneumonia 
for traumatic lesions of the thorax followed by pulmonary disease.) 

Prevention. — In the prevention of tuberculosis the most important factor 
is the destruction of the bacillus as soon as it leaves the body of the patient 
This is by no means as easy to accomplish as would appear at first sight, 
since it is often expelled in enormous numbers by sneezing and coughing. 
The moustache or beard of the consumptive is a veritable nest of infection, 
and his bed-clothing may be equally virulent unless he holds something in 
front of his face when he coughs. *v 

All sputum should be received into rags,which should be burned in a hot fire 
before they become dry, or into a paper spit-cup which can be burned. If a 
china cup is used, it should always contain bichloride of mercury solution. 

Largely through the efforts of Dr. Herman Biggs, of New York, the 
health department of that city has been active during the last ten years in 
stamping out tuberculosis, or consumption. Under an ordinance, physicians 
are required to report every case of this disease that comes under their care. 
In the poorer districts of the city this is followed by inspection, and, if 
necessary, disinfection of the quarters occupied by the sick man, and this 
again has been supplemented by the distribution of circulars in which 
directions are given whereby the patient can take precautions against the 
infection of his family, and the family can protect themselves. 

The second great preventive of tuberculosis is sunlight, for sunlight 
destroys the bacillus. If this w^ere not the case our streets w r ould infect 
more thousands than they do. Sunlight not only destroys the bacillus, but 
increases the vital resistance of the patient and of the uninfected as well. 
The absence of sunlight and the presence of bad air are the most potent 
auxiliaries to the disease. This is shown by the prevalence of the malady 
in tenement houses, in prisons, and in asylums which are badly arranged or 
managed. These facts have not only been proved on a gigantic scale by 
unintentional tests w T ith human beings, but experimentally as w T ell, particu- 
larly by Trudeau, who inoculated two sets of rabbits with the bacillus 
tuberculosis. He kept one set in a dark cellar and these animals suffered 
an unusually high mortality. The other set he turned out-of-doors, and 
these animals survived or were affected only by a modified form of the disease. 

In those who have an hereditary predisposition to the disease or w 7 ho have 
a faulty thoracic development, out-door life is in many cases an absolute 
necessity to prevent the disease. 

It is proven that tuberculosis can be conveyed from animals to man, and 
it would seem unwise to give up such precautionary measures as careful 
inspection of cattle in slaughter-houses and the proper control of cows 
supplying milk, and especially when the latter is to be used as an infant 
food. 

Frequency. — The prevalence of tuberculosis in its various forms is very 
great. About one death in every seven is due to this cause, and when we 
add to this fact the additional statement that a very large proportion of 
those who die of other diseases show more or less well-developed tuberculous 
lesions, it becomes evident that tuberculosis contributes to the death of a 
still larger proportion of persons. Thus Schlenker in 100 autopsies made 



294 DISEASES DUE TO A SPECIFIC INFECTION 

on adults and children dying of various diseases found that 65 per cent, 
had tuberculosis. Biggs found it in 60 per cent, of his postmortems, and 
out of 4000 consecutive autopsies in Breslau about 1300 showed tuberculosis. 
These statistics, which give some conception of the ordinary prevalence of 
the disease, are outclassed in an extreme degree by the reports of Naegeli 
in Zurich, who found in the Pathological Institute of that Canton that 
500 consecutive autopsies revealed tuberculosis in some form in 97 per cent. 
This percentage held true of adults as well as of children. Naegeli also 
found that tuberculosis is very rare in the first twelve months of life, un- 
common up to the age of five years, but so frequent from five to fourteen 
years that it was found in one-third of all bodies examined. In studying 
these statistics of Naegeli it must be remembered that in many of the autop- 
sies tuberculosis was not the cause of death, and in some cases was present 
in such a very slight degree that only careful search revealed its presence. 
Burrell believes that about 70 to 80 per cent, of all persons who reach the 
age of forty years have or have had some form of the disease. 

The far greater frequency of tuberculosis in cities as compared to country 
districts and villages is shown by the statistics of Paris, in which the number 
of cases per thousand is 4.9 per cent.; whereas in 662 villages in France it 
is only 1.81 per cent. 

Notwithstanding these facts it is interesting to note that in many parts 
of the world tuberculosis has undergone a most remarkable decrease in its 
frequency, although the mortality rate of 1 in 7 still holds true for nearly 
all cities. In New York the mortality has decreased from 4.6 to 2.6 per 
thousand in ten years, and a similar fall of about 40 per cent, has occurred 
in Philadelphia in that time. Abbott has shown that in 1853 the mortality 
of pulmonary tuberculosis in Massachusetts was 42 per 10,000 inhabitants, 
whereas in 1895 it was 21.8 per 10,000 inhabitants. The decrease in 
the entire United States has been from 25 per 10,000 in 1890 to 19 per 
10,000 in 1900. Hiller has shown that at the present rate of decrease 
the disease will be extinct in Prussia in 1927 and in England about 1947. 
In Prussia the mortality fell from 31 per 10,000 in 1886 to 19 per 10,000 
in 1901, and in England it has fallen 50 per cent, in the last forty years. 

A very great difference in frequency is found in different races. Thus, 
in the United States the death rate in those of English descent is 15 per 
10,000, whereas for the Irish it is 43, and 59 for the colored race. 

Occupation also makes great differences; thus, the death rate among 
tradespeople is 17 per 10,000, among barbers 33 per 10,000, book-keepers 
40, and stone-cutters 54 per 10,000. 

The average age at death from pulmonary tuberculosis is thirty-five years, 
but the actual incidence of the disease is from fifteen to thirty-five years. 

The relative frequency of the different forms of tuberculosis is difficult 
to determine. Statistics of deaths from tuberculosis in Ireland from the 
years 1891 to 1901 show T the following figures as to the relative frequency: 

Pulmonary tuberculosis 21.35 per 10,000 

Tuberculosis of the mesenteric glands . . . 2.2 " " 

Tuberculous meningitis 2.25 " " . 

Other forms of tuberculosis 2.3 " " 



TUBERCULOSIS 295 

Some difference exists, however, between the frequency of primary and 
secondary lesions. Thus, Heller, of Kiel, found but 1.45 per cent, of primary 
intestinal tuberculosis, but 37.8 per cent, in which the principal lesion was 
abdominal. 

Pathology and Morbid Anatomy. — As already stated, when discussing the 
etiology of tuberculosis, the bacillus enters the body usually through the 
respiratory mucous membrane, or through that of the alimentary canal. It 
is possible, however, for infection to take place through the skin, but this 
is usually followed by a localized lesion and rarely by visceral disease. The 
results which accrue from the entrance of the bacillus, in the manner indi- 
cated, vary greatly with the virulence of the micro-organism, the vital 
resistance of the individual and the organ or part in which the primary 
localization of the bacillus takes place. The effect of the bacillus upon the 
local tissues is to cause an accumulation of cells in the immediate neighbor- 
hood, followed in favorable cases by repair or, under less promising condi- 
tions, by necrosis. This aggregation of cells, composed of lymphoid, hyaline, 
endothelial, and, it may be, giant cells, and containing the bacillus, is the 
histological or rather anatomical characteristic of the disease, and is called 
a tubercle. 

In the great majority of instances the pathological process which is 
induced is inflammatory in type, and, as already stated, the lungs and their 
adjacent lymph nodes are the parts which are usually affected in adults, 
whereas in young children the gastrointestinal tract and its adjacent glands 
are commonly involved either alone or with the structures just mentioned. 
When the collection of the cells is small the growth is said to be a miliary 
tubercle, because it is thought to be the size of a millet-seed; but when a 
single tubercle grows to be so large as to be called a nodule its growth to 
these proportions is accomplished by the addition of a number of miliary 
tubercles. This growth usually is limited, in the miliary tubercle or nodule, 
by the fact that an exudate takes place, as part of the inflammatory process 
which the bacilli produce, which prevents the spread of the bacilli to 
adjacent areas, and so limits the field occupied by the micro-organisms. 

As the disease progresses this exudate becomes organized and is finally 
developed into a dense fibroid or cicatricial tissue, which acts as a protective 
barrier against the spread from that particular area of invasion. This barrier 
in a great number of cases remains effective and in a sense imprisons or 
restricts the production of poisons and lessens their dissemination. Within 
this limited zone of action the bacterial products cause necrosis and in 
the dead tissue the germ is suppressed or actually destroyed. After the 
local necrotic process is complete the necrotic contents are more or less fully 
absorbed and only a cicatrix remains to mark the site of the original lesion, 
or if this does not take place the caseous and degenerated mass undergoes 
calcification. In either instance a natural process tends to bring about a 
cure. 

If for any cause this protective barrier is removed by absorption while 
the imprisoned bacilli are still alive, or if the wall which is formed is incom- 
plete, the bacilli escape and speedily infect adjoining or distant areas, being 
conveyed by the lymph or blood streams. Such is the explanation of those 



296 DISEASES DUE TO A SPECIFIC INFECTION 

cases in which a patient who has suffered from some acute infection, like 
pneumonia, typhoid fever, or influenza, speedily develops tuberculosis during 
convalescence, although the acute illness may, by confining him to a healthful 
and well-ventilated room,have protected him from any recent infection. 

In still other cases the protective barrier of surrounding exudate is not 
formed and the amalgamation of tubercles produces a nodule which undergoes 
necrosis and softening and its bacterial contents become diffused into the 
surrounding tissues, thus spreading the infection. In still a third type of cases 
the lesions consist in a diffuse exudative process, with little or no tubercle 
formation, and as a consequence we find that it is possible for the entrance 
of the tubercle bacillus to be followed by a tuberculous pneumonia or pulmo- 
nary consolidation, tuberculous serositis, or lymphadenitis, the lesion not 
containing the characteristic tubercle. In other words, in certain instances 
the tuberculous inflammation is so intense and the poison formed by the 
bacilli is so abundant or virulent, or the resistance of the soil so inadequate, 
that no attempt at protection is made, but instead there occurs a profuse 
exudative process which is extremely liable to undergo necrosis, and this 
results in rapid breaking down not only of the exudate itself, but of the 
involved tissues as well. 

Under certain admittedly unusual conditions the tubercle bacillus becomes 
distinctly pyogenic and, rapidly developing in the lung, produces not only the 
degenerative and necrotic changes peculiar to tubercle formation, but fills the 
air vesicles with pus, serum, and dead epithelial cells and leukocytes, a state 
in which the part involved speedily goes on to widespread destruction. It 
is also to be recalled that in nearly all cases of tuberculous disease infection 
by other pyogenic organisms, such as the staphylococcus and streptococcus, 
aids in producing local inflammation and pus, and leads to the formation 
of toxins which cause local and general impairment of vitality. 

In some cases, on the other hand, the bacilli, in the presence of the resist- 
ance offered, do not seem capable of originating an acute inflammatory 
process, nor do they cause the formation of tubercles with caseation, but 
produce a condition in which an excessive formation of connective tissue 
occurs, which prevents the rapid spread of the disease and constitutes a 
form of infection called chronic hyperplastic tuberculosis in the intestine 
or in the lung which is closely allied to fibroid phthisis, so called ; but this 
fibroid process is by no means entirely dependent upon the presence of the 
bacillus tuberculosis, since other causes may produce it. 

It is fully established that the action of the tubercle bacillus in the human 
organism is due to its poisons, a number of which have been described. 
The early coagulation necrosis and subsequent caseation are clearly the 
result of bacillary toxins. The tendency to fibrosis seen in many cases has 
been thought to be due to a sclerogenous toxin and the frequent cheesy 
disintegration, so commonly present, to a caseogenous poison; it is probable, 
however, that the same noxious agent in some individuals induces caseation 
and in those more resistant to its action a fibroid or fibrocalcareous change. 
Progressing caseation may be looked upon as an evidence to low resistance, 
while fibrosis, with or without calcification, indicates strong reparative and 
antagonistic powers on the part of the affected tissues. 



TUBERCULOSIS 297 

With these preliminary remarks we may proceed to a discussion of the 
various manifestations, pathological and clinical, which are to be met with 
in persons affected by this disease. 

Acute Miliary Tuberculosis. — By acute miliary tuberculosis is meant 
a condition in which a single organ, or a number of organs, or perhaps 
the whole body, is infected by the Bacillus tuberculosis, causing the forma- 
tion of innumerable tubercles of the type already described. It arises not 
by the inhalation of dust laden by bacilli, but by the escape of bacilli in 
large numbers from some infected focus, as, for example, a caseous lymphatic 
gland. The escape takes place into a bloodvessel, and in a few hours at 
most the bloodvessels of the neighboring parts, or perhaps of the entire 
body, are swarming with bacilli, so that in a very brief space of time the 
lungs, the liver, and other parts are found studded, or, as it has been well 
expressed, "stuffed," with miliary tubercles. The caseous gland or primary 
cheesy nodule which gives origin to this acute secondary infection is usually 
so situated that it is adherent by inflammatory products to a vein, commonly 
the pulmonary vein or one of its branches, or to the thoracic duct, or the 
superior cava. By a process of extending necrosis the soft contents of the 
gland, laden with tubercle bacilli, break into the vessel or duct. Sometimes 
an active tuberculosis of the wall of the bloodvessel is present, so that tubercles 
may be found in the intima. Councilman has observed a tuberculous aortitis 
apparently resulting from infection through the vasovasorum. 

Weigert has divided the results of this vascular invasion by the bacilli 
into three classes: (1) that in which all the organs of the body become 
filled with tubercles of the miliary type; (2) that in which the disease, though 
widely disseminated, nevertheless appears in multiple but widely separated 
foci; and (3) that in which the tubercles are not so numerous, their growth 
is more chronic, and their size causes them to be classed as nodules. This 
is manifestly an artificial division which is not closely adhered to under 
natural conditions, for the process may represent all these types in one 
case, while in other instances it may be impossible to tell to which class 
the case belongs because the lesions shade into one another. 

Symptoms. — The symptoms of widely diffused miliary tuberculosis are to 
be carefully studied because they simulate those of enteric fever and other 
typhoid states so closely that not rarely an erroneous diagnosis is made. 
The chief manifestations may be said to be those of profound toxaemia 
without any localized lesion to explain the illness, which begins with the 
general wretchedness common to the early stages of all acute infections and 
which is followed by fever, rising each evening to 102° or 103°. The pulse 
is unduly rapid, and there are often profuse sweats. In such cases there 
are three symptoms which, while not pathognomonic by any means, are 
nevertheless of some value in separating this condition from typhoid fever. 
The fever is often irregular, sometimes breaking with a profuse sweat. In 
other cases it is higher in the morning than at night. The pulse is often 
exceedingly rapid in the early stages, a phenomenon which, as a rule, is not 
observed in typhoid fever. The temperature does not resist cold sponging 
in the first week as does that of typhoid fever, but, on the contrary, falls with 
great rapidity to below normal. Later there is the absence of rose spots 



298 DISEASES DUE TO A SPECIFIC INFECTION 

to lead one to a correct opinion, and careful examination of the lungs may 
reveal some area of infiltration or softening, or of dulness on percussion 
which should arouse suspicion. 

Additional differential factors are as follows: There is absence of the 
Widal reaction. This reaction, however, often does not appear in typhoid 
fever until after the tenth day. Tubercle bacilli may, by spinal puncture, 
be found in the cerebrospinal fluid, and in some instances the ophthal- 
moscope will reveal tubercles in the choroid. Rarely the bacillus can be 
demonstrated in the blood or urine. Enlargement of the spleen, the diazo 
reaction in the urine, the presence of active diarrhoea or severe constipation, 
and the fever are not differential points in favor of typhoid, for they 
all appear in miliary tuberculosis. Unlike typhoid fever, herpes labialis 
may be present in acute miliary tuberculosis. 

In other instances the disease has a much more abrupt onset. The 
patient is seized with a chill followed by high fever, or rapid pulse, pro- 
found prostration, and copious sweats. Emaciation proceeds with remark- 
able rapidity. The aspect of the patient is profoundly toxic or septic and his 
expression anxious. The tongue is dry and the cheeks flushed. 

When miliary tuberculosis involves the lungs the pulmonary symptoms 
are chiefly those of diffuse acute bronchitis, although careful examination 
may reveal at one apex, or at both, some impairment of resonance due 
perhaps to an ancient infection. The general symptoms are distinctly 
asthenic, as already described, and added to them there are fine rales over 
the greater part of the chest and a degree of dyspnoea far out of propor- 
tion to the lesions which can be discovered. The respirations may be unduly 
rapid. The cyanosis is very pronounced, the cough constant, and the patient 
may seem surprisingly ill considering that no cause can be discovered. The 
sputum may be rusty or blood-streaked, or a true hemoptysis may develop. 
Auscultation may reveal pleural friction due to tuberculosis of the pleura, 
and as the case progresses widely distributed rales may be heard in the 
back and front of the chest. In these cases great mental anxiety is often 
a marked symptom unless the disease attacks a child, when the patient 
usually lies limp and apathetic and perhaps stuporous. 

These patients usually die in from one to three months, but cases are 
occasionally met with in which death ensues as early as the fourteenth day. 
In still other instances the case becomes less fulminating in character, 
the symptoms moderate, and the patient passes into ordinary subacute 
pulmonary tuberculosis. Acute tuberculous bronchopneumonia is more 
frequently seen in children than in adults. 

Diagnosis. — The diagnosis is not difficult in the pulmonary form if there 
is a history of an old tuberculous lesion elsewhere, or if the marked cyanosis 
as compared to the apparent limited area of disease is considered. Here 
again the presence of tuberculous foci may, if found, show that an acute con- 
dition is imposed upon an older one. The physician must not be led into 
the belief that the lungs are normal because he is able to elicit a clear and 
resonant percussion note on the chest wall, for a compensatory emphysema 
often is present in these cases. 

When the miliary process chiefly or entirely involves the meninges the 



TUBERCULOSIS 299 

symptoms are of course cephalic in large degree, and we have that grave 
state known as acute tuberculous meningitis present. 

Spinal puncture to determine the cause of the disease is a most valuable 
aid. If tuberculosis is present the cerebrospinal fluid will be turbid and 
occasionally, if it is placed in a centrifuge, the bacilli can be found, or some 
of the fluid may be injected into a guinea-pig, which will develop tubercu- 
losis, if this be the cause of the illness. 

From typhoid fever of the meningeal type tuberculous meningitis is sepa- 
rated by the presence of spots, by the diazo reaction, and the Widal test. 
Again, the diagnosis of tuberculous meningitis may be confirmed if a focus 
of primary tuberculosis can be found in the other organs as in the lungs, 
the bones, or the mesenteric glands. 

Prognosis. — The prognosis is always fatal, although cases said to have 
recovered have been reported 

Treatment. — The treatment consists in the use of nutritious food and 
stimulants and in the relief of restlessness by chloral or the bromides. 

Glandular Tuberculosis. — Glandular tuberculosis, or tuberculosis of the 
lymphatic glands, is the condition which was formerly called "scrofula" 
before Koch demonstrated the existence of the tubercle bacillus. It is now 
known that no such disease exists as scrofula, or scrofulosis, in the sense 
of a separate entity. 

Tuberculosis of the lymph glands is often a very mild form of the infection 
and the mortality from its presence is very low. Indeed, it may be said that 
if the infection does not escape to other parts of the body life will not be 
seriously jeopardized. 

In studying this state it must be recalled that one of the important functions 
of the lymph nodes is to arrest and perhaps destroy such micro-organisms 
as may endeavor to enter the general system. As soon as pathogenic 
germs enter a healthy gland one of several processes takes place. In a 
strong individual with great vital resistance the gland becomes enlarged 
and active in an evident endeavor to destroy the invaders. In this it may 
succeed, or the few bacilli which escape are caught and destroyed by 
other adjacent glands. If the infection is virulent and the vital resistance 
is below par, the battle is more prolonged, the inflammation in and about 
the gland is more active, and the general system may be saved by the addi- 
tional safeguard of a wall of protective tissue thrown around the infected 
gland to protect the rest of the body. In still other cases the glands go 
on to caseation and the necrotic contents escape externally or even internally. 
It is a noteworthy fact, however, that this so-called pus is usually sterile 
or contains bacilli in such small numbers as to be demonstrable only by 
inoculation experiments. Again, if the infection wins the battle and the 
gland undergoes caseation, it is still possible for the area to be surrounded by 
a fibrous barrier which walls up the caseous mass and its bacilli and protects 
the body even though the gland is destroyed. 

When the protective processes fail the bacilli pass the lymph nodes, or a 
caseous gland in juxtaposition to a bloodvessel breaks, and general tuber- 
culosis ensues as already described. 

Tuberculous infection of the lymph nodes takes place in four chief areas : 



300 DISEASES DUE TO A SPECIFIC INFECTION 

the cervical glands, the mediastinal glands, and the mesenteric and retro- 
peritoneal glands. In the first class the infection takes place through the 
tonsils, in the nasopharynx, or because of the presence of bad teeth or a break 
in the gums. The mediastinal glands suffer by the entrance of the bacillus 
through the mucous membrane of the larynx, bronchial tubes, or smaller 
bronchioles, while the abdominal lymphatics receive their infection from 
the intestines. 

The diagnosis of cervical adenitis is not difficult, although occasionally, 
when the disease is bilateral and the swelling is great, the possibility of 
Hodgkin's disease may have to be considered. 

The involvement of the mediastinal glands by tuberculous infection 
results in a spread of the disease to the retroperitoneal lymphatics or in 
the growth of the tissues affected to such a degree that lymphatic tumors 
may be formed which cause serious symptoms by pressure. Thus, the 
recurrent laryngeal nerve may be pressed upon and laryngeal spasm result, 
or the superior vena cava or pulmonary vein suffers from compression, and 
in a similar manner bronchial obstruction may ensue. More important, 
however, than the pressure symptoms are possible perforation by ulceration 
of the bronchi or trachea, or even of the bloodvessels w T ith rapid diffusion 
of the infection all through the body. So, too, it is possible for bacilli to 
enter the lung, to pass to the lymphatics, to cause disease in these glands, 
and finally cause pulmonary tuberculosis, pleural tuberculosis, or pericar- 
dial tuberculosis by softening and rupture into these parts through the 
adhesions which are formed. 

In diseases of the retrobronchial glands auscultation over the upper end 
of the sternum, when the head is well thrown back, may reveal a tracheal 
hum, and careful percussion may elicit some dulness. 

When the mesenteric and retroperitoneal glands are involved, producing 
what is called "tabes mesenterica," the child is anaemic, poorly nourished, 
has constipation alternating with diarrhoea, and presents an enlarged abdo- 
men ("pot-belly")- The size of the belly as compared to the rather w r asted 
arms, legs, and thorax is noteworthy, and careful palpation may occasionally 
reveal enlarged glands deeply situated in the abdominal cavity. This con- 
dition is to be separated from tuberculosis of the peritoneum and from 
consumption of the bowels, for both of these structures are usually free 
from the disease in these cases, although they may be infected by softening 
of the glands themselves. These lesions probably exist in a far larger pro- 
portion of cases than is generally thought, and end by a process of fibrosis 
and calcification, for the involvement of these glands is met with in many 
cases at autopsy when death is due to another cause, and when no sus- 
picion of tuberculous infection has been present. 

Treatment of Glandular Tuberculosis. — Tuberculosis of the retrobron- 
chial glands and of the retroperitoneal glands can be treated only by 
sunshine and fresh air with residence by the sea, and by the internal 
use of tonics, of syrup of the iodide of iron and cod-liver oil to combat 
anaemia. 

Persistent enlargement of the cervical glands demands their surgical 
removal, not their incision, but their excision, because, as has already been 



TUBERCULOSIS 301 

stated, a tuberculous focus is always a threatening focus. On the other 
hand, it cannot be denied that large numbers of very healthy adults bear 
scars showing that they have had cervical adenitis in early life. In these cases 
the battle between vital resistance and tuberculous infection has been won 
by the individual. 

Tuberculosis of the Serous Membranes. — Tuberculosis of the serous 
membranes may be divided into the acute and chronic forms. The acute 
is further subdivided into (a) an acute serofibrinous form, macroscopically 
identical or indistinguishable from serofibrinous serositis arising from 
other causes; (b) an acute miliary tuberculous serositis due to the invasion of 
the serous membrane by tubercle bacilli and the formation of miliary tuber- 
cles. The two forms just mentioned may be distinct or coincident. The 
chronic tuberculous serositis may be (a) fibrocaseous or (b) fibrohyaline. 
The former results from the formation of tuberculous exudates, in which 
extensive caseation gives rise to cheesy accumulations of various sizes 
surrounded by granulations or more fully organized fibrous tissue. Marked 
calcareous change is frequently associated with this form. The fibrohyaline 
type is characterized by marked thickening, and the formation of adhesions 
by newly developed fibrous tissue of a peculiar, grayish, translucent form. 
Both the chronic forms may occur together, and the caseous masses may 
be enclosed by hyaline fibrous tissue of the type just mentioned. 

Acute Meningeal Tuberculosis.— Meningeal tuberculosis is an inflammation 
of the pia mater produced by an infection of this membrane with the bacillus 
tuberculosis and accompanied by an effusion of lymph, it may be the forma- 
tion of pus, and the development of tubercles. These tubercles are usually 
very minute, but occasionally are large from the amalgamation of several 
tubercles into one. They are most profuse at the base of the brain, hence 
the name basilar meningitis, and extend upward on its sides following 
chiefly the vascular pathways. In some instances, how T ever, the pia mater 
on the convexity of the brain contains more tubercles than exist at the base. 
Nearly always at the base there is a copious exudate of lymph which pro- 
duces a pearly, gelatinous appearance. The lateral ventricles are distended 
with fluid. Minot states that Robert Whytt, of Edinburgh, in 1768, first 
accurately described this condition, although he had no clear conception 
of its cause. Guersant, in 1827, reported that the pathological appearances 
of the membranes were of so peculiar a type that he suggested the name 
"granular meningitis." In 1830 Papavoine described the disease as a true 
tuberculous lesion, and the condition of moderate hydrocephalus which 
existed with the meningitis was recognized as having its origin in the tuber- 
culous infection. It was reserved for W. W. Gerhard, of Philadelphia, in 
1833, to show not only that this type of meningitis was tuberculous, but that 
it was practically in every instance secondary to some tuberculous lesion 
elsewhere. 

Symptoms. — The symptoms of acute meningeal tuberculosis are very 
characteristic, whether it occurs in children or adults. It is much more fre- 
quently seen, however, in children between two and seven years. These 
symptoms are best divided into three stages for study. At first the parent 
notices that the child is unusually peevish and irritable, or in other cases 



302 DISEASES DUE TO A SPECIFIC INFECTION 

peculiarly languid and indisposed to play. There is little restful sleep and 
the child often has night terrors. The appetite is capricious and the bowels 
irregular. After these symptoms have lasted for some days, during which 
time the tubercles have probably been deposited in the pia mater, the well- 
developed symptoms of the disease appear. Headache may be constant 
and is characterized by sharp exacerbations of pain which cause the child 
to give a peculiar high-pitched scream which is quite characteristic. Sudden 
attacks of vomiting of an explosive character may occur. At times a fleeting 
delirium may be present. 

It is almost impossible in many of these cases to exclude early typhoid 
fever, for a similar train of symptoms may be presented in its early stages. 

The temperature is usually elevated, rising as high as 102° or 103°. The 
pulse is slow and the respirations are irregular and sighing. Rapid emacia^ 
tion takes place, and if the child be very young, so that the fontanelle is 
open, there may be distinct hydrocephalic enlargement. The patient now 
lies stuporous or somnolent, with the eyes half closed. Indeed, the appear- 
ance may be that of deep sleep with sighing breathing. 

In some cases in which the onset of the affection is rather acute, the patient 
suffers from a series of convulsions. I have seen such a case with Dr. 
Brouwer, of Tom's River, New Jersey, while preparing this article, in which 
the child had as many as sixty convulsions in twenty-four hours. 

As the exudate increases symptoms of intracranial pressure and signs of 
interference with the cranial nerves appear, so that squint, twitching of the 
facial muscles, and chewing movements of the lips and jaws develop. 

Even as late as this the patient may be aroused and will seem so much better 
for a time that the friends are much encouraged, but a relapse inevitably occurs. 
The child is now too stuporous to be roused, the eyes are filled with sticky 
secretion, and the parents find solace in the belief that even if hopelessly ill 
the patient does not suffer. This solace is, however, occasionally rudely dis- 
pelled by a shrill, piercing cry which, interrupting the profound stillness, is 
more than usually startling. As death approaches the pulse becomes very 
rapid, probably from vagal paralysis, the pupils no longer react to light, and 
the eyeballs are rotated upward. 

The duration of the entire illness is about ten to eighteen days, as a rule, 
but cases may die as early as the end of five days, in a convulsive seizure, or 
they may last for several weeks. 

Diagnosis. — The diagnosis of acute miliary tuberculous meningitis must 
be made with the recollection that the following conditions simulate it: 
Acute meningitis not due to tubercle is rare in children, has a more sudden 
onset, as a rule, and ends in a week in most cases. The delirium accom- 
panying it is more marked, the febrile movement is more sharp, and there 
is usually no history of tuberculosis in the parents, as there is in the tuber- 
culous case in many instances. 

From cerebrospinal meningitis of the epidemic type it is separated by the 
sudden onset of that disease, by the absence of its eruption, and by the 
fact that no cases of cerebrospinal meningitis have occurred in the vicinity. 
By spinal puncture the meningococcus may be obtained in one case and the 
tubercle bacillus in the other, although the latter is not frequently discovered. 






TUBERCULOSIS 303 

The fluid in cerebrospinal fever contains polymorphonuclear cells and 
hyaline leukocytes, while in tuberculous meningitis recent studies seem to 
show that a lymphocytosis is the rule. (See Cerebral Spinal Fever.) 

Tuberculous Pleurisy. — Tuberculous pleurisy is, in the vast majority of 
cases, secondary to tuberculous infection in other parts. Most commonly 
the primary focus is in the lungs or in the mediastinal glands. In some 
instances the process is the result of a general infection which results in 
miliary tuberculosis, and in these instances it not infrequently happens that 
the pleura is involved without there being any tuberculous process in the 
lungs. Thus Hodenpyl, in 91 autopsies on persons in whom the lungs were 
free from tubercle, found miliary tuberculosis of the pleura in 41, both the 
parietal and visceral layers being affected. He also believes that miliary 
tuberculosis of the pleura is apt to undergo fibrous changes. 

The tuberculous lesions are of three types. In the first type we find 
scattered patches of tuberculous deposit which are the continuation of a 
tuberculous process in the lung beneath the visceral layer of the pleura, 
or similar patches are found which are independent of lung involvement, 
or again patches appear upon the parietal pleura. In the second type the 
lesions are simply those of a widespread miliary tuberculosis of the pleura, 
and in the third type, which is representative of a more chronic or slow 
process, there is great thickening of the pleura, partly as the result of the 
organization of formed exudates and also of proliferative changes in the 
primitive serous layers. Throughout this tissue and exudate miliary tubercles, 
or masses of miliary tubercles, appear. These undergo coagulation necrosis 
in some instances. 

The presence of any one of these processes usually results in the out- 
pouring of a certain amount of effusion which is often serous and by no 
means rarely purulent. When it is serous it is lacking in fibrin and it may 
be tinged with blood. The physician should recall the important clinical 
fact, in connection with these tuberculous pleural effusions, that whether 
they be serous or purulent, an examination of the fluid will rarely reveal 
the tubercle bacillus unless in some manner these organisms are dislodged 
from the pleural surface by scraping. In some cases the effusion is not 
due to the bacillus tuberculosis alone, but to an associated infection. Thus, 
in the purulent type the pneumococcus, streptococcus, or staphylococcus 
pyogenes are often found. (See Empyema.) 

Reference has already been made to the fact that the visceral layer of the 
pleura is often infected by a tuberculous process in the lung as a result of 
direct extension. It may be added that in nearly every case an inflammatory 
area — that is, a localized pleuritis — exists over the seat of the disease in the 
pulmonary tissues. This condition often gives rise to pain in the chest 
and not rarely causes adhesions between the layers of the pleura. The 
inflammatory process, while tuberculous in origin, is not necessarily tuber- 
culous in character, but it often becomes tuberculous as already stated. 

Sometimes when the tuberculous mass in the lung softens and breaks 
down the visceral layer of the pleura is perforated and sudden dyspnoea and 
pain ensue, with the production of pneumothorax. (See Pneumothorax 
and complications of Pulmonary Tuberculosis.) Through this opening 



304 DISEASES DUE TO A SPECIFIC INFECTION 

infection with pyogenic bacilli occurs or the Bacillus tuberculosis becomes 
pyogenic, and as a consequence pyopneumothorax develops. (See Pyopneu- 
mothorax.) 

Tuberculosis of the Pericardium. — Like tuberculosis of the pleura, peri- 
cardial tuberculosis is usually secondary to primary infection elsewhere. It 
may, however, be primary. It occurs in two forms: the miliary, in which 
the small tubercles are scattered or profuse, and in a form in which the 
entire pericardium, both in its visceral and parietal layers, is thickened by 
an inflammatory exudate which is associated with the development of 
tuberculous masses which undergo cheesy change. In this type the peri- 
cardial space may be nearly obliterated by the adhesions which are formed 
between its layers. It is a noteworthy fact that although the pericardium 
is so near the lungs and pleura it is, comparatively speaking, rarely infected. 
Out of 1048 autopsies Wells found tuberculous pericarditis only 16 times 
and in 4500 autopsies Baginsky found it 15 times. In 1317 autopsies on 
phthisical patients Willigk found tuberculosis of the pericardium 11 times. 
Leudet found it 8 times in 299 autopsies. In 1000 autopsies Osier found 
7 cases of tuberculous pericarditis. Ellis has recently reported from the 
laboratories of the Jefferson Medical College a case in which the heart, the 
pericardium, and the mediastinal tissues formed one large, adherent mass 
of tuberculous nodules. 

The symptoms presented by tuberculosis of the pericardium may be so 
slight that no suspicion of the pericardial disease exists during life, or they 
may resemble those of mediastinopericarditis, or adherent pericardium. 
(See Adherent Pericardium). 

Tuberculosis of the Peritoneum. — Aside from tuberculosis of the lungs, 
tuberculosis of the peritoneum is the most frequent and most important 
manifestation of tuberculous infection met by the physician. The statistics 
of Grawitz and Brunn show that in 13,422 autopsies tuberculosis of the 
peritoneum was found 284 times. 

In 2802 autopsies on tuberculous subjects, collected from various sources, 
the peritoneum was involved in 571, a percentage of 20.36. These figures 
represent all ages. Steiner found the peritoneum affected in 92 out of 800 
cases of tuberculosis occurring in children, or in 11.5 per cent. 

As to the relative frequency of the disease in adults and children Aldibert's 
statistics, based on 326 cases, are of interest. Of these 326 cases, 274, or 
84.05 per cent., occurred in adults and the remaining 52, or 15.95 per cent., 
occurred in children. It is in a very large proportion of cases secondary 
to tuberculous foci elsewhere. The combined statistics of Munstermann, 
Borschke, and Pribram, comprising 437 cases of tuberculous peritonitis ex- 
amined postmortem, showed that only 3 were primary. 

A tuberculous family history is present in 53 per cent, of cases. The 
disease is much more common in the female than in the male; according 
to Nothnagel 90 per cent, of the cases are females. Konig's statistics make 
it 78 per cent. 

Tuberculous peritonitis is of especial interest not only because of its 
frequency and gravity, but because it is, in one type at least, more readily 
cured than any other well-developed form of internal tuberculosis. It occurs 



TUBERCULOSIS . 305 

in three chief varieties, viz., as an acute miliary tuberculosis, as a chronic 
tuberculosis with large nodules and adhesions, and as a still more chronic 
form with fibroid changes. The relative frequency of the different forms 
of tuberculous peritonitis is shown by the following facts: In 46 cases 
which came under the observation of Munstermann, 25 were exudative, 
21 were plastic, and 8 were chiefly caseous. Of the 21 plastic cases 8 were 
fibrous. Herringham found fibrous adhesions in 18 out of 50 cases. Borschke 
found the miliary form in 16 out of 226 cases which came to autopsy. 

The acute miliary form is usually secondary to infection of the mesenteric 
and retroperitoneal glands, but occasionally in women the infection comes 
from the Fallopian tubes, or in males from the bladder or other part of the 
genito-urinary apparatus. The miliary tubercles are scattered widely over 
the peritoneum on both its visceral and parietal layers (Fig. 45), and 

Fig. 45 



Miliary tubercles of the surface of the small bowel and mesentery. (Kast and Rumpler.) 

the surface of the liver is often profusely peppered by these formations. In 
these cases there is a serous effusion into the peritoneum which in some 
instances is very profuse, particularly if the case is rather subacute in the 
rapidity of its course. 

The mode of its development is well illustrated by a case I saw some years 
since with my associate, Dr. Thornton. A girl of about twelve or thirteen 
years, while in apparently perfect health, was bathing in a pond and playing 
with a small row-boat, the sharp prow of which struck her a severe blow 
on the epigastrium, which made her nauseated and faint. She speedily 
20 



306 DISEASES DUE TO A SPECIFIC INFECTION 

began to lose weight and strength, became distinctly emaciated, and rapidly 
developed a marked ascites. The abdomen was opened and every peritoneal 
surface was found literally covered with tubercles. The fluid was allowed 
to escape, drainage was permitted, and perfect recovery followed. Un- 
doubtedly the blow on the belly ruptured a tuberculous mesenteric or retro- 
peritoneal gland, and so produced general peritoneal infection. In such 
a case no nodules can be found in the belly on palpation, but the presence 
of ascites in a child, or in an adult, without any signs of hepatic disease 
should lead the physician to suspect tuberculosis of this type, particularly 
if in addition there is present some fever of an irregular type, which is 
commonly moderate, but which may rise at times as high as 103° or even 104° 

How opening the belly and permitting drainage cures these cases is not 
known, but the clinical fact that such a result is often achieved is not to be 
denied, and this holds true even if this condition develops in adults. Walter's 
statistics show that 50 per cent, of adults who are subjected to laparotomy 
recover, and Herzfeld's statistics give a recovery percentage of 62 per cent, 
for children. Marganecci gives 85 per cent., von Krencki 71.5 per cent. 
Thomas 73 per cent. Hall reports 94 cures out of 110 operations. 

The second caseous type of peritoneal tuberculosis with nodules is charac- 
terized by the presence of caseous masses of tubercle which tend to ulcerate, 
which are associated with seropurulent, or purulent, effusion in moderate 
amount, and in which the belly cavity is not distended by fluid nor the 
intestines by gas, as in the miliary form just described, but is apt to 
present a peculiar pasteboard rigidity. The effusion in these cases is 
often sacculated by reason of the fact that there are formed adhesions 
which wall off spaces in which the fluid collects. These spaces may be 
between coils of intestine or contiguous mesentery, between the intestine 
and omentum, and between the omentum and the parietal peritoneum. 

In some instances these sacculations are capable of containing but a few 
drachms of fluid, but in those cases in which fairly large peritoneal areas 
are separated from the general peritoneum by adhesions very large accumu- 
lations of fluid may be present. If this takes place in the flanks or lower 
zone of the abdomen, where it usually occurs, the symptoms may very 
closely resemble ovarian cyst, and many cases have been operated upon 
with the idea that ovarian disease was the cause of the fluctuating mass. 
Careful palpation under ether may reveal an irregular nodular edge to the 
growth, or nodules elsewhere may explain the real state. 

The chronic fibroid type may resemble the nodular type just spoken of, but 
in it the matting of the abdominal contents into a small compact mass is 
quite extraordinary, the intestines and omentum being glued together in an 
adhesive bundle which cannot be separated. In this type the belly is often 
remarkably scaphoid and the degree of general emaciation extraordinary. 
Some idea of its degree may be gathered from the illustrations shown in 
Figs. 46 and 47. 

The symptoms of chronic fibroid peritoneal tuberculosis are characteristic. 
In addition to the general emaciation it will often be found that the skin over 
the abdomen looks and feels peculiarly rough and scurf-like, or as if there 
was marked "goose flesh" over this part. In addition it is often stained a 



TUBERCULOSIS 



307 



Fig. -16 




A case of peritoneal tuberculosis of the fibroid type in a man aged twenty-one years, with great general 

atrophy and scaphoid belly. 



Fig. 47 




Extreme emaciation in a woman due to thoracic and peritoneal tuberculosis of the fibroid type. 



308 DISEASES DUE TO A SPECIFIC INFECTION 

curious dirty yellow or is light brownish in hue. The abdominal wall is 
not only hard, but the abdominal muscles are readily felt by the finger- 
tips, while deep palpation reveals nodules or gives the sense of abdominal 
vacancy as if the patient had been eviscerated. The temperature range is not 
markedly febrile, and often is subnormal, ranging from 96° in the morning 
to 99° at night. 

It is not, however, in these well-advanced forms of the disease that the 
physician has difficulty in making a diagnosis, but in those cases in which 
there is general impairment of health without marked general emaciation; 
and it may be without distinct abdominal symptoms save obstinate consti- 
pation, with occasionally attacks of active purging, or in those instances in 
which the patient is still hale and robust, but suffers from some abdominal 
distress. These cases often present a distinct abdominal tumor, or tumors, 
composed of tuberculous nodules, or of nodules combined with thickened 
knuckles of intestine which may be so firmly held by adhesions of exuded 
lymph that gas and feces produce a tumor that cannot be readily dispelled 
by pressure. 

Sometimes a tumor is met with in the epigastric area extending across 
the abdomen at this level, or just above the umbilicus, formed by a 
peculiar rolling of the omentum as a workman would roll up his apron 
and stow it under his belt. A similar condition is sometimes found in carci- 
nomatosis of the peritoneum, but such a roll is usually due to tuberculosis. 

When the mesenteric glands or retroperitoneal glands are gravely infected, 
a single nodule or several nodules may be easily palpated. When multiple 
they are usually tuberculous, but where it is single a careful exclusion of 
malignant growth must be made by finding a tuberculous focus elsewhere 
or by the tuberculin test. 

Treatment of Tuberculosis of the Peritoneum. — The treatment of the 
subacute or chronic forms of peritoneal tuberculosis consists in operation. 
The first thing to be looked for at operation in peritoneal tuberculosis in 
the female is the Fallopian tubes, for they are the cause in the majority of 
cases. If diseased they must be removed, for such tubes will persistently 
infect the peritoneum. 

The operative treatment is most successful, as a rule, when the state is 
characterized by sufficient effusion to keep the intestinal coils apart, and 
so prevent adhesions. The operation consists in a single opening of the 
peritoneal cavity and a free entrance into it of atmospheric air. Any attempt 
to remove the tuberculous masses is useless, unless a single mass can be 
excised without damaging the tissues and without the danger of setting 
free bacilli to cause infection elsewhere. In sacculated cases the sac 
should be incised, drained, and packed with iodoform gauze. In the 
chronic fibroid type operation will not be productive of much good, for 
it cannot result in the loosening of the shrivelled omentum or of the cica- 
tricial contractions about the intestines, but in these cases cceliotomy may 
arrest the disease. When there are sacculations with accumulations of fluid 
or pus, the operation is of value in that it evacuates these collections and 
may arrest the process, but it does not promise complete cure as in the cases 
with large ascites. (For statistics see page 306.) 



TUBERCULOSIS 309 

The medical treatment consists in active feeding with easily assimilated 
foodstuffs and in the use of cod-liver oil. If anaemia is marked the syrup 
of the iodide of iron may be given in alternate weeks with the oil, and I 
have certainly seen good results follow the use of nightly iodoform inunc- 
tions over the abdomen, a mixture of olive oil and iodoform in the pro- 
portion of 10 grains to the ounce being used. Iodoform suppositories, 
5 grains each, may also be employed. 

Pulmonary Tuberculosis. — Pulmonary tuberculosis, or pulmonary 
phthisis, as it is sometimes called because it causes such emaciation or 
wasting, is the most prevalent disease to which man is susceptible. It 
affects, as a rule, young adults or adolescents (see Frequency of Tuber- 
culosis), but it may occur at any period of life, being comparatively rare 
in the first five years of existence and in the period of well-developed 
old age. 

As a result of infection of the lung by the Bacillus tuberculosis we find 
three types of pulmonary disease: the miliary, the chronic or caseating, 
ulcerative type, and the so-called fibroid type. Of these the second form is 
by far the most common and the most important from the clinical stand- 
point. The infection takes place as a primary process through the entrance 
of the bacillus by the respiratory passages, or secondarily as a result of the 
transference of the bacillus from some primary focus by the bloodvessels 
or lymphatics. 

Much discussion has arisen as to the mode by which the first focus of 
tuberculosis in the lung is produced. Birch-Hirschfeld proved that, in many 
cases at least, the bacilli gain their primary lodgement in a bronchiole, where 
the lung is least able to get rid of foreign matter by coughing, and that, from a 
primary tuberculous lesion at this point the rest of the lung becomes infected. 
Aufrecht also proved that the primary infection sometimes takes place 
through the circulation, to which the bacilli gain access by the tonsils and 
the alimentary canal, the pulmonary focus being due to a plugging of a 
vessel by their presence. 

Whether the means of infection be respiratory or vascular, the ultimate 
lesions are often the same ; but the early lesions differ, and the prognosis 
may be governed to some extent by the finding of a primary focus elsewhere 
which is responsible for the pulmonary lesions. 

The early lesions of pulmonary tuberculosis, due to infection by inhalation 
(aerogenous infection), are found chiefly in the wall of a bronchiole and in 
the alveoli grouped around it and forming lobules. Either by extension from 
this infected lobule or by the fusion of a number of similarly affected 
lobules, large tuberculous masses are speedily formed. They are also 
characterized by the extension of the tuberculous infection to the tissues 
around the bronchioles, giving rise to an extending bronchopneumonia 
which is nodular in its character owing to the primary lobular limitations. 

The early lesions of the form of tuberculosis of the lung which is due to 
infection by way of the bloodvessels or lymphatics are found in the walls 
of the alveoli — that is to say, in the connective tissue between the alveoli 
and in the interlobular capillaries. The disease may be well scattered 
through both lungs in either instance, but in the first type the patches are 



310 DISEASES DUE TO A SPECIFIC INFECTION 

larger, involving, it may be, a lobule at a time, whereas in the second form 
they are diminutive and more of the nature of miliary tubercles as observed 
elsewhere. This we would naturally expect from what has been said of 
the cause of miliary tuberculosis. After the disease has existed some 
time the areas of tuberculous deposit in either case may attain the same size. 

The discovery that there is a primary seat of tuberculosis, which has given 
rise to the pulmonary lesions, requires a graver prognosis because it indicates 
that there is more than one focus, and because such a primary lesion which 
has caused pulmonary disease by infection through the vessels may have 
caused other foci of infection elsewhere by the same means. Again, the 
disease is more apt to be generalized throughout the lung in this case than 
in the inspiratory form of infection. 

Tuberculous infection of the lung, therefore, produces the following changes 
in the pulmonary tissues: The gray and yellow tubercles, which differ in 
no way from those tubercles already described as occurring elsewhere, 
become amalgamated and form caseous masses, with, sooner or later, the 
characteristic softening of the growth; if the tubercles do not undergo 
necrosis and fail to coalesce, the accompanying low-grade irritation or 
inflammation may lead to fibroid changes. Along with these changes in the 
tubercles themselves there is always associated a considerable amount of 
inflammation, which often results in the formation of an exudate which fills 
the air vesicles just as it does in croupous or catarrhal pneumonia. Side by 
side with the development of the tubercles in the lungs, and of the pneumonic 
exudate, there develops in the interstitial tissues themselves a process w T hich is 
tuberculous and which causes thickening. This is the so-called tuberculous 
infiltration of Laennec. The lung, therefore, becomes solidified, partly as 
the result of the tuberculous growth, and partly as a result of the inflam- 
mation caused by the bacillus. 

Sooner or later a large part of the infiltrated area undergoes caseation. 
Around this focus or area of active tuberculous process inflammatory 
changes occur, which may cause the neighboring parts of the lung to 
present lesions like those of catarrhal pneumonia. On making a section 
of such an area the lung presents a smooth, homogeneous surface, as does 
a piece of Castile soap or cheese (Figs. 48 and 49), but if the process 
is not far advanced in caseation it may show a peculiar gelatinous appear- 
ance, the so-called gelatinous pneumonia. 

The fourth condition, which is noteworthy, is the lack of bloodvessels in 
the diseased portion of the lung, for no new ones are formed with the morbid 
growth and the ones naturally present are occluded by the disease which 
involves their coats and causes thrombosis; the resulting thrombus in turn 
undergoes caseation so that the vessels disappear in the tuberculous mass. 
These vascular changes possess great interest for this reason, and also 
because by this means the tubercle bacillus may enter the blood and infect 
other points, or by a process of ulceration of the vessel wall hemorrhages 

mav occur. 

«/ 

All tuberculous lesions in the lungs are, therefore, very similar in character; 
all manifest a disposition to undergo similar reparative or degenerative 
changes, the alterations being differences in degree rather than in kind. 



rriiK/uTLOSis 



311 



When the restrictive efforts of the affected organ are inadequate caseation 
extends until a bronchus is reached, through which the products of necrosis are 
removed by drainage and expectoration. Air takes the place of the material 
removed, and so a cavity is formed, the walls of which are lined by broken- 
down tubercle-containing material, which continually softens (caseation) and 
melts down, thereby enlarging the cavity. This cheesy material is loaded with 
bacilli in far greater numbers than they exist in the solidified part of the lung. 
The cavity is also infected by the pathogenic bacteria inhaled in the air, and 
these aid in the destructive local process and increase the general toxsemia. 



Fin. 48 




Caseous consolidation in the upper lobe and bronchiectasis in the lower lobe. (Kast and Rumpler.) 

It is interesting to note that the smaller bronchioles are usually closed 
by tuberculous infiltration as the disease progresses and only the larger ones 
remain patulous. These communicate with the cavities by small lateral 
orifices as the tube courses along the wall of the excavation, or open into 
the cavity like the small papilla of a duct. The walls of the bronchial tubes 
which provide drainage for the cavities are often the site of tuberculous 
ulceration. 

Tuberculous cavities are of two classes, moist or secreting, and dry. The 
first is that met with in the acute types of the disease and it often increases 
in size very rapidly. The contents of this cavity are usually composed of 



312 



DISEASES DUE TO A SPECIFIC INFECTION 



caseous matter, broken-down lung-tissue, pus cells, and tubercle bacilli, and 
the walls of the cavity suffer from active ulceration. 

The dry cavity, on the other hand, is found in the chronic cases which 
often last for years; efforts at repair smooth the wall, in which fibrous tissue 
develops, and it not rarely happens that by the fibroid process already 
described as occurring in this disease the size of the cavity is greatly 
decreased. These cavities contain but little material beyond a small amount 

Fig. 49 




Caseous consolidation above. Red hepatization below, f Kast and Rumpler.) 

of pus, and from their walls hemorrhage may rarely occur as the result of 
erosion of large vessels. Secondary cavities are due to the spread of the 
infection by the vessels or bronchi, and follow the secondary caseation 
process already described. 

We have now passed over the stage of pulmonary infection, consolidation, 
caseation, and disintegration, and come to the study of the processes often 
instituted in reparation. This is not a part of the tuberculous process. The 



TUBERCULOSIS 



313 



small-cell infiltration and exudation in the inflammatory zone surrounding 
the area of infection sometimes escape speedy involvement in the tuberculous 
process, and instead of degenerating rapidly aids in the production of 
fibrous tissue. At first it is immature and imperfect in character, but as 
time passes it becomes firm, dense, and fully-formed fibrous tissue. If 
the tuberculous focus is small it may be completely encapsulated by this 

Fig. 50 




2 cm. 



Left lung, superior lobe and upper part of lower lobe, the former containing a number of communica- 
ting caverns, brought about by tuberculous infiltration, caseation, and evacuation of the contents 
through the bronchi: A , aneurysmal dilatation of an artery spanning one margin of a large cavity; B, 
communication with another cavity; C, C, thickened and adherent pleura between the two involved 
lobes. The pleura over both lobes is thickened, and at the autopsy the cavity had been obliterated by 
universal adhesion; D, the pointer from the letter D leads to a small group of tubercles in which casea- 
tion is just beginning; E, a fused group of tubercles, further advanced than at D. 

fibrous covering, with the result that the caseous mass becomes calcareous 
or is gradually absorbed so that only a puckered scar results. 

When a cavity heals its walls undergo cicatricial contraction, but it is 
probably never obliterated unless it has been exceedingly small before the 
healing process began. 

The growth of fibrous tissue is most marked in those parts of the lung 



314 DISEASES DUE TO A SPECIFIC INFECTION 

which ordinarily possess the greatest amount of connective tissue, as in the 
interlobar and interlobular portions of the pulmonary tissues. 

If a large cavity is present bands of fibrous tissue may persist, and, stretch- 
ing across it, form trabecular (Fig. £0). At times these trabecular consist 
largely of good-sized bloodvessels which have not been plugged by the 
tuberculous process. If they are perforated by ulceration, so violent a hemor- 
rhage may occur as to cause death, even though the process of advancing 
cicatrization is endeavoring to limit the progress of the disease. At times 
the lesion in the bloodvessel develops into an aneurysm, and this may rupture, 
causing haemoptysis. 

Finally, we find still another process designed to arrest the disease and 
save the patient, namely, thickening of the pleura which protects the 
pleural cavity from pneumothorax and which, as it undergoes fibroid change, 
contracts and so acts as a sort of fibrous capsule of the entire diseased 
lung. 

Fibroid tuberculosis of the lungs is a very chronic condition, already 
described from the pathological standpoint, and characterized by marked 
overgrowth of fibroid tissue in the affected organ. A somewhat similar state 
exists when no tubercles have been present. The primary areas of tubercu- 
lous invasion become invested by fibrous tissues so that tuberculous broncho- 
pneumonia becomes gradually changed into one of fibrous overgrowth, 
with shrinkage of the parts so that the lung becomes much decreased in 
size and even the chest may be sunken and deformed. These thoracic 
changes are, however, more marked in those cases in which the visceral 
pleura is also involved in the cicatricial or fibroid process. The disease 
loses many of the symptoms of ordinary pulmonary tuberculosis, and while 
the constricted cavities may contain bacilli and the bronchial tubes provide 
copious material for expectoration, the process of general wasting goes on 
very slowly and the strength does not decrease with any speed. Such con- 
ditions are usually seen in patients of middle life and may last for ten to 
twenty years. Death finally comes from dilatation of the heart or from an 
acute complicating pneumonia or a hemorrhage from an ulcerated bronchial 
vessel. 

Symptoms of Pulmonary Tuberculosis. — The onset of this, the most com- 
mon type of the disease, is often such as to mislead the physician. In some 
cases there is no cough, but only a slight rise of evening temperature preceded 
by chilly sensations. If the number of cases in which these symptoms 
have given rise to the diagnosis of "malarial poisoning" could be gathered 
together they would be a " multitude which none can number." In many 
instances this error has been a deserved reproach to the physician who 
made it, because he has not searched for tuberculosis as a cause but has 
simply prescribed quinine. 

Another type of onset is found in those cases which present insidious 
pleural effusion. (See Pleurisy with Effusion.) In still a third series the 
primary symptoms are laryngeal. As these lines are written I am sending 
a case of active tuberculosis of the lungs to New Mexico. He was told by 
several skilled laryngoiogists that his husky voice was due to gout of the 
larynx, whereas if they had examined his chest marked signs of phthisis 



TUBERCULOSIS 315 

would have made the diagnosis evident. All cases presenting signs of per- 
sistent hoarseness should cause the physician to search for tuberculosis, 
syphilis, papilloma of the larynx, and aneurysm of the aorta. 

In the fourth type the very earliest sign of the disease is spitting of blood. 
There can be no doubt that in the vast majority of instances the bringing 
up of blood from the bronchial tubes means tuberculous infection. The only 
other causes which are at all frequent in the production of hcemoptysis are 
acute pneumonia or pulmonary infarction due to cardiac lesions. It not 
infrequently occurs that haemoptysis in the stage of onset is scanty and 
associated with no demonstrable physical signs, the lesion being situated in 
such a position that it readily perforates a vessel. (See p. 316.) 

The symptoms of pulmonary tuberculosis may be divided for study into 
those which are complained of by the patient, those which can be readily 
observed by the physician, and those which can be demonstrated by the aid 
of physical diagnosis. It must be remembered, however, that the severity 
of the symptoms of all kinds varies to an extraordinary degree in different 
cases and at different times in the same case. It is necessary, therefore, in 
speaking of the symptoms to adhere to the description of the three types of 
the disease named when discussing its pathology. At the outset, however, 
it may be said that two symptoms are present in all cases at some period, 
namely, loss of flesh and fever. 

It may be said of the fever of tuberculosis that it is usually moderate, 
varying from 100° to 102°, although at times it may reach 103°. When the 
temperature reaches higher than this it is probably not due solely to the 
tuberculous infection, but to septic or hectic fever, depending upon asso- 
ciated staphylococcic, pneumococcic, or streptococcic infection. In all 
instances in which the fever is high it is prone to run a very uncertain and 
aberrant course, save that it is high at night and low in the morning, as in 
nearly all fevers, particularly that due to sepsis. It is very easily broken, 
as a rule, by the use of any antipyretic medicine, but this effect of drugs 
is, of course, very temporary. 

The loss of weight depends upon several causes for its existence. The 
loss of appetite, the cough, which is exhausting and sleep destroying, the 
sweats, the disorders of digestion, and the anaemia are all active factors in 
decreasing flesh. Last, but by no means least, as a cause of loss of weight, 
is to be considered the toxcemia of the disease itself. 

The rapidity of loss of flesh is sometimes remarkable, amounting to as 
much as four or five pounds a week. This rapidity of loss is a good guide 
to the activity of the tuberculous process, for if it be rapid the outlook as to 
the progress of the patient's illness is gloomy. On the other hand, gain in 
weight is correspondingly encouraging in that it indicates a very slow, or 
arrested, progress of the disease. 

A third symptom, often of very great annoyance to the patient, is sweating, 
which is particularly prone to occur at night. These sweats vary greatly in 
severity, and seem to occur because of the relaxation of sleep, but in many 
cases their true cause is the hectic or septic state of the patient. If they are 
not severe enough to exhaust the patient or disturb his rest, they are to 
be regarded as an effort to diminish toxaemia, but if they become so profuse 



316 DISEASES DUE TO A SPECIFIC INFECTION 

as to be called colliquative they are deleterious. At times the sweat follows 
a sharp rise of septic temperature. It is hardly necessary to add that profuse 
night sweats, while a common symptom in well-developed phthisis, are by 
no means pathognomonic of this disease. 

Aside from the loss of flesh, fever, and sweats, the most constant symptom 
of pulmonary tuberculosis is cough. It varies in its character and in its 
degree in different cases of the subacute or chronic form of the disease. 
In the early stages it is apt to be worse on going to bed or on getting up 
in the morning, and in the early stages is usually annoyingly unproductive 
and persistent. As the disease advances and the process of softening 
begins to take place in the consolidated part of the lung, the cough 
becomes less dry and more productive. When cavities are formed, marked 
increase in morning cough is very prone to occur in order that the cavity 
may be well cleared of the accumulations which have occurred in it during 
the night. Cough is to be regarded as a useful attempt on the part of the 
system to keep the lungs clear. Only when it provokes hemorrhage or is 
so excessive as to cause exhaustion, loss of sleep, or vomiting is it to be 
regarded as an evil. 

Aside from the general symptoms of tuberculosis already described, 
patients with pulmonary tuberculosis often have severe pain in the chest, 
which is due to an extension of the inflammation to the visceral layer of 
the pleura. They also suffer from dyspnoea on exertion partly because of the 
diminished area of lung and lessened ability of the blood to carry oxygen, 
partly from cardiac feebleness, and partly because the general nervous 
system and the muscles are so feeble that any exercise leads to exhaus- 
tion. 

The sputum is composed of mucopurulent material from the associated 
chronic bronchitis, or if the lung is beginning to undergo softening the 
expectorated material is thin, with small, pale and greenish-looking masses 
in it — the so-called "nummular sputum." Sometimes when a cavity is 
being emptied or there is a marked bronchorrhoea the sputum is very 
purulent. 

The quantity of sputum varies greatly. The average amount in an 
active case varies from 1 to 4 ounces a day, but I have known a patient 
with several cavities to raise a pint or more in twenty-four hours. 

Complications. — A frequent symptom of the ulcerative type of pulmonary 
tuberculosis is haemoptysis, but a large number of cases pass through all 
stages of the disease without bringing up a particle of blood. It is absent, 
according to West, in from 20 to 30 per cent, of cases. Haemoptysis is more 
than three times as frequent in males as in females. The quantity of blood 
lost varies from a mere streak in the sputum to 3 ounces in the average case. 
Occasionally it amounts to 4 or 6 ounces, but a little blood "goes a great 
way," and patients will state that they have spit a quart when only a few 
ounces have been raised. It is rare for as large an amount as a pint to be 
coughed up in twenty-four hours. Very rarely a large gush causes death 
by suffocation. Sometimes the hemorrhage is concealed and unaccom- 
panied by blood-tinged sputum. If of a dribbling type it may inundate a 
large part of the lung or even fill a cavity and cause death without any 



TUBERCULOSIS 317 

external manifestation; such cases are rare. A free hemorrhage nearly 
always means the presence of an ulcerating cavity. The blood in haemop- 
tysis may come from the pulmonary vessels or from the bronchial vessels, 
but it is usually from the former. Flick, Ravenel and Irwin believe that 
haemoptysis is usually due to pneumococcus infection. 

All ages may suffer from hemorrhage from the lungs, but the period 
from eighteen to thirty-five is of course that of greatest frequency. 
Hoffnung has recorded a case in a child of ten months and Powell one in a 
child at seven months of age. 

The blood which is expelled in true haemoptysis is usually frothy and is 
brought up by coughing. It is also usually red except in instances of slow 
oozing into a cavity, when it may appear as a dark clot or clots. When 
the bleeding is profuse the blood gushes out of the mouth. Often before 
the spitting of blood actually takes place a salty, or bloody, taste in the 
mouth is persistently present for some time. 

Haemoptysis due to pulmonary tuberculosis is to be separated from 
haematemesis by the fact that the first occurs with coughing and the second 
with retching or vomiting. It is further differentiated by the fact that 
the blood is frothy and filled with mucus and bubbles and is usually 
bright red in haemoptysis, whereas in haematemesis it is usually pure or 
discolored by contact with the gastric juice. In one state the history of 
pulmonary disease, or the discovery of lesions in the lungs, reveals the seat 
of the hemorrhage; in the other gastric symptoms are present. In haemop- 
tysis the blood is often brought up in small degree for several days, 
whereas in haematemesis it is usually brought up once or twice on one 
day and then the bleeding ceases. 

In this connection it must not be forgotten that haemoptysis, or blood 
spitting, is not always due to tuberculosis of the lungs. It is sometimes 
present in the stage of onset in acute croupous pneumonia. It is not rarely 
met with in thoracic aneurysm, and its occurrence, unless it be very profuse, 
does not necessarily mean immediate death in the latter type of cases, since 
it not rarely happens that the vessel oozes blood for several days before it 
finally completely gives way. Sometimes by the pressure of the aneurysmal 
sac some small vessel may be eroded so that the blood escapes from it alone. 
Slight haemoptysis occurs in some cases of malignant intrathoracic growth, 
and swollen glands by pressure may rupture a neighboring vessel and cause 
leakage of blood. Again, haemoptysis often develops in mild degree as a 
result of pulmonary infarction. 

Among the other causes of haemoptysis may be mentioned hemorrhage 
from a superficial vessel in a bronchial tube in bronchiectasis, and from 
the larynx in malignant and non-malignant growth or tuberculosis of this 
organ. Haemoptysis is sometimes due to a varicose condition of the veins 
at the root of the tongue. 

A peculiar form of haemoptysis which lasts in some cases for years is 
seen in Formosa and Japan, due to the presence of the parasite Para- 
gonimus Westermanni. (See Parasitic Haemoptysis.) 

Although haemoptysis in the great majority of cases indicates pulmonary 
tuberculosis, it must not be forgotten that this symptom sometimes occurs 



318 DISEASES DUE TO A SPECIFIC INFECTION 

for years without any other signs of the disease appearing. I have one case 
in mind in which the young wife of a student at the Jefferson College had 
repeated hemorrhages during an entire winter without any physical signs 
being present, and continued to have them for many years afterward. 
Eight years after they began she still had them on exertion, but was the 
picture of health, had no signs of aneurysm or tuberculosis, and had gained 
thirty-five pounds. 

In regard to the distribution of the cavities Ewart has collected the fol- 
lowing interesting statistics. In 791 cases cavity occurred at the apex in 
282 cases, in the dorsoaxillary region in 227, in the mammary region in 189, 
in the sternal region in 61, and at the base in 32. 

Many of the other complications of pulmonary tuberculosis in addition 
to vomiting, diarrhoea, and haemoptysis have already been considered when 
discussing the disease as it affects serous membranes, as in pleurisy and 
pericarditis. The most important is pneumothorax, which follows the 
perforation of the tuberculous lesion into the pleura. It occurs in from 3 to 10 
per cent, of all cases, is often fatal if sudden in onset, and may cause dis- 
tressing dyspnoea. West says that of 39 cases, 2 died in an-hour, 8 others in 
twenty-four hours, and 29 out of the 39 inside of two weeks. The mortality is 
about 90 per cent. Effusion usually speedily develops. I have seen great relief 
follow gentle aspiration of the air from the thorax, but aspiration is to be 
avoided save when the pressure produces urgent dyspnoea. Very rarely the 
pneumothorax develops insidiously without severe symptoms, producing what 
is called "latent pneumothorax." (See Pneumothorax.) 

A still more rare affection seen in some cases of the chronic forms of 
pulmonary tuberculosis is pulmonary osteoarthropathy (which see). 

Diagnosis. — Before the physical signs of pulmonary tuberculosis are 
dealt with the sites of the lesions usually present may be discussed, so that 
they may be examined with particular interest in every case. The apices 
are the parts affected in the vast majority of cases, and it is here that the 
primary lesion is usually found, even if other parts become more severely 
diseased later on. The process as it extends is prone to travel back- 
ward rather than forward. No satisfactory explanation of this fact is 
obtainable. 

Next to the apices the upper part of the middle lobe on the right side is 
most frequently the site of infection, or the upper part of the lower lobe on 
the left side is diseased. The area of the upper part of the middle lobe 
on the right side is one which is often overlooked, owing to the fact that 
it is covered by the right scapula. Only when this scapula is raised by the 
hand being placed on the top of the head is the spot of impaired reso- 
nance exposed at its lower margin. 

Tuberculosis of the bases rarely occurs except after the disease has lasted 
long enough to involve the whole lung. 

Physical Signs. — The two methods of physical diagnosis which give us 
the most information in cases of pulmonary tuberculosis are percussion and 
auscultation. Throughout that period in which there is consolidation of 
the lung percussion gives impaired resonance or dulness over all the part 
affected, unless the lesion be deep seated, in which case light percussion over 



TUBERCULOSIS 319 

this part may produce a sound which is high pitched or slightly tympanitic. 
With the development of cavity the percussion note over it undergoes a 
change and there is developed a high-pitched tympanitic resonance, which 
careful percussion will show to be surrounded by an area, or ring, of impaired 
resonance representing the surrounding area of infiltrated lung-tissue. At 
times in the neighborhood of tuberculous lesions in the lungs hyperresonance 
is developed on percussion, as the result of a compensatory emphysema of 
the lung. If the cavity communicate with a bronchus and the patient takes 
a breath and holds it, with the mouth open, percussion may develop the 
so-called "cracked-pot sound." 

Auscultation reveals, in the earliest stages of infiltration, prolongation 
of expiration in the part involved. This is a physical sign of very great 
importance. Again, it may reveal some harshness of the inspiratory 
murmur and both inspiration and expiration may be more distinct and 
rougher than in health. 

Occasionally careful auscultation will also reveal a few very fine rales on 
forced inspiration. In lesions of the apex on the left side such a forced 
inspiration not rarely produces an inspiratory sound which is interrupted 
by the action of the heart three or four times during the act of drawing air 
into the lung. 

It must not be forgotten that negative signs may be as valuable as positive 
ones, and therefore if the infiltration produces an absence of breath sounds 
at the infected spot this may indicate disease as surely as do the more 
positive signs already named. 

If the physician listens carefully over the area of consolidation with his 
disengaged ear closed by his finger-tip, and the patient will say one, two, 
three in a stage whisper, the area of consolidation will give greater vocal 
resonance than the same area in the healthy lung. 

With the development of softening the fine dry rales which have been 
heard at first become coarse and moist, and as a cavity is formed they may 
become even bubbling or gurgling. These rales sometimes possess a curious 
metallic sound. 

As the cavity is formed the vocal resonance over it increases and may 
become startlingly clear, so that when the patient speaks the sound of 
the voice is transmitted with great clearness through the chest wall. This 
is called pectoriloquy. 

Over such a cavity cavernous breathing is often heard, or, if the cavity is 
a small one, the breathing may be hollow, tubular, or amphoric, as if he 
patient w T ere blowing with his lips over the mouth of an open bottle. 

Moist cavities also present on auscultation, in addition to large moist 
rales, metallic tinkling due to the dropping of fluid from their walls. This 
metallic tinkling is to be separated from the metallic tinkling of hydro- 
pneumothorax by the absence of the physical signs of fluid in a dependent 
part of the chest, and by the fact that such a cavity is near the upper part 
of the lung and so produces this sign in the upper zone of the chest. 

The sounds arising from a dry cavity are blowing or amphoric. When 
such a cavity has existed long enough for marked fibroid change to occur 
it often happens that the chest over the affected part is greatly flattened, 



320 DISEASES DUE TO A SPECIFIC INFECTION 

and it may be decreased in all its diameters. Compensatory hypertrophy 
of the opposite lung causes an increase in the size of the chest on that side, 
and this emphasizes the difference between the two sides. Further than 
this, the contraction process may greatly displace nearby organs. Thus, if 
the left lung undergoes this change, the right lung, partly from enlargement 
and partly from traction, may extend as far as three inches to the left of 
the sternum, the heart may be drawn upward and tilted to the left of the 
nipple as high as the third interspace. Even the stomach may be drawn 
upward. On the other hand, when the right lung is affected by the disease 
the heart may be drawn to the right under the sternum, the liver may be 
pulled upward, and the left lung drawn well over to the right side of the 
chest. Most of these marked changes are due to associated pleural 
adhesions, and these may cause deformity of the entire chest. 

The diagnosis of cavity from bronchiectasis is made by the recollection 
that a cavity is usually near the apex, and bronchiectatic spaces are at the 
base, as a rule, although they may develop as high as the third or fourth 
rib. If so, they are nearer the sternum than is the cavity. Again, in 
cases of cavity the area around the hollow space is usually dull on 
percussion, whereas in bronchiectasis it is usually hyperresonant from 
emphysema. 

It is to be remembered that tuberculosis may occur as a complication 
of bronchiectasis, but that well-developed bronchiectasis rarely occurs in 
tuberculosis except in old chronic cases with much contraction due to fibroid 
change. 

Palpation. — Palpation over that portion of the chest which is infiltrated 
by a tuberculous process, or in which a cavity has already formed, also 
presents very definite physical signs when the patient speaks, namely, a 
marked increase in vocal fremitus. If the cavity is superficial and of any 
size it may be possible to feel the bubbling rales which are produced by 
its contents. 

Inspection. — Inspection of a well-advanced case of pulmonary tubercu- 
losis occurring in one whose configuration is naturally phthisical reveals a 
very typical picture, but in those with well-developed chests very advanced 
lesions of the lungs may be present before any change in the appearance of 
the chest is manifest. 

The physical signs of acute pneumonic tuberculosis are at first the same 
as those of acute pneumonia. There are bronchial or tubular breathing, 
dulness on percussion, and fine crepitant rales. As the disease progresses 
these signs become modified to the extent that the rales become coarse and 
more moist in character, and signs of softening are therefore developed. 

In the diagnosis of a case of this character it may not be possible to 
state accurately the true cause of the disease for several days, but the fol- 
lowing points are of some value, namely, the discovery in the history of the 
patient, or in the body at the time, of a tuberculous infection, as of enlarged 
cervical glands or of tuberculous masses elsewhere, as in a Fallopian tube or in 
a testicle or joint; the general appearance of the patient as to nutrition, for 
the pale, anaemic patient with the typical slim bones and large joints, large 



TUBERCULOSIS 321 

orbital spaces, and delicate features is more apt to succumb to the bacillus 
tuberculosis than to the pneumococcus. On the other hand, it is to be 
remembered that robust and hearty persons may develop acute tuberculous 
pneumonia and die in a short period. The presence of the pneumococcus 
in the sputum is of little diagnostic value, but the discovery of the tubercle 
bacillus will be of great aid in determining the cause of the illness. 

Microscopic Diagnosis. — An examination of the sputum by the aid 
of the microscope reveals shreds of mucus mixed with particles of caseous 
substance and small round cells, leukocytes, and pus corpuscles. Crystals 
of the triple phosphates, oxalates, and of tyrosin and leucin are often present. 
All these constituents of the sputum are, however, of little importance as 
compared to two others, namely, the presence of elastic-tissue fibres pos- 
sessing the morphology and arrangement of pulmonary reticulum, showing 
that breaking down of the lung is taking place, and tubercle bacilli, the 
presence of which reveals the fact that they are the cause of this condition. 
The bacilli are indisputable evidence of the presence of the disease, but 
their absence from a specimen of sputum does not exclude tuberculosis, 
because they may happen to be absent from that individual sample, or they 
are absent because the sputum does not come from a part of the lung in 
which breaking down is taking place. Even an old cavity, if it is well 
drained, may not provide bacilli constantly. 

Yellow, elastic fibres are to be sought for by spreading the sputum in a 
thin layer on a pane of glass placed over a blackened surface. A second 
sheet of glass is placed over this and the sputum smeared by moving the 
upper piece laterally. The particles of elastic tissue are usually contained 
in small masses of yellowish-gray material, which, if crushed and placed 
under the microscope, are found to consist of characteristic, double-contoured, 
interlacing, yellow, elastic fibres, having the arrangement of the pulmonary 
elastica. Elastic-tissue stains are of value in the hands of experienced 
microscopists. As many meats are rich in elastic tissue which may lodge 
in the mouth, the mere finding of such structures in the sputum does not 
justify the diagnosis of " breaking down " of the lung. The recognition of 
pulmonary elastica must be based on the shape and arrangement indi- 
cated. Occasionally small pieces of calcareous matter are found in the 
sputum. 

The bacilli are sought for in the following manner : A microscope slide 
is thoroughly cleansed and dried. From the sputum spread out on a glass 
plate, or in a Petri dish, nummular particles if present are selected, or if 
absent the thicker portion of the sputum is spread in a thin layer over the 
surface of the slide and allowed to dry spontaneously. The dried film on 
the slide, surface upward, is passed three times through the flame in order 
to fix the thin layer firmly to the slide. Cover-glasses may be used instead 
of slides, but possess no special advantages. Of the many stains recom- 
mended Ziehl's carbol-fuchsin gives satisfactory results. It is prepared by 
dissolving 1 gm. of powdered fuchsin in 10 c.c. of alcohol; to this solution 
90 c.c. of 5 per cent, aqueous solution of carbolic acid is added; the stain 
is ready for immediate use, and if prepared from proper ingredients keeps 
21 



322 DISEASES DUE TO A SPECIFIC INFECTION 

well. The prepared stain is poured over the slide, which is then heated 
over a Bunsen burner or alcohol lamp until steam begins to rise, when the 
heat is withdrawn. After staining five minutes the excess is poured off and 
the slide freely washed in clean water. It is then flooded with Gabbett's 
solution, which consists of 1.5 gm. of methylene blue dissolved in 100 c.c. 
of a 25 per cent, aqueous solution of sulphuric acid. This is allowed to act 
for one minute; it is then poured off and the slide washed in water; if any 
of the red dye be retained the application of the Gabbett solution is repeated 
until all macroscopic evidence of the fuchsin has disappeared from the 
thoroughly washed slide, which is then stood on end and allowed to 
dry. 

A drop of immersion oil is placed on the stained film and the specimen 
examined with a one-twelfth-inch immersion lens. If it be desired to pre- 
serve the specimen, balsam is applied to the dried slide and a cover-glass 
placed on it. In properly prepared films the cellular elements and bacteria, 
other than the tubercle bacillus, will have selected the blue dye; the tubercle 
bacillus, however, will appear red on the bluish background. 

X-Ray. — A valuable aid in determining the presence of consolidation of 
the lung in tuberculosis is the use of the fluoroscope or x^ray photograph, 
for such a lesion often reveals a very distinct opacity. 

Tuberculin. — In the diagnosis of pulmonary tuberculosis there can be no 
doubt that tuberculin when properly employed is a valuable agent, although 
I believe that in the majority of instances it should not be used, since careful 
examination of the patient and consideration of his history will in most 
instances reveal the presence of tuberculosis, or point to its presence with 
such a degree of certainty that the patient should certainly be sent away 
for his health on the ground that he is a fair mark for a tuberculous infec- 
tion, and that his lung is in such a condition that he is at all times liable to 
the rapid development of a true tuberculous process. 

Tuberculin, which is used hypodermically, for these diagnostic purposes 
is usually given to adults in the dose of a milligram, and if tuberculosis 
is present it causes a reaction in the form of a rise in temperature of 
two or three degrees within a few hours. If the dose is larger than this, 
susceptible persons may have a violent reaction. If the patient fails to 
react to the smaller doses, before deciding that the tuberculin test has 
proved him free from tuberculosis, doses of 2 mg. or 3 mg. or even more 
should be given at intervals of three or four days, or a week. 

The use of tuberculin for diagnostic purposes has a larger field in cases 
of suspected renal or abdominal tuberculosis than it has in the diagnosis 
of pulmonary lesions, in which the physical signs can usually be demon- 
strated. 

It is to be remembered that the tuberculin reaction sometimes occurs in 
persons who have syphilis, and it is thought by some that the reaction 
which is produced may actually increase the rapidity of the tuberculous 
process. 

In order that a careful record of its effects may be obtained the tempera- 
ture of the patient should be taken after the injection at intervals of every 
two hours for six hours, and after that every hour for twelve hours. Before 



TUBERCULOSIS 323 

the test is made it must be determined that the patient is afebrile by a careful 
record of his temperature for several days, as otherwise the usual fever may 
be mistaken for a reaction. 

Tuberculin may be used in hypodermic tablets, each of which contains 
1 mg., or in the form of the tuberculin (Koch), which is a liquid prepa- 
ration. If the tablet is used it is dissolved in water as is an ordinary 
hypodermic tablet. If the liquid tuberculin is employed the bottle con- 
taining it is uncorked and a small pipette, which is graduated, is dipped 
into the contents and then withdrawn, with the finger-tip over the outside 
end to hold the fluid in the pipette, as in testing urine. The quantity of the 
fluid as expressed in milligrams is then allowed to run out into a sterile 
porcelain dish, and pure water is drawn up in the pipette to wash it free 
of any residue of the original fluid. This wash-water is then added to the 
contents of the dish, and, after mixing, the fluid is drawn up into a hypo- 
dermic syringe and given to the patient through an ordinary hypodermic 
needle. 

It has been urged against Tuberculin R. that there is a possibility of its con- 
taining living bacilli which may infect the patient. For this reason many 
clinicians employ a tuberculin prepared by filtration and subsequent con- 
centration of sterilized bouillon cultures, whereby a germ-free product is 
assured. (See Treatment.) 

Prognosis. — It is not long since it was almost universally thought that sub- 
acute pulmonary tuberculosis was an utterly hopeless and incurable disease. 
At present we know that it is in many instances a readily curable affection, 
even when it is not possible to obtain the very best conditions for cure. 
Further, we know that hundreds of persons have the disease and get well 
without even knowing that they have had it. It is manifest, however, that 
only those cases can recover in which the disease is not far advanced and 
in which the vital resistance of the individual can be maintained at such a 
level that the protective processes of combat and repair, already described 
may be carried out to completion. 

The degree of vital resistance of the patient is of very great importance 
in deciding the prognosis. Often the most powerfully built individual falls 
a victim to rapid phthisis while his comparatively feeble comrade manifests 
the most remarkable vitality. Additional factors in determining the outlook 
in an individual case are the maintenance of the body weight, the absence 
of anaemia (but red cheeks do not necessarily mean good blood), and the 
presence of a good digestion, particularly in respect to starches and fats. A 
good family history is not as important a factor for good as a bad history is 
important for evil. 

A large number of statistics as to the curability of this disease by climate 
and feeding and by out-door life are now obtainable, and some statistics 
will be found discussed under Treatment. 

F. C. Wood believes that the diazo reaction can be used to aid in deter- 
mining the question of prognosis, stating that if no reaction occurs and the 
kidneys are intact the outlook is favorable, but that if the urine reveals a 
strong and persistent reaction the outlook is evil. (For the diazo test, see 
article on Typhoid Fever.) 



324 DISEASES DUE TO A SPECIFIC INFECTION 

The average duration of life in a case of pulmonary phthisis is limited 
to two years. 

Marriage should be forbidden for either sex if suffering from tuberculosis, 
even if it be in a mild form. The woman who is tuberculous may survive 
her first pregnancy only to pass into a hurried decline after the birth of her 
child or during lactation. Several pregnancies almost always destroy her. 
The man not infrequently loses nervous vigor by marriage, and this is the 
more prone to occur, as it is notorious that tuberculous men are cursed with 
a degree of sexual desire which is in excess of that of health. 

o 

The prognosis of haemoptysis so far as its causing immediate death is 
concerned is favorable. Patients rarely die during the hemorrhage unless 
it takes place in those who are already very feeble and anaemic. Rarely 
the hemorrhage is so profuse as to cause death by suffocation. West gives 
the proportion of deaths from this cause as but 1 or 2 out of every 100 
cases that die of this disease, whereas 60 per cent, of tuberculous cases are 
supposed to suffer from haemoptysis at some period of the malady. 

The secondary effects of hemorrhage may, however, be disastrous, for if 
the neighboring part of the lung is inundated with blood and with bacilli, 
the bronchioles in that part become filled with the extravasation and a 
traumatic tuberculous pneumonia speedily ensues. 

Treatment of Pulmonary Tuberculosis. — The treatment of pulmonary 
tuberculosis in its subacute or chronic forms may be considered in several 
parts. 

1. Its treatment by proper diet, proper exercise, and rest. 

2. Its management by suitable out-door life, and particularly by climate. 

3. The employment of drugs to control or modify symptoms which are 
severe enough to demand attention. 

4. The use of tuberculin as a curative remedy. 

5. The avoidance of the use of drugs with the idea that they can cure 
the disease; for he who tries to cure pulmonary tuberculosis by drugs does 
not know the morbid anatomy of the malady. 

It is of vital importance in the treatment of pulmonary tuberculosis that 
the disease be recognized at the earliest possible moment and that curative 
measures be immediately instituted. The possibility of cure depends solely 
upon the limitation of the lesion, and this is difficult to accomplish in direct 
proportion to its size and the degree to which degenerative changes have 
advanced. 

Diet. — There can be no doubt that the proper nourishment of the patient 
is the most important matter demanding the attention of the physician; 
for tuberculosis is not only a disease in which emaciation progresses rapidly, 
but it is one in which the outlook depends entirely upon the ability of the 
patient to carry out protective processes through which alone he can hope 
to recover his health. Under these circumstances it is evident that the 
physician must do everything in his power to keep the digestion in the best 
possible order, to administer foods which are easily digested and readily 
absorbed, and, equally important, to prescribe no drugs or foods which by 
disordering the stomach will interfere with the function of this important 
viscus. It must also be remembered that the digestion of food requires 



TUBERCULOSIS 325 

nervous energy just as does the performance of any other vital function, 
and care must be taken that food is not ingested at a time when, by reason 
of exercise or other cause, a considerable quantity of nervous energy has 
been recently expended. The physician is, therefore, in the difficult position 
of knowing that the patient must take large quantities of nutriment if 
recovery is to be expected, and at the same time be careful that the digestion 
is not overburdened by the too frequent administration, or too free employ- 
ment, of nutritious articles. If the patient's digestion is moderately strong, 
he may follow a line of diet about as follows: 

Before getting up in the morning he should receive a teacupful of hot 
milk, which should be sipped and not gulped down in one or two large 
swallows. After taking this, he should rest in bed for fifteen or twenty 
minutes; should then bathe, or be bathed, and clothed, and for his breakfast 
have wheaten-grits, oatmeal, or some of the more modern cereal preparations 
which are known to possess real nutritive value. If his appetite is good 
he may also have at this time a tender chop or a small piece of steak, and 
if accustomed to the use of tea or coffee, these beverages may be allowed 
unless it is found that they increase nervous irritability. In some instances 
the patient may desire to take an orange or some other fruit with his break- 
fast, and to this there can be no objection. The meal should be adequate, 
but not large enough to be heavy. 

Half-way between his breakfast and his mid-day meal the patient should 
receive some light luncheon, consisting of a cup of broth, a piece of toast, 
a glass of koumyss, or a sandwich made of scraped beef; or, if he tires of 
this, one made with toast and anchovy or caviar. Often an egg, cooked 
or raw, may be taken between meals with advantage. If desired, a glass 
of sherry or some red wine may also be taken at this time ; or, in its place, 
Scotch or rye whiskey may be given. 

The dinner should be the heaviest meal of the twenty-four hours, and should 
be taken between twelve and two o'clock. It should consist of a nutritious 
and somewhat stimulating soup which is easily digested and absorbed ; one of 
the clear soups being preferred rather than a puree, unless it is known that 
the patient readily digests thickened and rich soups. This may be followed 
by a small piece of fresh fish, great care being taken that the fish is really 
fresh, and then by a hearty course of any one of the roast or broiled meats, 
accompanied by two or three wholesome vegetables, such as potatoes, string 
beans, asparagus, spinach, carrots, macaroni, and similar substances. With 
this meal it may be well for the patient to take a little sherry wine or whiskey 
and water, particularly if he is accustomed to stimulants with his meals. 
Some plain, nutritious dessert like cornstarch or rice-pudding may also be 
taken. 

During the afternoon a light luncheon should be given him, somewhat 
similar to that which has been taken in the middle of the forenoon, two 
or three hours after his dinner. In the evening another light meal should 
be taken, which should consist of arrow-root or an egg cooked in some 
simple form, or a few stewed oysters or milk-toast may be used, and again 
before going to bed at night a cup of broth, a glass of koumyss, a cup of 
hot milk, or some curds and whey may be given. 



326 DISEASES DUE TO A SPECIFIC INFECTION 

The patient who is able to take the quantity of food which has just been 
described is, of course, one whose digestion is in fairly good condition. But 
if careful attention is paid to the digestive tract by the administration of 
aids to digestion, such as pepsin, pancreatin, and taka-diastase, if the bowels 
are moved regularly by the use of proper laxatives, and if, above all, the 
patient is required to conserve his nervous energy in order to expend it upon 
his digestive apparatus, it is quite remarkable what large quantities of food 
may be taken, even by the consumptive who otherwise seems quite feeble. 

The actual quantity of the food at each feeding must be varied from day 
to day with the patient's appetite and with the conditions which may arise. 
If the patient has passed a restless and feverish night, the quantity of food 
at each feeding should be small; whereas, if he has had a restful night, and 
therefore has been able to gain nervous energy, larger quantities may be 
given. So, too, limited quantities should be ordered when the tongue is at 
all foul, and larger quantities ordered when it is comparatively clean. It 
is of vital importance that these daily variations should be made in the diet, 
for the digestive apparatus of no one is prepared day in and day out to 
take exactly the same quantity of food, and digest it satisfactorily. Both 
the physician and the patient must remember that professional advice as 
to food and digestion is much more important for the patient than advice 
as to the treatment by drugs. 

Exercise. — The majority of cases of pulmonary tuberculosis do not 
require much exercise provided they are supplied with sufficient fresh 
air. Patients, however, differ very greatly in regard to this matter. Some 
of them seem capable of taking moderate exercise with great advan- 
tage, and others cannot take any exercise without suffering either from a 
disordered digestion or from a restless night caused by inordinate fatigue. 
In many instances the patient's health can best be preserved by giving 
him fresh air, and supplanting exercise by massage and gentle Swedish 
movements. Of course, these remarks do not hold true of those cases in 
which a small area of the lung is involved, with almost no impairment of 
the general health and muscular strength. These patients should take 
healthy exercise, being careful to avoid excessive fatigue, and they should 
be impressed with the idea that exercise in sufficient degree to approach 
exhaustion is not only bad on general principles, but actually diminishes 
their ability to prevent the spread of the infection in their lungs. The 
whole question of exercise must, therefore, be gauged in each case by the 
real strength of the individual rather than by his ambition to be up and about. 

Climate and Out-door Life. — In these two factors we have our greatest 
aid in the treatment of pulmonary tuberculosis, although, of course, these 
agents must be prescribed with the same care as governs our employment 
of ordinary remedies. There can be no doubt whatever that an out-door 
existence is capable of curing pulmonary tuberculosis under certain circum- 
stances, even when the climate is by no means theoretically suitable for 
pulmonary cases. This is a matter of importance when it is remembered 
that a very large proportion of consumptives find it impossible to travel 
great distances to obtain those climatic conditions which are most favorable 
to them. 






TUBERCULOSIS 327 

At every modern resort for consumptives every measure is taken to keep 
the patients for many hours each day in the open air, the essentials being 
that they shall be exposed to sunlight, and, if possible, to the direct rays of 
the sun, and protected from high winds. These conditions can be obtained 
by the erection of suitable sheds facing the sun, and providing wind 
guards which will place the patient in a quiet atmosphere. Even should 
the patient be unable to go to the country for fresh air, good results have 
been found to follow this plan of treatment while he remains in a city resi- 
dence, either in a suitably arranged room or in a tent or shed erected upon 
the roof of his house. 

The climate to which the patient should resort, if it is possible for him 
to travel, should, in the great majority of instances, be one which is found 
at an altitude varying from 3000 to 6000 feet. There are two great essentials 
in such a climate: first, that there shall be an unusual number of hours 
of sunshine in the course of the year, and, second, that the atmosphere 
shall be dry. A third point of importance, but by no means an essential 
one, is that the atmosphere shall be quiet, in order that there may be little 
dust. The temperature is of comparatively little importance, provided it is 
not accompanied by humidity, for it is quite remarkable how patients 
suffering from this disease often thrive in temperatures which in winter 
are far below the freezing point, and in summer are often as high as 90°. 
At those altitudes of from 5000 to 6000 feet which are suited to this class of 
patients the atmosphere is so clear that the sun's rays are not interfered 
with, and even if the thermometer shows that a zero temperature is present, 
the patient, if properly clad and protected from wind, can very frequently 
lie out-of-doors all day, warmed by the heat of the sun. This is beneficial 
to an extraordinary degree. 

A high altitude is advantageous for the tuberculous patient, not only 
for the reasons which we have given, but also because the rarity of the 
atmosphere requires that he use all possible portions of the lung tissue, 
and, this being the case, he gradually expands and calls into functional 
activity all those parts of the lung in the neighborhood of the tuberculous 
lesion which have a tendency to become functionally inactive. This develop- 
ment of active circulation of air and blood does much toward aiding nature 
in walling off the tuberculous focus and preventing its further spread. A 
high altitude is also advantageous because it seems to increase the quantity 
of haemoglobin in the blood. Whether it increases the number of red blood 
cells is still a matter of debate, some asserting that the increased number 
of corpuscles, found in the superficial bloodvessels after a patient has been 
some weeks at a high altitude, depends more upon an altered distribution 
of blood than upon any actual increase. 

Of the high-altitude resorts which are most popular because of their 
excellent climate for consumptives may be mentioned Colorado Springs, 
Colorado, certain parts of Arizona and New Mexico, and parts adjacent in 
America, and the so-called Engadine, in Switzerland, of which the most 
celebrated places are Davos, Pontresina, and San Moritz. 

A high, dry climate is contraindicated in tuberculous patients who are 
suffering from tuberculous laryngitis, since the dry air increases the laryngeal 



328 DISEASES DUE TO A SPECIFIC INFECTION 

irritation. It is also contraindicated in patients who have dilatation or 
degeneration of the heart muscle, and great care should be taken to deter- 
mine the state of the heart in all tuberculous patients before sending them 
away from' home. A persistently high pulse rate is a distinct contraindication 
to altitudes. If valvular disease exists, and there is a tendency to failure 
of compensation, a high altitude is also contraindicated; but where com- 
pensation is adequate, the mere presence of a murmur does not necessarily 
contraindicate resort to an altitude, provided that the patient is cautious 
not to overexert himself. 

Emphysema associated with pulmonary tuberculosis usually contrain- 
dicates a high altitude. 

It has been taught by some that a tendency to haemoptysis also renders 
a high altitude inadvisable, but very eminent phthisiologists, on the con- 
trary, have asserted that a tendency to hemorrhage does not contraindicate 
health resorts of this character. My own personal feeling is that the 
patient who has a tendency to haemoptysis should approach a high altitude 
very gradually in order that his heart and lungs may become accustomed 
to the altered atmospheric conditions, and certainly, for the first few weeks 
after his arrival, should rest constantly. 

Still another contraindication to such an altitude, unless perchance the 
climate is very mild and the temperature fairly constant, is renal disease 
of any kind, or tuberculosis of the genito-urinary tract. Should any of these 
contraindications exist, the climate of choice is one which is represented 
by San Diego, California, where the air is pure, where sudden changes of 
temperature do not occur, and where a flood of sunshine is constantly 
obtainable. 

In those cases which have a great deal of secretion, excessive cough, and 
excessive expectoration, dry climates, such as are found near Phoenix, Ari- 
zona, and Silver City, New Mexico, are the climates of election. 

For those who are unable to take a long journey, and for those who are not 
thought to be suitable cases for high altitudes, the Adirondacks in the neigh- 
borhood of Saranac Lake, New York; White Haven, Pennsylvania; or 
Asheville, North Carolina, can be recommended. These altitudes are in 
the neighborhood of 2500 feet. Lower altitudes which have been found 
advantageous for these cases exist at Thomasville, Georgia, and Lake- 
wood, New Jersey, where the curative elements are the sunshine and 
pure air. 

It is interesting to note, in regard to the treatment of pulmonary 
tuberculosis by fresh air, proper diet, and moderate or high altitudes, that a 
large percentage of cases can be cured. Thus, Trudeau reported, at the 
Adirondack Cottage Sanitarium, where the altitude is less than 2500 feet, 
for the years 1897, 1898, and 1899, cures in 72 per cent, of incipient cases 
and 17.8 per cent, in advanced cases; and Clapp and Bowditch, of the 
sanatorium at Rutland, report for the year ending September 1, 1901, 
cures in 72.5 per cent, of incipient cases and 46.11 per cent, in ad- 
vanced cases. 

Still more recently Trudeau has presented the results obtained by an analysis 
and study of all the cases under his observation in the last seventeen years. 



TUBERCULOSIS 329 

Of the 1500 cases under consideration, which have been discharged from 
two to seventeen years, 434 could not be traced, leaving 1066 which have 
been traced. Of these 1066, 46.7 are still living, 31 per cent, are known 
to be well at present, in 6.5 per cent, the disease is still arrested, 4 per cent, 
have relapsed, 5.2 per cent, are chronic invalids, and 53.3 per cent, are dead. 
As to the influence of the stage of the disease on the permanency of the 
results obtained, he found 66 per cent, of the 258 incipient cases discharged 
are well at present. Of the 563 advanced cases 28.6 per cent, are well, 
and of the far-advanced cases 2.5 per cent, only remain cured. Thus we 
learn that 31 per cent, of all cases discharged from two to seventeen years 
ago have remained well, and that 66 per cent, of the incipient cases dis- 
charged during the same time continue well at present. Surely these results 
are encouraging and he has shown us the way in a great work. Thirty years 
ago physicians were of the opinion that cures did not take place from pul- 
monary tuberculosis in more than 2 per cent, of cases. 

Sea voyages, which at one time were very popular in the treatment of 
tuberculosis of the lungs, are no longer regarded with much favor. The 
possibilities of seasickness, bad weather, and of consequent close confine- 
ment are naturally not looked upon with favor, when we consider that free 
feeding and fresh air are absolutely essential for these patients. Further 
than this, the atmosphere at sea is never dry, but always more or less damp. 
Again, there are practically no comfortable sailing ships at the present time, 
and steamers make such rapid voyages that the patient is not long enough 
at sea to be materially benefited. 

Before the physician decides to send his patient away from home for the 
climatic treatment of his disease, he should determine whether such treat- 
ment really offers fair chance of benefit; for it is a vital mistake to exhaust 
the strength and finances of the individual in a vain endeavor to arrest 
an inevitable process. If it is decided that the disease has advanced so 
little that such a trip can promise good, the next question which arises is 
as to whether the patient is strong enough to stand the journey, and, again, if 
he can stay away long enough to be benefited; for in all instances it is useless 
for a patient to leave home with any expectation of returning in less than 
six months or a year, and usually he had better give up the hope of return- 
ing except for a visit, if he wishes to preserve his health after the climate 
has done its good work. It is also a grave mistake to send such patients 
far from home unless they can be accompanied by some relative or friend, 
as homesickness exercises a deleterious influence upon vitality. 

Drugs. — I have already mentioned the use of the various digestants 
when speaking of the diet. The ever-present anaemia of many of these 
patients is to be overcome by the careful administration of iron and arsenic. 
Arsenic for many years has had the reputation of being a drug of great 
value in tuberculosis. Iron is also very useful, but it should not be given 
in the large doses ordinarily employed. As I have repeatedly pointed out, 
the quantity of iron in the body is exceedingly small, not more than about 
10 grains, and therefore the administration of 2 or 3 grains of reduced iron 
two or three times a day provides in twenty-four hours far more iron than 
can possibly be utilized, and at the same time tends to produce constipation 



330 DISEASES DUE TO A SPECIFIC INFECTION 

and so disturb digestion. Most cases will do better if they are given in the 
neighborhood of yg- to \ grain of reduced iron three times a day. 

Strychnine may be used in moderation as a bitter and as a nervous tonic, 
but it is a mistake to use it as a circulatory stimulant, as it is only an irri- 
tant to the nervous system, and produces fictitious strength. Quinine 
cannot be given in doses which are adequate to control hectic fever, and 
if any attempt of this kind is made it disorders the stomach and pro- 
duces headache; 2 or 3 grains, twice or thrice a day as a bitter tonic, are 
quite sufficient for the average patient. 

The syrups of the hypophosphites and lactophosphates have been popular 
with the profession for many years. In many instances the improvement 
which follows their use depends upon the iron or strychnine which they 
contain, and too frequently these syrupy preparations disorder the stomach 
and spoil the appetite. If it is desired to administer calcium, potash, 
and soda to such patients, it is better, in the writer's experience, to give 
an elixir of the glycerophosphates in the dose of a dessertspoonful three 
times a day to an adult. 

When the heart is weak, particular care should be taken in regard to 
rest, and digitalis may be given, but it should be used in small doses over a 
long period of time rather than in full doses for a short period. It is quite 
remarkable what good results follow the use of 2 or 3 minims of a physio- 
logically tested tincture of digitalis three times a day. These doses, main- 
tained for some time, produce a true improvement in the heart muscle and 
do not disorder the stomach; whereas, larger doses soon upset the cardiac 
balance, and almost certainly disturb digestion, and even produce vomiting. 

For the control of night sweats no remedy equals camphoric acid in my 
experience, given in the dose of 15 to 20 grains, two or three hours before 
the time that the sweat usually comes on. The best way to administer it 
is in cachet or capsule, or dissolved in a little brandy. The difficulty of 
the use of atropine for this purpose is that it checks other secretions and 
sometimes by so doing renders the cough more dry and annoying. 

Fever, as a rule, requires treatment only if it becomes excessive. The 
patient may be sponged with tepid water and alcohol, and even cool water 
may be used. But care must be taken that the temperature does not break 
rapidly and become subnormal. The use of the coal-tar antipyretics is 
entirely inexcusable. They diminish vital resistance, are apt to produce 
profuse sweats, and increase cyanosis and dyspnoea when the pulmonary 
lesions are well developed. 

The use of creosote or of any of its derivatives, with the idea that they 
are beneficial for pulmonary tuberculosis, is based upon an utterly erroneous 
view of the disease and of the action of these drugs. When bronchitis is 
present as a complication their value as stimulating expectorants is worthy 
of consideration, and under these circumstances, by improving the con- 
dition of the bronchial mucous membrane and aiding expectoration, they 
may eventually help the patient, but they certainly do not exercise any influ- 
ence upon the tuberculous process itself. Worse than this, in many instances 
they do not even act as expectorants, unless given in doses so large as to 
disorder the stomach. The number of unfortunate consumptives whose 



TUBERCULOSIS 331 

struggle with their disease has been lost through disorder of the digestion 
arising from the administration of expectorants is not comforting to con- 
template. 

Cough is to be controlled by the use of such cough sedatives as heroin 
in the dose of ^V to -^ of a grain three or four times in twenty-four hours. 
A very useful plan of treatment under these circumstances is the adminis- 
tration of the elixir of terpin hydrate and heroin in the dose of a teaspoonful 
every four hours. In some instances cannabis indica is useful as a cough 
sedative. In still other cases, if the cough seems to be due to a dry and 
irritable condition of the bronchial tubes, quiet and sleep is obtainable if 
there is disengaged in the air of a room, from a bronchitis kettle, steam 
which arises from water into which is poured creosote, oil of pine, and 
oil of eucalyptus, equal parts, to the extent of J to 1 drachm. Care should 
be taken that the patient does not go out-of-doors into the cold atmosphere 
after inhaling the warm steam-laden atmosphere. 

When a laryngeal tuberculosis develops, these steam inhalations are often 
exceedingly valuable. 

Sometimes an excessive cough at night can be stopped by giving the 
patient a drachm of Hoffmann's anodyne, or a little spirit of camphor. In 
other instances morphine in the dose of -^q- to ^ of a grain is required, 
but opiates are to be carefully avoided if other measures of relief are 
sufficient. 

When the cough depends upon the accumulation of large quantities 
of material in the bronchial tubes or in cavities, it is of vital impor- 
tance that it should not be arrested by the administration of drugs; 
for it is an effort on the part of nature to get rid of materials which, if they 
are retained in the lung, will greatly increase septic poisoning. This is 
particularly true of morning cough, which, though it is often exceedingly 
annoying, is really an effort to empty a cavity which has become filled 
during the night. Such coughing can frequently be aided by placing the 
patient in such a position that the cavity will readily drain into its supply- 
ing bronchus. 

Whenever the physician in the treatment of pulmonary tuberculosis is 
tempted to employ a drug, the question of its influence upon the stomach 
and digestion should be carefully decided, even though the indications for 
the use of the remedy which exist in other portions of the body seem 
very clear and conclusive. Thus, the use of cod-liver oil in the treatment of 
pulmonary tuberculosis is undoubtedly to be commended, provided that 
the patient can digest it, and at the same time take ordinary food. Even 
a healthy person cannot exist on cod-liver oil alone, and it is a vital mistake 
to impair the appetite and digestion by giving full doses of this sometimes 
valuable drug. Any sign of indigestion of the oil, as in eructations, or in 
the passing of oily stools, should be the signal for stopping its use at once. 
The digestion of good food does more for a patient's vitality than the diges- 
tion of good oil. 

Serum Therapy. — An endeavor has been made to treat tuberculosis by 
means of antitubercle serum, but so far the results which have been 
obtained have not been sufficiently encouraging to cause the plan to be 



332 DISEASES DUE TO A SPECIFIC INFECTION 

very popular, although in the early stages of the disease the use of this 
serum may act as an aid to the control of the tuberculous process. 

Antistreptococcic serum has been used on the ground that nearly all 
cases of tuberculous cavity are infected by the streptococcus as well as the 
tubercle bacillus, and that if the former malign organism was removed, or 
its toxins antagonized, the patient could the better combat the original 
cause of the illness. If streptococci are found in the sputum in large numbers 
it may be used to aid the patient, but otherwise its use is futile. 

Tuberculin. — The employment of tuberculin as a specific remedy for 
pulmonary tuberculosis has not as yet received general professional endorse- 
ment. It is true that a very large number of physicians who are especially 
engaged in the treatment of tuberculous patients have written papers in 
which they have highly praised the employment of this substance, and that 
statistics are numerous which tend to show that it produces advantageous 
results. It must be admitted, therefore, that at times it does good. But, 
on the other hand, it is a good rule in practice to follow the majority in the 
use of new remedies ; for new remedies which really are advantageous are 
taken up and constantly employed by everyone. Probably the conclusions 
as reached by Trudeau, in regard to tuberculin, represent the real facts of 
the case when he says: "My experience with tuberculin treatment at the 
Sanitarium thus far has led me to believe that when carefully tried, in 
suitable cases, it has proved apparently free from danger, and that it has 
seemed to have some favorable influence in bringing about healing of the 
lesions, probably by inciting the formation of fibrous tissues." 

The tuberculin which should be employed is that which is prepared 
by the more modern methods. It is now made by a number of reliable 
concerns, and it can be obtained both in this country and abroad. This 
remedy is not one which is suitable to all cases and should only be given 
by an expert in its use. 

When tuberculin is used for curative purposes the so-called " Tuberculin 
R." is always employed. It is a very much more powerful product than 
ordinary tuberculin. This preparation bears this name because of the fol- 
lowing facts: Tubercle bacilli are coated with fatty acid. This fatty acid 
is removed by triturating them in a mortar and washing the mass with dis- 
tilled water. This mixture is then placed in a centrifuge and it is found 
that the fluid separates into two layers. The upper layer contains no tuber- 
cle bacilli, and it is called "Tuberculin Oberst" (T. O.), but the lower layer, 
which contains bacilli, is called "Tuberculin Residuatum," or T. R. This 
lower layer is repeatedly treated by triturating and centrifuging until all the 
bacilli are removed. The advantage of this product, T. R., is that it does 
not cause suppuration, but does cause immunization. By care in grading 
the dose it may be possible to produce a curative effect without causing 
reaction. 

When the physician desires to use T. R. as a curative agent he begins by 
employing -g-^-g- milligram or less if that dose produces a reaction. This 
dose is prepared by adding 1 c.c. of Tuberculin R. to 500 c.c. of normal 
saline solution (0.8 per cent.). One c.c, therefore, represents one dose 
of -j-^-g- milligram. As the solution when used should not be more than 



TUBERCULOSIS 333 

twenty-four hours old, this method necessarily involves wasting a great deal 
of the product. 

The dose is injected into the tissues of the back by means of a sterilized 
syringe on every alternate day. It is desirable to avoid reaction, and all 
febrile movement that may be induced by one injection must have disap- 
peared before another dose is given. After repeated doses the patient 
may be able to stand very large doses without any reaction and with good 
effect. 

When vomiting complicates pulmonary tuberculosis, its cause must be 
discovered. If it follows excessive cough, the cough must be controlled in the 
manner already described. If it arises from gastric irritability, 2 to 5 grains of 
subnitrate of bismuth and 1 to 2 grains of oxalate of cerium may be given 
an hour before meals. In other instances, where the stomach is depressed 
rather than irritated, 1 or 2 drops of Fowler's solution before meals is 
advantageous. 

The treatment of haemoptysis consists in the administration of a hypo- 
dermic injection of -g- of a grain of morphine if the patient shows great 
mental perturbation because of the hemorrhage. It does not have any 
direct influence upon the flow of blood by producing nervous quiet, but it- 
relieves the patient's mind and so quiets the circulation. If the flow of 
blood is profuse, the patient should be allowed to occupy that position in 
which it is most easy for him to rid his bronchial tubes of fluid. I have 
seen relief produced by permitting him to lie flat on his chest with his head 
resting on the edge of the mattress in such a way that the blood readily 
flowed from his mouth without violent efforts at coughing. 

A multitude of measures have been recommended for the control of the 
hemorrhage. Manifestly, none of them can exercise much power for good. 
No one would think of attempting to control the hemorrhage from a ruptured 
varicose vein in the leg, or from a small artery on the surface of the body, 
by the internal administration of any drug of which we have knowledge. 
Such indirect styptics as tannic and gallic acid are useless. When the 
hemorrhage ceases after the administration of these, or other styptics, by 
the stomach, it is evident that the arrest must be due to the natural clotting 
of the blood rather than to any effect of drugs. That this is the correct 
view of the case is still further emphasized by the fact that the pulmonary 
bloodvessels are very poorly supplied with vasomotor nerves and with 
muscular fibres, and therefore drugs which act by contracting bloodvessels 
cannot exercise any powerful influence in this area. Finally, absorption is 
so slow from the stomach that it is incredible that styptics can exercise a 
material effect before the hemorrhage destroys the patient or is stopped 
by clotting. If the circulation is bounding, a dose of chloral or aconite may 
be given as a circulatory sedative. Nitroglycerin is also of value. 

The use of adrenalin by the stomach is of doubtful value, first, because, 
as just pointed out, the pulmonary bloodvescels are poorly supplied with 
muscular fibres upon which the adrenalin can act, and, second, because it 
is very doubtful whether when adrenalin is placed in the stomach it is not 
decomposed, or at least largely prevented from exercising its constricting 



334 DISEASES DUE TO A SPECIFIC INFECTION 

influence upon bloodvessels at distant parts. The use of astringent sub- 
stances in atomizers is equally futile. All of the fluid strikes against the 
pharyngeal wall, and may run down into the stomach, but it does not reach 
the lungs. Only fluid which can be used in a vaporizer, such as that which 
is driven by a cylinder of compressed air, can by any possibility reach the 
bleeding spot. 

Some practitioners have recommended the application of ice upon the 
perineum in cases of haemoptysis, believing that in some reflex manner it 
diminishes hemorrhage from the lungs, and others have applied a small 
ice-bag over the cavity from which the hemorrhage takes place. There 
is much more danger of these measures adding to shock by chilling 
the patient than there is chance of their doing good. As already stated, 
haemoptysis rarely produces death as the immediate result of the loss of 
blood, and remedies which receive credit for arresting the flow are probably 
unworthy of the confidence imposed in them. 

Tuberculosis of the Alimentary Canal. — Tuberculosis of the alimentary 
canal may occur in any of its parts from the tonsils to the anus, and, while 
its development is a comparatively rare primary form of the infectiqn, it is 
nevertheless met within sufficient frequency to make it of importance. In 
an analysis of 5142 autopsies William Hunter, the Government Bacteriolo- 
gist of Hong Kong, found that this condition was rarely present in children 
under five years, notwithstanding the very great prevalence of tuberculosis 
among the Chinese. 

Tuberculosis of the Tonsils. — The tonsils may contain tubercle bacilli, on 
their way to the infection of neighboring lymphatic glands, or they may 
be actually tuberculous themselves, containing in their substance miliary 
tubercles or caseous foci. These lesions are more frequently met with in 
children than in adults, and may depend upon autoinfection — that is, the 
tonsils may be infected by tuberculous sputum which is expectorated 
(secondary), or they may become infected by the entrance of tubercle bacilli 
in dust by the nose or mouth or perhaps in the milk of tuberculous cows 
(primary). Koplik has recently made an interesting report on this subject 
in the American Journal of the Medical Sciences. 

Even more important than tuberculosis of the tonsils is tuberculosis of 
the so-called third or pharyngeal tonsil, constituting the " postnasal adenoid." 
As is well known, these growths are not rarely tuberculous in origin. 
From these adenoids the bacilli may pass through the lymphatics and 
so cause tuberculosis of the mediastinal and bronchial lymph nodes. 

Tuberculosis of the Pharynx and (Esophagus. — The pharyngeal wall is not 
uncommonly the site of miliary tubercles, in the course of chronic pulmonary 
tuberculosis, and even more commonly tuberculous ulceration extends from 
the larynx and epiglottis to the pharynx and adds greatly to the discomfort 
of the patient. Tuberculosis of the oesophagus is exceedingly rare, but some 
cases have been recorded. It may complicate general miliary tuberculosis, 
being a part of the systemic infection, or it may arise from the swallowing 
of tuberculous sputum, or, again, from the extension of the disease from 
a tuberculous lymph node or vertebra. The ulceration may lead to 
perforation from within or the reverse. 



TUBERCULOSIS 335 

Tuberculosis of the Stomach. — Tuberculosis of the stomach rarely occurs, 
probably because its juices protect it from infection. When it does occur, 
it appears as a miliary tuberculosis due to circulatory infection, or as single 
or multiple tuberculous ulcers involving the mucous membrane. These 
ulcers are usually the result of a process starting from an ulcerating gland 
which becomes attached to the stomach and so causes disease by the exten- 
sion of the inflammatory process. Van Wart has recently reported an 
instance of solitary tubercle in the muscular layer of the stomach which is 
believed to be unique. 

Tuberculosis of the Intestines. — Tuberculosis of the intestines is a much 
more common condition, and in the great majority of instances is secondary 
to infection elsewhere. Primary intestinal tuberculosis occurs usually in 
children, and as the result of the ingestion of milk which is infected by the 
specific bacillus. This primary form has been denied an existence by such 
excellent men as Leube and others, but so many other pathologists, of 
whom Bollinger may be taken as a leader, have observed it that its existence 
is proved. 

The secondary or common type of intestinal tuberculosis is usually the 
result of pulmonary tuberculosis, and arises from the swallowing of tuber- 
culous sputum. When the pulmonary lesions have lasted for a long time 
intestinal infection will be found at autopsy in a large proportion of cases, 
about 25 per cent. Statistics have been published by certain pathologists 
giving over 50 per cent. The lesions are found chiefly in the ileum (80 
per cent, of the intestinal cases) just before it joins the csecum, or in the 
ileum and colon 45 per cent., in the colon alone 3 per cent., and in the 
rectum 7 per cent., according to Frerichs. These statistics as to the relative 
frequency of the various lesions hold true of the disease, as it appears in 
children as well, even when the malady appears as a primary affection. 

Tuberculous infection of the intestine primarily involves the lymph nodes 
of the bowel, causing them to become swollen by reason of the characteristic 
cell proliferation which the tubercle bacillus always produces. The solitary 
glands project markedly above the surface as yellowish-white masses which 
finally undergo caseation and softening, and then the mucous membrane 
covering them breaks down, forming an ulcer which is surrounded by 
somewhat overhanging edges. The ulcers are not very numerous; at times 
only one node may be involved. If the agminated glands, or Peyer's patches, 
are infected, separate caseous masses develop, several ulcers form, and 
finally coalesce, forming a large necrotic surface of very irregular outline. 
It is interesting to note that this condition is quite different from the process 
in enteric fever, in which disease the glands are affected generally and the 
individual agminated mass is uniformly infiltrated. Tuberculous ulcers of 
the agminated glands usually extend transversely across the gut, whereas 
the lesion of enteric fever extends longitudinally. 

The overlying serosa is commonly thickened, it may contain distinct tuber- 
cles, and at operation the diagnosis of tuberculous ulcer may be made 
without opening the bowel. Fibrosis and thickening with associated con- 
traction may cause stricture and symptoms of obstruction; perforation is 
not common and is usually overlooked. 



336 DISEASES DUE TO A SPECIFIC INFECTION 

Tuberculosis of the caecum in the neighborhood of the appendix may 
give rise to the belief that appendicitis or tumor of the bowel is present. 
(See Symptoms.) 

When the rectum is affected the ulceration is preceded by infiltration 
and caseation in the submucosa, it often encircles the bowel, and the tissues 
near the seat of the ulcer are frequently dotted with small, yellowish or 
whitish tubercles, which add to the area of the ulcer as they undergo degen- 
erative change. They also give rise to tuberculous infection of the perito- 
neum and perirectal tissues and to tuberculous abscesses and fistulse. 

With the distinct and specific lesions just described tuberculous disease 
of the bowel presents an associated condition of acute and chronic catarrh 
or, in other words, a true enterocolitis. 

Of recent years much has been written of chronic hyperplastic tuberculosis 
of the intestine. In this form the intestinal wall is greatly thickened, the 
lumen commonly narrowed and sausage-like. Distinct cylindrical seg- 
ments of the involved tissue may be recognized through the thin abdom- 
inal walls. Neoplastic masses which may attain the size of a fetal head 
occasionally develop, and polypoid growths may occur on the interior of 
the bowel. The condition is most common in the ileocecal region, and 
is rarely restricted to the small intestine, but may involve one or more parts 
or the whole of the colon, causing strictures with interposed dilated areas, 
although actual dilatation is rare. The stenosis may be almost complete. 
Histologically there is marked hyperplasia of the connective tissue of the 
intestinal wall, and the great thickening, sometimes attaining 5 cm., is due 
largely to this cause. Caseous areas and even typical tubercles may be 
absent. The newly formed tissue is often but scantily supplied with bacilli. 

Symptoms of Intestinal Tuberculosis. — The symptoms of intestinal 
tuberculosis consist chiefly in the manifestations met with in most cases of 
enterocolitis. The patient complains of looseness of the bowels, or diarrhoea, 
and a considerable amount of colicky pain. With these signs there is wasting 
and decrease in strength. The tongue may be coated, but it is often un- 
duly clean and the normal roughness of its mucous membrane is replaced by 
a raw-beef appearance. Palpation of the abdomen may reveal tenderness 
at certain points, which is not, however, very well marked, and auscultation 
will show an excessive amount of peristaltic movement and rumbling. At 
times the appetite may be excessive owing to the fact that the diarrhoea 
causes starvation of the tissues, which is recognized by the system and shown 
in a desire for more food. At such times, in particular, the stools may 
contain undigested particles of food. There are, however, no symptoms 
in this early stage that can be considered typical, and the presence of 
tuberculosis elsewhere may be the chief reason for believing that the 
alimentary canal is involved. 

When ulceration occurs the presence of mucopus, blood, and, more im- 
portant, the discovery that tubercle bacilli are in the stools make it possible 
for us to state positively the cause of the disease. If the disease develops 
farther, as it is prone to do if life is prolonged a sufficient length of time, 
the peritoneal coat of the intestine is involved and gradually a general 
adhesive peritonitis, such as was described in the article on peritoneal 



TUBERCULOSIS 337 

tuberculosis, is produced, with its characteristic thickening of the peritoneum 
and cicatricial contraction of the omentum and mesentery. This produces 
constrictions in the intestine, which may be due to the peritonitis or to the 
ulcerative process inside the bowel. 

In some cases the inflammatory process produced by tuberculosis of the 
caput coli is so intense that pain in the region of the appendix may give 
rise to the belief that an acute appendicitis or appendicular abscess is 
present. In a case known to be tuberculous the possibility of this condition 
is manifest, but in one which has a small and unrecognized tuberculous 
focus elsewhere, as in the lungs, operative procedures for appendicitis may 
be hurriedly resorted to when no necessity for them exists. 

So, too, the finding of a mass in this region, without sharp pain, may mislead 
the physician into a diagnosis of malignant growth if the rest of the body be not 
well investigated for a tuberculous focus. Such a mass may be differentiated 
from carcinoma by the fact that there is a focus of tuberculosis elsewhere. 
If the growth be slow it is probably tuberculous ; whereas if rapid it is probably 
cancerous, for csecal tuberculosis may last two years and csecal cancer 
rarely lasts longer than eight months. Further than this, if the patient is 
below thirty years of age tuberculosis is more likely than cancer; whereas 
after forty years the reverse is true. The tumor when outlined by palpation 
in tuberculosis is elongated and the thickened intestine can be felt, whereas 
in cancer it is usually sharply circumscribed and the rest of the bowel 
cannot be outlined. Fever is usually present in tuberculosis and absent in 
cancer. The presence of tubercle bacilli in the stools will, of course, decide 
the diagnosis, and even if they cannot be found, the presence of a tuberculous 
focus elsewhere, in a person below forty years, should be considered as point- 
ing strongly to this bacillus as the cause of the growth. 

At times the tumor found at the ileocecal region results in obstruction 
of the ileocecal valve, and the colon becomes greatly distended with gas, 
appearing as a large mass in the sides and in the epigastrium. In other 
cases the colon undergoes atrophy, and can be felt through the emaciated 
belly wall as a narrow, thickened band. I have seen the entire colon in 
a case of this character shrunken to such an extent that it was smaller than 
the ileum. In doubtful cases resort may be had to tuberculin to determine 
the true nature of the mass. 

Prognosis in Intestinal Tuberculosis. — The prognosis in intestinal 
tuberculosis is not as grave as in pulmonary tuberculosis, as far as early 
death is concerned. In the majority of instances the patient dies of the 
primary focus before the state of the bowel is grave enough to cause death. 
Such cases often last for several years and have periods of improvement 
followed by relapse, and characterized by gradual loss of vitality. If death 
is caused by the intestinal state it comes as a direct result of profound 
feebleness and exhaustion. 

Treatment of Intestinal Tuberculosis. — The treatment of intestinal 
tuberculosis, as in tuberculosis of the lungs, consists to a great extent in the 
maintenance of the greatest degree of nutrition and vitality that is possible, 
and this can only be accomplished by an out-door life, plenty of sunshine, 
the avoidance of fatigue, and the use of such foods as are easily digested in the 
22 



338 DISEASES DUE TO A SPECIFIC INFECTION 

stomach or in the duodenum, so that the greater part of the nourishment will 
be absorbed before the lower part of the ileum is reached. In those cases in 
which excessive peristalsis rapidly carries the contents of the small intestine 
to the large bowel before absorption can occur, it is needful to insist on small 
quantities of food being taken at a time, and to order that no water be taken 
at meals. It is also essential that the patient shall immediately after taking 
food lie down and rest in order to apply all the nervous energy possible to 
the process of digestion and to prevent stimulation of the bowel to active 
movement. For the purpose of arresting peristalsis and diarrhoea the 
salicylate of bismuth in the dose of 10 to 15 grains three or four times a day 
may be given, or salol and the subnitrate of bismuth may be used. Another 
valuable drug is eudoxine in the dose of 10 to 20 grains three times a 
day in capsule, or bismuth subgallate may be given in the same dose. In 
some instances iodoform given in keratin-coated pills in the dose of 5 grains 
four times a day to exercise the influence of this substance on the tuberculous 
lesions; or if the disease is in the rectum or colon, 20 grains may be injected 
dissolved in 4 ounces of olive oil, or 5 to 10 grains may be given in suppository. 
Some relief and comfort can also be obtained by the use of a hot-water 
bag over the abdomen and by painting the belly wall every few days with 
tincture of iodine. 

Tuberculosis of the Liver. — Tuberculosis of the liver occurs as part of a 
general miliary tuberculosis, as a form characterized by the formation of 
fairly large aggregations of tubercles in which the nodules may be as large 
as a walnut. Tuberculosis of this organ is practically always secondary 
to disease elsewhere. (See Tuberculosis of the Peritoneum.) 

The miliary form is characterized by the formation of miliary tubercles 
which are intralobular or interlobular in position. They may even be in 
the walls of the biliary ducts, and vary in size from those so small that they 
cannot be seen with the naked eye to others which are several millimetres 
in diameter. When the tubercles are massed together so that they form 
small nodules, the cells of the liver are of course destroyed, the surrounding 
cells suffer coagulation necrosis and infiltration with spheroidal cells, and 
tubercle bacilli may be found in large numbers in the cheesy masses. 

Tuberculosis of the Genito-urinary System. — Tuberculosis may involve 
any part of the genito-urinary tract, and is by no means rarely met with in 
the testicle, the Fallopian tube, the bladder, and the kidneys. 

Tuberculosis of the Testicle. — When tuberculosis appears in the testicle 
it develops in one or two forms. In one of these the onset is abrupt and 
accompanied by acute inflammation, and in the other type the disease 
develops slowly, with no inflammation and without pain. When the acute 
inflammation of the first type disappears the testicle presents irregular 
nodules, which also develop in the chronic form. In a large proportion of 
cases the disease is secondary to lesions elsewhere, but it may be primary, 
particularly if it begins in the epididymis. Verneuil believes with others 
that infection may occur during coitus if tuberculous disease of the uterus 
exists, but that state is very uncommon. Bab£s has found tubercle bacilli 
in the vagina. 

In nearly all cases, whether the disease be primary or secondary, the 



TUBERCULOSIS 339 

lesion begins in the head of the epididymis, forming nodules which undergo 
caseous changes. The infection spreads to the vas, which becomes thickened 
and nodular, and to the testicle, the vaginal tunic of which is infected. In 
more than three-fourths of the cases this secondary infection of the testicle 
takes place. 

When primary infection of the testicle occurs the tubercles also produce 
nodules, which soften and may form a sac of cheesy matter. Sinuses may 
form after adhesion to the scrotum has taken place and discharge exter- 
nally. 

Symptoms of Tuberculosis of the Testicle. — In the form of the # 
disease characterized by sudden onset the symptoms closely resemble those 
caused by gonorrhoea! orchitis, for sickening pain and swelling are present. 
Instead of subsiding in the course of a week or ten days, the swelling 
persists, although the pain disappears; but before many days have passed 
softening occurs and the so-called abscess is formed escaping by one or more 
sinuses. The swelling is often bilateral, and in some instances massive 
caseation does not take place, but hydrocele develops. In the chronic 
painless form there is gradual enlargement, usually of one testicle, with the 
development of one or more nodules and a sense of weight. In place of 
caseation a fibroid process may develop. 

Diagnosis. — The diagnosis of acute tuberculosis of the testicle can be 
made only after care has been exercised to exclude the possibility of injury, 
metastasis in mumps, gonorrhoea, syphilis, and the orchitis of some of the 
acute infectious diseases such as typhoid fever. A previous history of 
gonorrheal orchitis is, however, of importance, for this condition predis- 
poses to tuberculosis of this part. The absence of any of these causes, the 
presence of tuberculous lesions elsewhere, as in the seminal vesicles or pros- 
tate, or in organs farther removed, and the fact that the patient is in young 
adult life, all favor the diagnosis of this disease being present. The develop- 
ment of suppuration" and the finding of the bacilli in the cheesy pus will, of 
course, decide the diagnosis. 

The chronic type must be separated from sarcoma and from the thicken- 
ing following gonorrhceal orchitis. The absence of any recent history of 
gonorrhoea, or of urethral discharge, and the presence of an irregular tumor 
which increases in size, all point to tuberculosis as the cause. The finding of 
the bacilli proves tuberculosis, but the presence of the gonococcus does 
not prove the absence of tuberculosis, for obvious reasons. If hydrocele 
is present the injection of some of the fluid into the peritoneal cavity of 
a guinea-pig may decide the diagnosis by producing tuberculosis in that 
animal. 

Treatment. — In most cases it is far safer to remove the gland. The 
palliative treatment consists in the ordinary hygienic measures used in 
tuberculosis and, if the disease is localized, in incision and drainage with 
iodoform gauze; or in other cases, after the abscess is evacuated, the cavity 
may be injected with iodoform in glycerin or in olive oil to the extent of 
15 drops. In other cases a few drops of this mixture may be injected into 
the gland at different points every three or four days, care being taken 
that antisepsis is preserved. 



340 DISEASES DUE TO A SPECIFIC INFECTION 

Tuberculosis of the Bladder. — This condition may be either primary or 
secondary, and when secondary it may be due to infection through the 
bloodvessels from a distant point, or by direct extension from the prostatic 
urethra, which is diseased through infection of the prostate gland, which 
is affected in 97 per cent, of cases of genito-urinary tuberculosis according 
to Kazywicki. In other instances the tuberculous lesions are transferred 
from the kidney by the ureter to the bladder. In still other instances the 
infection passes from the vas deferens or epididymis or seminal vesicles to 
this viscus. Primary vesical tuberculosis is quite rare, and when it occurs 
js due to infection from tuberculous female genitals (Fournier). In many 
instances a case of tuberculosis of the bladder which is seemingly primary 
is really secondary to an unrecognized infection of the kidney. This renal 
condition in other instances may be known to exist during life, but it may 
develop so synchronously with the vesical lesions that it is difficult to tell 
which organs were first affected. In many other cases the primary lesion 
may really exist in the prostate or in the seminal vesicles. 

The bladder, when affected by tuberculosis, develops grayish miliary 
tubercles in its epithelial lining, which can rarely be seen through the cysto- 
scope as small gray spots, which, like all other tuberculous growths of small 
size, tend to amalgamate and form patches which in turn may ulcerate, 
and so destroy the mucous membrane. The ulcers may be single or mul- 
tiple, and, like tuberculous ulcers of the bowel, may have irregular outlines 
with the base covered by greenish or grayish pus. Sometimes they are deep, 
at others superficial, and in the severe cases they may penetrate the walls of 
the bladder and cause abscesses, which in turn may perforate the rectum, 
the vagina, or even the tissues in the suprapubic area. The chief lesions 
are usually in the area of the trigonum. Tubercle bacilli may be found in 
the pus in the urine. 

Symptoms. — The symptoms of tuberculosis of the bladder are usually 
not well marked in the early stages, and the onset of the malady may be so 
gradual that the disease is well developed before it is recognized. At first 
nothing more than a little vesical irritability may appear, and the urine 
remains clear and normal in appearance. The microscope may, however, 
reveal a few red blood cells, and later distinct hematuria develops, which is 
characterized by the appearance of a few drops of clear blood at the end of 
urination. As soon as the mucous membrane of the bladder becomes 
eroded infection is prone to occur and cystitis develops, and with the appear- 
ance of cystitis fain comes to be a prominent symptom, associated with 
tenesmus and a constant desire to urinate, which exhausts the patient and 
prevents sleep. The earliness with which these symptoms develop depends 
upon the seat of the disease. If it be in the trigonum, they arise promptly; 
if elsewhere, they may be postponed for months. Retention of urine may 
follow ulceration, or in other cases as the neck of the bladder ulcerates 
incontinence is produced. 

Diagnosis. — The diagnosis of vesical tuberculosis depends upon the pres- 
ence of these symptoms and the finding of the bacillus in the urine, or by 
inoculation of a rabbit or guinea-pig with the urine, with the subsequent 
development of the disease in that animal ; but the failure of either of these 



TUBERCULOSIS 341 

tests does not exclude tuberculosis. If gonorrhoea, stone in the bladder, 
stricture of the urethra, or a history of the use of irritating drugs can be 
excluded, and if no spinal disease exists to cause secondary bladder trouble, 
tuberculosis should be suspected. The presence of tuberculosis elsewhere, 
of course, suggests that this disease is the cause of the bladder trouble. 

Treatment. — For the general plan of treatment in these cases reference 
must be made to treatises on genito-urinary disease. The bladder must be 
soothed by alkaline diuretics if the urine is acid, hyoscyamus may be given 
for vesical irritability, and if the disease is active iodoform in olive oil may 
be injected into the bladder every day, using a 10 per cent, solution. The 
bladder should be carefully emptied before the iodoform is injected. In 
other cases corrosive sublimate 1 : 5000 may be employed by injection. In 
severe cases perineal drainage is to be resorted to. 

Tuberculosis of the Kidneys. — With regard to the pathway by which the 
bacillus reaches the kidney two views have generally been held. Hsema- 
togenous infection is admitted. Until recently an ascending infection has 
been thought not uncommon, but there is at present a decided tendency to 
doubt that infection travels from below upward ; it has been shown by many 
observers that tubercle bacilli are occasionally present in the urine of tuber- 
culous patients, even when subsequent examination at autopsy discloses no 
tuberculosis of the genito-urinary organs, and hence it is not necessary to 
invoke ascending infection to explain renal lesions secondary to tuberculosis 
elsewhere. 

Tuberculosis of the kidneys appears in an acute and chronic form. The 
former is of the miliary type and is associated with the signs of tuberculous 
infection elsewhere, and cannot be treated separately from the general state. 
The chronic form may arise as a primary lesion, or, far more commonly, 
as a secondary process due to disease of the lower genital tract. When the 
disease is primary the bacillus probably gains access to the kidney through 
the blood; this type is that usually met with in children. But the form 
ascending from the genitals is that met with in adults, as a rule. Males 
are more frequently affected than females. The disease is most frequent 
between twenty-five and forty years of age, but it has occurred in an infant 
at the breast and in very old men. The lesions are often bilateral. 

The pathological process in primary and secondary renal tuberculosis 
is quite different. In the primary form, in which the infection comes by 
the blood, the bacilli, resting in the vessels of the tufts and tubules, form 
small tubercles, which gradually undergo necrosis and so cause a spread of 
the disease to other parts of the kidney, particularly the calices and the 
pelvis. The necrosis of tuberculous nodes gives rise to areas of softening 
or abscess cavities, and these are filled with cheesy material which rarely 
contains blood and urine, although lime salts are frequently present in the 
dead tissue. Not only tubercle bacilli but pyogenic and other micro- 
organisms are often present. The capsule of the kidney is thickened and 
may show scattered tubercles. The size of the organ is considerably 
increased by the growth of the tubercles and the associated inflamma- 
tion, forming the so-called massive tuberculosis of the kidney. Finally, the 
kidney may be shrunken. 



342 DISEASES DUE TO A SPECIFIC INFECTION 

As the tuberculous process in the pelvis of the kidney increases the ureter 
is usually infected, and as a result is often partly occluded. This produces 
a retention of urine in the kidney and so a secondary hydronephrosis 
develops, or it may be a pyonephrosis. Sometimes in the early, and much 
more frequently in the later, stages of the affection the tissues surrounding 
the kidney become more or less affected and a peri nephritic tuberculosis may 
appear from rupture of a softened area through the capsule of the kidney. 

When that form of renal tuberculosis which is secondary to tuberculosis 
in the lower genito-urinary tract develops, the ureter, is first involved, and 
thence the pelvis of the kidney. The disease then attacks the tips of the 
pyramids and so gradually the entire gland is involved, but to a less degree 
than in the form first described. Pyonephrosis is very common in these 
cases, and obstruction in the flow of urine is usual. 

Symptoms. — Often no symptoms appear until the pelvis of the kidney is 
diseased, when pain becomes a marked symptom. This pain may be dull 
or acute, as if due to a renal calculus, with the characteristic radiation of 
the pain to the penis and inner side of the thigh. The urinary symptoms 
are frequent urination, slight incontinence, and, later, distinct signs of 
cystitis develop. Before the pelvis of the kidney is affected the urine may 
be normal, but afterward it contains pus and blood, the pus coming from 
this area or from the necrotic ulcerating tubercle. Attacks of violent pain, 
arising from acute hydronephrosis due to blocking of the ureter by cheesy 
masses, may occur, followed by a free flow of purulent urine as the obstruc- 
tion gives way. Tubercle bacilli can usually be found in the urine, but care 
must be taken that the smegma bacillus is not mistaken for the specific 
bacillus, and, as indicated above, the demonstration of the tubercle bacillus 
does not prove that the infection is in the genito-urinary organs. 

The associated symptoms are those of anaemia, debility, and loss of flesh. 
A lumbar tumor may also appear. 

When the case is grave the question of operation must be considered, 
and it is important to discover if the disease is bilateral or unilateral before 
operating. This may be done by unilateral catheterization. 

Tuberculosis of the Fallopian Tubes, Ovaries, and Uterus.— The fre- 
quency of tuberculosis of the Fallopian tubes is notable. It forms the 
largest part of all statistics involving the female genitalia, for, as stated 
below, the ovary and uterus are rarely affected. Tuberculosis of these 
parts was recognized and reported as early as 1744 by Morgagni. In 
1886 Hegar published an important paper on this subject which marked 
an epoch in its study. To illustrate the great frequency of tuberculosis of 
the female genital tract the statistics of eight European pathologists may 
be cited. In 8627 cases of tuberculosis in females, this disease had infected 
the genitals 208 times. These relative proportions are probably too small. 

Unlike tuberculous disease elsewhere, tuberculosis is quite frequently a 
primary lesion in these parts, the infection being received in some cases from 
the male during coitus (Verneuil, Cohnheim), but in the majority of instances 
taking place through the blood or lymphatics. According to the statistics 
of Schramm, Spaeth, Mosler, and Frerichs, genital tuberculosis is found 
to be primary in about 18 per cent, of cases of genital tuberculous disease. 



TUBERCULOSIS 343 

Genital tuberculosis is most common during the period of sexual life. 
Pathologically the condition under these circumstances is like that of an ordi- 
nary salpingitis, the tubes being thickened and filled with cheesy material. 
Because of the inflammation associated with the tuberculous process the fim- 
briated extremity of the tubes becomes adherent to the ovaries and the uterus 
may become infected. This condition may develop in children as well as in 
adults, and it is usually bilateral. True abscess of the tube may arise from 
this cause and a tuberculous parametritis and peritonitis often start from 
this nidus. In some cases a miliary tuberculosis of the tube develops. 

The ovary is rarely involved, but when this occurs it is always a secondary 
infection from an infected tube or other adjacent parts or from the blood. 
The uterus is affected only in very rare instances. 

Prognosis. — The prognosis in tuberculosis of the female genitalia is more 
favorable than would be imagined, provided an early diagnosis is made and 
operative treatment resorted to. It is, of course, more favorable in these 
instances if the lesion be a primary one, for if severe disease is present else- 
where, operation may be contraindicated and general recovery impossible. 

Treatment. — The treatment is entirely surgical. 

Tuberculosis of the Heart. — Ferrend and Rathery have reported a case 
of tuberculous vegetative endocarditis following primary tuberculosis of 
the spleen. Tubercle bacilli were found in these vegetations and in the 
clotted heart blood. 

Tuberculosis of the myocardium is very rare. In 1902 Anders collected 
71 cases of tuberculosis of the myocardium, and reported one of his own, 
which were all he could find in literature. Out of 3999 autopsies reported 
by Valentin and Sangelli this condition was found in only 9 instances. 
Weigert, however, states that he has found minute tubercles in different 
portions of the heart in nearly ail his autopsies on patients who died from 
acute miliary tuberculosis. 

Tuberculosis of the Thyroid Gland. — Fraenkel and Chiari in 480 
autopsies on tuberculous subjects found the thyroid gland affected 13 times. 

Tuberculosis of the Brain and Cord. — Tuberculosis of the meninges 
of the brain and cord has already been mentioned when discussing the tuber- 
culous infection of the serous membranes. The tissues of the brain and 
cord are, comparatively speaking, very rarely affected. When tuberculous 
lesions occur in these parts they are practically always secondary to tuber- 
culous lesions elsewhere, but there are a few exceptions to this rule. Thus, 
Demme has recorded a unique case of tuberculous tumor of the cerebellum 
in a child of twenty-three days, and he has also had a case in which infection 
seemingly took place through the nose. 

When tuberculous tumors develop in these parts of the nervous system 
they appear as solid or caseous, rounded masses, which resemble the ordinary 
tuberculous growth as it is seen elsewhere. They vary in size from a 
millet-seed to an orange. When incised they are caseous, fibrocaseous, or 
hyaline and calcareous, or all of these changes may be found associated. 
The surface of the growth is sometimes soft and translucent, and the adjacent 
brain-tissue may be filled with miliary tubercles, which, coalescing with the 
main growth, in this way increase its size. The growth does not undergo 



344 DISEASES DUE TO A SPECIFIC INFECTION 

the rapid changes usually met with elsewhere. Sometimes these nodules 
become encapsulated by fibrous tissue just as does the ordinary tuberculous 
growth in the lung, or rapid softening in the surrounding tissues develops 
and suppuration takes place. 

These tuberculous growths do not tend to infiltrate the surrounding tissues. 
They generally occur in the brain tissue itself, and while it has been asserted 
that they always spring from the pia mater, this view is of doubtful value. As 
they often project above the surface, the cerebrospinal fluid is readily infected. 
One-third of these tuberculous growths occur in the cerebellum, in one of its 
hemispheres or in the middle lobe. After the cerebellum, the cerebrum 
is the most common site, and after this Gowers gives the following order: 
the pons, the cerebral ganglia, the quadrigeminal bodies. As a rule, more 
than 1 growth exists; but sometimes 2 and sometimes as many as 10 or 12 
are present. Thus, Trevelyan found them multiple in 17 out of 33 cases, 
which is a smaller proportion than is usual, and the largest number in any 
one case was 4. In a case reported by Middleton there were 20, and 
in a case reported by Homen there were 12. West and Henocli have 
each reported a case in which there were 12 tuberculous tumors. There 
are a few cases recorded in which recovery has taken place notwithstanding 
the presence of a tuberculous tumor in the brain, and without operation. 
(For literature see Trevelyan's article in the Lancet for November 7, 1903.) 
The symptoms and treatment of tubercle of the brain are discussed under 
Brain Tumor. 

LEPROSY, 

Definition. — Leprosy is a chronic infectious disease caused by a specific 
bacillus, and is characterized by the occurrence of granulomatous new- 
growths in the skin, mucous membrane, peripheral nerves, and viscera. The 
lesions are partly anaesthetic and there is a marked tendency to destructive 
ulceration and trophic lesions. 

History. — The history of leprosy is as old as the written history of the 
human race. The earliest known records are in two Egyptian papyri of 
4260 B.C. and 2400 B.C. The detailed description of leprosy in the third 
book of Moses is familiar to all. In India and China the earliest writings 
that unmistakably describe leprosy appeared about 700 B.C. The disease 
appears much later in European history. It was not mentioned by Hippoc- 
rates, and we may assume that it was unknown in his time. It appeared 
in Greece before 375 B.C. and gradually spread over all Europe, its exten- 
sions being generally along the track of conquering armies. Its extensive 
distribution in the Middle Ages finally brought about stringent restrictive 
regulations which, beginning in the thirteenth century, served to gradually 
decrease the disease until now it occurs only in isolated centres of infection. 

Distribution. — At present the distribution of leprosy is very extensive, 
principally in tropical and subtropical countries. It is a mistake to con- 
sider that leprosy is essentially a disease of warm climates. In Europe 
it appears only in small, scattered centres or in isolated cases. It prevails in 
greatest numbers in Finland, Sweden, Iceland, and Norway, particularly 



LEPROSY 345 

the latter. In Russia it is found in forty-nine provinces, most frequently in 
the Baltic provinces of Lifu with 609 and Kurland with 201 cases. Isolated 
cases occur in England, Germany, Brittany, and Italy. The total number 
of cases in Western Europe at present is estimated at 3000. The disease 
is found all over tropical Asia. In British India the number of lepers is 
estimated at 105,000, or one in every two thousand of population. It is 
believed that leprosy prevails in the southern provinces of China more 
than anywhere else, although no accurate figures are available. It is 
very common in Japan, the number of cases being estimated at 23,660 
(Souton), and in Ceylon, Persia, Arabia, and the Malayan country. In 
the Philippines there are probably 15,000 lepers. The disease is widely 
distributed in Africa, particularly along the upper Nile and the countries 
bordering along the Red Sea and the Mediterranean. Leprosy was intro- 
duced into the Sandwich Islands in 1859, and in 1891 one in thirty of the 
population was affected. 

Much has been said of the early existence of leprosy in America. There 
is no evidence to show that the disease existed prior to the Spanish discovery. 
The so-called evidence of pre-Columbian leprosy in America is entirely too 
vague to justify any deductions. In point of fact it suggests syphilis or 
sacrificial mutilation more strongly than leprosy. At present lepers are 
found in large numbers in Mexico and many countries of South America. 
In Colombia there are said to be seven in every one thousand in the popula- 
tion. There are some cases in New Brunswick and British Columbia. Cuba 
and the Antilles are severely infected; the latest figures give 1297 lepers in 
Cuba. In the United States the disease is generally distributed. A recent 
official report shows that nearly every large city has at least one case, the 
aggregate number for the United States reaching over 900. The disease 
occurs in three main foci, namely, one in Louisiana, which has existed since 
1785, and has lately been estimated as containing about 500 cases; another 
in California, the infection having been brought in by the Chinese, and a 
third in Minnesota, where it is estimated that there are 170 lepers, the num- 
ber being almost entirely made up of emigrants from the infected districts in 
Norway, from which region infected persons also carried the disease into the 
Mormon settlements of Utah. These settlements in Utah have also been 
infected from Hawaii. 

Etiology. — The specific cause of leprosy is the Bacillus leproe, discovered 
by Hansen in 1871. This bacillus is about the same size and has the same 
morphology as the tubercle bacillus. Like it it is also acid fast; that is to 
say, when stained with an aniline dye it does not decolorize readily in the 
presence of mineral acid. It stains a little more easily than the tubercle 
bacillus and decolorizes more rapidly. It has not been grown successfully 
on artificial culture media. It is found packed in very great numbers 
inside the leprosy cells, but it does not invade the nucleus. It is also found 
in zooglea masses in the lymph spaces, in the granulomatous lesions, and 
in the infiltrated nerve tissues. A number of cases have been reported in 
which the bacillus has been found in the circulating blood. 

Manner of. Infection. — There is one case of experimental inoculation on 
record in the person of a Hawaiian convict reported by Arning. Four weeks 



346 DISEASES DUE TO A SPECIFIC INFECTION 

after inoculation the disease began to develop with acute pain and thicken- 
ing of the nerve trunks, and a little while after a typical leprous nodule 
appeared at site of inoculation. The patient died of the disease in six years. 
Unfortunately this experiment was made in a leprosy country and the man 
had a leprous family history, so that the evidence derived from it cannot 
be regarded as absolutely conclusive. There can be no doubt that in a large 
number of instances the bacillus gains admission through abrasions of the 
skin and mucous membrane, and possibly also from the friction of infected 
clothing. 

Corroboration of the idea that the bacilli gain entrance through local 
lesions is found in the fact that where people go habitually without shoes, 
as in tropical countries, the disease first appears in the feet in a large 
proportion of cases. Ehler states that in Iceland the face and hands are 
most frequently attacked because the remainder of the body is so fully pro- 
tected by clothing. Boinet, in Hanoi, considered infected earth to be the 
probable carrier of the disease to the feet of the natives. He found the earth 
saturated with sputa, crusts, and discharges of the lepers. He was able 
to demonstrate that the soil of the cemetery at Hanoi was highly charged 
with bacilli, but this evidence is of little value, as acid-fast bacilli are 
widely distributed. Carasaquilla believes that leprosy may be conveyed 
by the bite of fleas, and infection by the mosquito must also be borne 
in mind, since the bacilli are sometimes found in the blood and have also 
been demonstrated in mosquitoes. Scabies may transfer the infection. 
A large proportion of cases are undoubtedly infected in sexual intercourse. 
The contagion of leprosy is, however, feeble. 

The immunity of physicians and nurses is proverbial, although several 
striking instances, as that of Father Damien, are on record in which 
attendants on lepers have fallen victims to the disease. It would seem 
that long intimate contact were necessary to contract it. Hutchinson sug- 
gests that leprosy may be conveyed from person to person by commensal 
contagion; that is to say, by eating food prepared by the sore hands of a 
leper, and by eating out of infected dishes and utensils. Von Bergmann, in 
a study of 106 cases of leprosy in Riga, found that 60 per cent, occurred in 
people who had lived in intimate contact with lepers. In the workhouse 
at Riga there were 23 cases: 4 who entered with it, 19 who contracted it in 
the house; 9 cases developed in women whose neighbors in the next beds 
had leprosy. 

Great significance was formerly attached to the factor of heredity in 
leprosy, but recent studies of the epidemiology of the disease have disproved 
its importance. Boinet cites a case in which grandfather and grandmother 
were lepers, while the father and five children escaped although living in a 
leprous community. Children of lepers removed soon after birth from 
the infected districts do not develop leprosy, while their brothers and sisters 
who continue to live in the leper community may contract it. None of the 
children of Norwegian lepers who have emigrated to the United States 
have developed the disease. Tonkin, in a careful study of lepers in Algeria, 
found that only 10 per cent, of the cases had any leprous taint in their ances- 
try; so that 90 per cent, at least must have derived the disease from other 



LEPROSY 347 

sources. He found, further, that less than 10 per cent, of the children of 
lepers developed the disease, which is certainly a low percentage of con- 
tagion for persons living in close intercourse with lepers, even disregarding 
the question of heredity. There is nowhere a record of a leprous foetus, 
although one or two cases of infants born with leprosy has been reported. 

The disease is exceedingly rare under one year; and, in fact, before the 
fifth or sixth year. It must be recognized as very feebly contagious, 
therefore, when close and prolonged contact is eliminated. Of the various 
types the tuberculous is far more contagious than the anaesthetic. 

Many writers have maintained that defective nutrition and diet play an 
important role in this disease. Hutchinson is at present the foremost ex- 
ponent of the theory that the disease is conveyed by food and that the germs 
gain entrance to the body through the stomach. He believes that tainted 
fish carry the infection, although leper bacilli have never been found in them. 
This idea of fish serving as the medium for the infection of leprosy is not a 
new one. They have been suspected in all ages, and it is true that leprosy 
occurs chiefly in countries where fish forms a staple article of food, and where 
a large proportion of the inhabitants are engaged in fishing. There is noth- 
ing inherently improbable in the theory that fish may carry the infection, 
or that a fish diet may represent a common additional factor in the develop- 
ment of the disease. As against this theory, Hansen maintains that it is 
necessary to demonstrate the bacilli in fish. He states that the people of 
Norway are using more fish than ever at present, but nevertheless leprosy 
is constantly decreasing. 

Morbid Anatomy. — In tuberculous leprosy the lesions consist in granulo- 
matous growths or diffuse infiltration of the skin and mucous membrane. 
The granulomatous growths are built up of small round and fusiform cells 
and large vacuolated cells, called by Virchow leprosy cells. These cells 
are probably of endothelial origin and are packed full of bacilli. They 
frequently develop into giant cells. The bloodvessels are increased. In 
diffuse leprous infiltration the same histological elements are observed. The 
new-growth invades the bloodvessels, hair follicles, and sweat glands. The 
bacilli are found everywhere, but in greatest numbers in the giant and 
leprosy cells. 

In the macular lesions there is a larger proportion of connective tissue, 
the bacilli are fewer, and none of the large types of cells are seen. In the 
anaesthetic type, diffuse or nodular infiltrations are found in the nerve 
trunks. The nerves are firmer than normal and darker in color. The 
interstitial connective tissue is markedly increased and the axis cylinders 
are atrophied. 

Leprous nodules and infiltrations are found in the liver, spleen, testicle, 
intestines, and kidneys. In the bones osteomyelitis, necrosis, and atrophy 
are observed, the bone being replaced in many instances of leprous mutila- 
tions by connective tissue. In the larger joints changes occasionally are 
observed that are very similar to the trophic joint changes of tabes. 

Symptoms and Clinical Forms. — Leprosy shows itself under an extreme 
variety of forms. Its beginning is very insidious and at first the progress 
is very slow. Even after a number of years the lesions may be very insig- 



348 DISEASES DUE TO A SPECIFIC INFECTION 

nificant and not at all conclusive to the casual observer. The incubation 
period is uncertain, and is usually accepted as very long. The average 
incubation is assumed to be between two and three years, although cases 
are reported in which it is supposed to have lasted from ten to twenty-seven 
years; these prolonged instances must be viewed with suspicion as to their 
accuracy. In many other cases periods as brief as from three or four weeks 
to three or four months are given. It will be recalled that the incubation 
of the Hawaiian inoculation case was four weeks. 

Another disputed point in the symptomatology of leprosy is the existence 
of the primary sore or the leprous chancre, as it has been called. It has 
been shown that all evidence points to direct inoculation as the source of 
leprosy, and it is not unreasonable to assume a primary sore at the point 
of inoculation of the germ. Many observers hold that such a sore does 
occur, and that in a large majority of cases it is located on the nasal septum. 
Thus, Stickler was able to demonstrate ulceration of the septum in 128 
out of 153 early cases. 

Leprosy begins with marked prodromata, of which fever is the most 
common. It comes in crises of several days' duration and is usually mistaken 
for malaria. It is entirely analogous to the pre-eruptive fever of syphilis. 
Head and joint pains are common as well as general malaise, with frequent 
drenching and exhausting sweats unassociated with fever. Epistaxis is a 
common and early symptom and corroborates Stickler's observation of the 
existence of a primary ulcer in the nose. After lasting from a few months 
to two years, an unusually severe attack of fever ushers in the primary 
eruption or macular stage of leprosy. 

Macular eruptions consist in erythematous patches, smooth, shiny, and 
slightly elevated. They occur all over the body, but are more profuse on 
the face, the backs of the hands, and forearm. The supraorbital ridges 
and malar prominences are commonly affected. The hairy scalp is not 
invaded. The patches come and go, although the later crops show a tendency 
to persist and for the skin to become slightly thickened. When the macules 
invade the hairy portion of the body, the hair is lost or becomes white and 
downy. The macules are anaesthetic, particularly in the centre of the 
patches. 

Next follows the stage of development of the leprous nodules or the 
deposit of specific leprous infiltration. Here the disease may be broadly 
divided into three clinical types: first, tuberculous or nodular leprosy, in 
which the skin and mucous membrane are invaded by the specific new- 
growth; second, the anaesthetic or nerve leprosy, where the leprous deposits 
take place in the nerve trunk; third, the mixed type of leprosy, which 
combines both of the foregoing and to which class all cases ultimately tend. 

Tuberculous or nodular leprosy may begin with or without the mac- 
ular stage. The leprous nodules appear under the skin, particularly about 
the face and ears; the nodules are palpable as distinct, tough, flattened masses 
under the skin. They have a peculiar, rubbery consistence, are painless, 
and freely movable. Diffuse infiltration of the skin takes place, and large, 
flat, leprous patches are formed. The leprous lesions grow steadily larger, 
until on the face large folds and masses of tissue are formed, producing the 



LEPROSY 349 

condition known as Leontiasis, or the lion-like face of leprosy. New nodules 
appear and other portions of the body are invaded until practically the 
leprous lesions cover the entire skin surface. In the early stages the nodules 
occasionally diminish in size or may be entirely absorbed. Later they 
break down and extensive ulceration occurs. At this stage the mucous 
membrane becomes extensively involved. The cartilaginous structures of 
the nose are completely lost, and leprous ulcerations of the larynx occur, 
with loss of voice and ultimately cicatricial stenosis, which may cause intense 
dyspnoea. Extension of the leprous ulceration into the corneal structures 
may cause blindness. The ulcerations produce horrible and characteristic 
deformity. 

Death takes place from exhaustion or intercurrent infection. 

Anaesthetic Leprosy. — Ansesthetic leprosy shows a very different picture 
from the foregoing. The macular stage continues and is marked by increased 
pigmentation and complete ancesthesia of the macule. Gradually extensive 
neuritis is developed in the trunks of various nerves, causing pain, severe 
and neuralgic in character, and later large areas of anaesthesia or numbness. 
The superficial nerve trunks, the posterior auricular, and the ulnar where 
it winds about the internal condyle, are palpably thickened. Bullous erup- 
tions occur on the hands, feet, and elbows, and along the course of the 
nerves breaking down and leaving extensive spreading and destructive trophic 
ulcers. As a further result of these trophic disturbances extensive con- 
tractures develop, and fingers and toes slough away. In the older cases the 
areas in the distribution of the affected nerves, which at the beginning of 
the disease were painful or numb, become completely ansesthetic and the 
muscles become extensively atrophied. When this condition occurs in the 
hand, a typical claw-like hand of leprosy is produced. The atrophied skin 
is particularly prone to injuries and to extensive ulceration. The course 
of this type of leprosy is excessively chronic. 

The mixed leprosy presents a combination of the features of tuberculous 
and ansesthetic leprosy. In all cases of extensive tuberculous leprosy the 
nerve trunks eventually become involved, and the evidences of neuritis and 
trophic disturbances are added to the clinical picture. 

Diagnosis. — In advanced cases leprosy could hardly be mistaken for any 
other disease. The lesions are too striking and distinctive. Difficulties in 
diagnosis arise in early undeveloped cases, particularly in the macular and 
ansesthetic types. Here, as Manson says, the touchstone of diagnosis is the 
ansesthesia. It should be sought for in the centre of macular areas, and in the 
centre of recent nodules, if any exist. Advantage may also be taken of 
the fact that leprous areas do not perspire. Baelz uses an ingenious plan not 
only for diagnosis, but also for mapping out the involved areas. Aniline 
is rubbed on the skin and pilocarpine is administered hypodermically. The 
leprous areas do not sweat and consequently remain unstained. 

The most satisfactory diagnosis consists in identification of the bacilli. For 
this purpose a leprous nodule may be clamped, punctured with a needle, 
and the exuding drop of fluid properly stained and examined. Even in the 
very earliest cases, long before other symptoms appear, leprous thickening 
can be demonstrated in the ulnar or posterior auricular nerves. In doubtful 



350 DISEASES DUE TO A SPECIFIC INFECTION 

cases the minute fragment of one of these nerves should be excised and 
stained for the bacilli. 

Morrow calls attention to the fact that leprosy and nasal catarrh go hand 
in hand, and that in the large proportion of cases bacilli can be demon- 
strated in the nasal secretion. It has also been shown that where nasal 
secretion is scanty a few doses of potassium iodide will cause a sharp 
catarrhal flow, in which the bacilli may be demonstrated. 

Prognosis. — In the vast majority of cases leprosy slowly tends to a fatal 
ending from exhaustion or intercurrent infection. Isolated cases, however, 
occur in which the disease is arrested or cured. These instances of arrest 
are more common in anaesthetic leprosy than in the tuberculous type. Many 
of these cases survive twenty or thirty years, and in a large proportion of 
these the specific process is probably ended, although the extensive damage 
by nerve involvement and trophic lesions remain. Even tuberculous leprosy 
has been known to disappear. 

Many cases are arrested, and, after a long period of years, death occurs 
from some other disease not associated with the leprosy. These reported 
cures must, however, be accepted with extreme caution. It is probably 
more fair to speak of them as arrests. Mention must also be made of 
the marked amelioration that occasionally follows the removal of a leper 
from the country in which he has developed the disease. 

Treatment. — The treatment of leprosy comprises careful attention to 
cleanliness, provision of good hygienic surroundings, abundance of nourish- 
ing food, proper clothing, hygienic dwellings, and light occupation. As 
special remedies gurgun oil and chaulmoogra oil have been extensively 
used, The former has been abandoned. Chaulmoogra oil (oleum gyno- 
cardii) may be administered by the mouth in doses of 2 drachms, or by the 
rectum, in an emulsion with hot milk, when it is badly borne by the stomach. 
In some cases this drug seems to have almost a specific action. In a few 
cases apparent cures and in a great many cases very marked improvement 
is observed. The oil may also be administered hypodermically. 

Unna advises the internal use of massive doses of ichthyol combined with 
inunction of pyrogallic and chrysophanic acid externally. The treatment 
is supplemented by hot baths. Several cures have been reported following 
this plan. Crocker reports improvement from subcutaneous injection of the 
bichloride of mercury, and De Luca from intravenous injections of mercury 
according to Bacelli's method. Raynaud reports marked improvement fol- 
lowing the administration of sodium cacodylate. Roussel reports an apparent 
cure following the administration of potassium chlorate, and Manson a case 
of nerve leprosy apparently cured by thyroidin. Tuberculin, antivenene, 
and the iodides have been used and do more harm than good. Danielsen 
recommends salicylate of soda in ascending doses combined with tonics. 
He believes that it cures leprosy if administered early. Baelz uses salicylic 
acid locally. He treats about one square foot of skin at a time by rubbing 
the diseased area with pummice stone until blood appears. Salicylic acid 
is then applied in a 20 per cent, ointment with lanolin and vaselin. This 
treatment is combined with the oil of gynocardium internally and hot 
baths. 



FEBRICULA 351 

Nerve stretching has been recommended and practised for the relief of the 
painful complications and trophic disturbances of nerve leprosy. 

Prophylaxis. — The only means of limiting leprosy is by isolation. While 
absolute segregation is the ideal and proper measure, it meets with so 
much opposition, and so many cases are concealed, that in the long run a 
better purpose is served by adopting a reasonable compromise similar to 
that followed in Norway. This includes caring for indigent lepers in an 
asylum and allowing those whose people are able to take care of them to 
do so at their homes under proper restrictions. The Russian laws only 
isolate the tuberculous and mixed cases. Although it is true that the nerve 
cases are much, less contagious, this regulation must be regarded as a 
mistake. 

FEBRICULA. 

Definition. — Febricula, sometimes called ephemeral fever, is a condition 
usually met with in children, and is undoubtedly a disturbance of the heat 
mechanism of the body produced by the action not of one but of several 
agents; that is to say, many different causes are responsible for it rather 
than one specific cause. 

Etiology. — The causes of febricula are very numerous. In some instances 
it is probably the result of some infection which is overcome by the pro- 
tective process of the body before it can develop into a full-fledged disease, 
such, for example, as an aborted influenza, or even one of the specific 
eruptive fevers, or some infection entering by the tonsils. Some years ago 
physicians believed that infectious diseases could be aborted in their early 
stages by proper measures designed to aid nature. This view fell into 
disrepute, but our knowledge of protective processes and of antitoxic bodies 
makes it probably true. In children an ephemeral fever is often due to 
gastrointestinal catarrh. Sometimes it is due to gastrointestinal intox- 
ication. 

Symptoms. — The patient after a feeling of wretchedness, rarely lasting 
more than a few hours, is found to be mildly febrile, the temperature being 
about 102° to 103° at the most. There may be -flushing of the face and 
even delirium in young neurotic children. The pulse and respirations are 
quickened. The fever usually, but not always, ends by lysis in about three 
days to a week. 

Diagnosis. — The diagnosis of febricula is made in most instances after the 
patient is well, for until then no one can tell that the symptoms are not the 
early signs of one of the acute infectious fevers. The important point is, 
not to be content with a diagnosis of febricula, which is but another way 
of saying that the condition is uncertain, but to search carefully for the 
real cause. 

Treatment. — This consists in rest in bed, the use of a little calomel followed 
by a saline, and the employment of a mixture of citrate of potassium and 
sweet spirit of nitre to keep the kidneys active. 



352 DISEASES DUE TO A SPECIFIC INFECTION 



MILK SICKNESS. 

Definition. — Milk sickness is a disease which is usually communicated to 
man by the milk, or by the butter or cheese made from the milk of cows 
ill of a malady called, when it affects cattle, "trembles," or "slows." 
When man is infected it is given this name and the additional one of " puking 
fever." The malady is one which exists in the Southwestern United States, 
and apparently does not affect animals on the Atlantic seaboard. It is said 
that the flesh of affected animals, if not cooked, may convey the infection. 
It is important to know that the infection may be transmitted from a 
seemingly healthy cow some time before it develops symptoms of the 
disease. 

Symptoms. — The symptoms in the cow consist in refusal to eat, redness 
of the conjunctiva, staggering gait, and muscular tremors, whence the name 
"trembles." In man, after a day or two of ill-health, the patient is seized 
with epigastric distress, followed by vomiting and constipation, fever, and 
thirst. Muscular tremors also appear. The breath is peculiarly foul and 
offensive and the tongue swollen. If the disease is severe the patient may 
develop typhoid symptoms, and even become delirious, comatose, or con- 
vulsed. In fatal cases death may come as early as the fourth day, or be 
deferred for two or three weeks. The more severe the cerebral symptoms, 
the more grave the prognosis. 

Treatment. — The treatment is purely symptomatic and consists in the 
use of stimulants or sedatives as they may be needed. 

WEIL'S DISEASE. 

Weil's disease is a very rare infectious malady, first described by Weil 
in 1886, which for some unknown reason seems particularly prone to attack 
butchers. It is characterized by the development of fever and acute jaundice, 
and appears usually in the warm months of the year. The victims of its 
onset are usually young and middle-aged adults, and the symptoms are 
severe headache, lumbar pain, and cramp-like sensations in the legs and 
arms. The masseter muscles also suffer from severe pains. Jaundice 
develops as an early symptom, and the liver and spleen are found swollen 
and tender on deep palpation. The stools may be putty-colored, as if from 
obstruction of the gall-ducts. The fever may last two weeks, often rises 
to 103° or 104°, and is characterized by sharp remissions, as in sepsis. 
Albuminuria may occur, and even coma may develop. Recovery usually 
takes place, but convalescence is slow. 

Weil's disease must be separated from bilious remittent fever, catarrhal 
jaundice, and phosphorus poisoning. This separation is readily accom- 
plished if the characteristic symptoms just described are compared to those 
presented in the course of these conditions. Remittent fever, which is the 
malady most closely resembling Weil's disease, is differentiated by finding 
the sestivo-autumnal parasite in the blood, and phosphorus poisoning 
by the history of the case and the phosphorescent character of the vomit, 



GLANDULAR FEVER 353 

which can be noted if it is examined in the dark. Treatment is entirely 
symptomatic. 

GLANDULAR FEVER. 

Definition. — Glandular fever is an acute infectious disease characterized 
by a moderate febrile movement and a painful enlargement of the cervical 
lymphatic glands. 

History. — The first accurate account of this disease was published in 1889 
by Pfeiffer, although it is probable that the condition described some years 
before by Filatow, of Moscow, under the name of idiopathic inflammation 
of the cervical glands, was in reality glandular fever. 

Cases have been reported from different countries on the Continent, and 
from England and the United States. J. Park West, of Bellaire, Ohio, has 
reported an epidemic in which ninety-six children were attacked, this being 
the most extensive epidemic on record. 

Etiology. — The specific micro-organism of this disease, if there be one, 
has not been discovered, but that the disease is infectious in nature is shown 
by the fact of its occurrence, as a rule, in small epidemics involving several 
members of a family. The disease generally occurs before puberty, although 
Galvagni and A. E. Roussel have observed it in adults. 

Symptoms. — The onset is sudden and is characterized by moderately high 
fever, restlessness, headache, pain in the limbs, and soreness and pain in 
the neck, which is increased by turning the head or by swallowing. The 
temperature ranges from 101° to 103° and may even go as high as 104°. 
The bowels are usually constipated, although in some of the severe cases 
observed by West copious discharges of thin, green feces mixed with mucus 
took place shortly before the beginning of convalescence. Abdominal pain 
is a common symptom, and pressure over the lower part of the abdomen, 
particularly in the midline between the umbilicus and the symphysis pubis, 
often elicits pronounced tenderness. The swelling of the anterior cervical 
glands, which usually begins on the left side and then extends to the right, 
attains its maximum between the second and fourth days. The glands are 
hard, easily distinguishable from one another by palpation, and are very 
sensitive to pressure. Suppuration rarely occurs. Examination of the 
pharynx reveals either a normal condition or a slight hyperemia. The 
liver is always enlarged, and not uncommonly there is considerable swelling 
of the spleen. Acute nephritis is the most frequent and most serious compli- 
cation. The duration of glandular fever is variable. European physicians 
have described a mild or abortive form in which the temperature falls to 
normal on the second or third day, although the cervical glands remain 
swollen several days longer. The average febrile period, however, is from 
seven to ten days. In West's ninety-six cases the average duration of the 
disease from its onset until the complete disappearance of glandular swelling 
was sixteen days. 

Diagnosis. — The occurrence of a sudden febrile attack accompanied by 
an early, painful enlargement of the anterior cervical lymph glands, without 
any inflammatory involvement of the pharynx, makes recognition of the 
disease easy. 
23 



354 DISEASES DUE TO A SPECIFIC INFECTION 

Prognosis. — Prognosis is always favorable. Convalescence is rapid, as a 
rule, although in some instances it is retarded by a considerable degree of 
depression and anaemia. 

Treatment. — Experience has demonstrated that there is no drug which 
will influence the duration or course of this disease. The patient should 
be confined to bed and a mild aperient given to overcome constipation 



MOUNTAIN FEVER. 

So-called mountain fever really does not exist as a separate entity. It 
has been proved to be an aberrant form of typhoid fever infection in a 
number of instances, particularly by the United States Army surgeons or 
those attached to the United States Health and Marine Hospital Service. 
In some cases the infection may be paratyphoid. (See Paratyphoid Fever.) 
In still other instances the fever may be due to an anaemia depending upon 
intestinal parasites such as the Anchylostomum duodenale. Some cases 
may be "tick fever." (See below.) 



TICK FEVER. 

Definition. — Under the name of "tick" or "spotted fever," a febrile 
malady has been carefully described within the last few years. It is 
prevalent in Western Montana, particularly among the eastern foothills of 
the Bitter Root Mountains. Curiously enough, it is chiefly limited to the 
western side of the Bitter Root Valley, in an area from four to ten miles wide 
and fifty miles long. Fewer and milder cases occur in Idaho, Wyoming, 
Nevada, and Oregon, at a level of from 3000 to 4000 feet. Its occurrence 
is limited to the period of from the middle of March until the middle of 
July. Herders and ranchmen are usually the persons affected. 

This form of so-called spotted fever is not to be confused with cerebro- 
spinal meningitis. 

Etiology. — According to the studies of Wilson and Chowning, and of 
Anderson, this disease is due to a parasite which is conveyed to man by 
the bite of the tick. To this parasite they gave the name Pyroplasma 
hominis, and therefore suggested that tick fever be called pyroplasmosis 
hominis. According to these observers this parasite in its smallest form 
slightly resembles the small hyaline bodies of malarial fever, but it is at 
no time pigmented. Stained with Laveran's or Nocard's stain chromatin 
masses are seen, as a rule, near one end of the parasite. It appears free 
in the blood or in the body of a red corpuscle. Often two parasites are 
present in one blood cell, but rarely more than this. They may be joined 
together by their lesser extremities, either when in the corpuscle or when 
floating free in the blood. Sometimes the so-called parasite seems to change 
its position in a blood cell, but no amoeboid movement has been seen. 

In the second phase of its development the organism in the red blood 
corpuscle appears to be solitary and distinctly larger than in the first phase 



TICK FEVER 355 

just described. During this stage of its development they claim that it also 
presents active amoeboid movements. 

The red cells of the general circulation are not infected in great numbers, 
but if the blood in the capillaries of congested tissues is examined, it is 
found that a large number of the red cells have become infected. The 
greatest degree of corpuscular infection is said to be met with in the spleen, 
liver, lungs, and kidneys. 

Since these observations of Wilson and Chowning, Stiles and Craig 
claim to have proved the non-existence of these so-called parasites, the 
former asserting his inability to discover any structures which lead him 
to a belief in the presence of a protozoon as a cause of the malady. Craig 
believes that the changes seen by Anderson in the red blood cells are not 
due to a parasite, but dependent upon certain alterations chiefly taking 
place in the haemoglobin, such as are often seen during the course of 
epidemic influenza, typhoid fever, measles, variola, and other acute infec- 
tions. The cause of this disease, if indeed it ultimately proves to be a 
separate entity, is, therefore, at present of uncertain character, the more 
so as there is reason to believe that the Pyroplasma bigeminum, which is 
the organism of Texas cattle fever, is incapable of infecting man. 

Symptoms. — The disease makes its appearance in from three to ten days 
after the bite, with chilly sensations, malaise, nausea, headache, and muscular 
soreness. The bowels are constipated, the conjunctiva congested, the urine 
scanty and albuminous, and slight bronchitis occurs. Episiaxis is a constant 
symptom. The fever rises sharply after the chill, but has morning remissions 
like typhoid fever. The rapidity of the pulse is out of proportion to the 
fever, often amounting to 110 or 140 per minute, and there \s a very moderate 
leukocytosis. Respiration is rapid. 

Its acme is reached by the twelfth day, when it gradually falls by lysis for 
four days more, and so convalescence begins. In fatal cases the fever remains 
high, about 104° or 105°, or even 106°. The pulse is usually very rapid and 
thready, and the blood rapidly becomes anaemic. 

The rash usually develops about the third day on the wrists, arms, legs, 
and forehead, and later on the back, chest, and abdomen. This rash, 
except on the abdomen, is often exceedingly profuse. 

The skin presents an eruption of bright-red macules, varying from a 
pinhead to a split pea in size, and in severe cases they become petechial in 
character. They fade as the fever falls, and the skin may desquamate. 
Sometimes in the later stage of the eruption they appear like the marks on 
a turkey's egg. Anderson states that slight gangrene of the fingers, toes, 
and scrotum may occur. Albuminuria is a constant symptom. 

Diagnosis. — The section of the country in which the disease occurs, the 
history of tick bites, and the finding of the changes in the blood are the 
factors which make the diagnosis positive. From ordinary purpura the dis- 
ease is separated by the lack of sore throat and the absence of arthritis. 
From typhoid fever the diagnosis may be quite difficult. In that disease, 
however, the rose rash appears first on the belly on the ninth to the twelfth 
day, whereas in tick fever it appears as early as the third day, and on the 
wrists. The discovery of a positive Widal test in the blood will settle the 



356 DISEASES DUE TO A SPECIFIC INFECTION 

diagnosis. Typhus fever is conveyed from man to man; tick fever is not 
directly transferred. Typhus fever breaks out in groups of persons. Tick 
fever always appears sporadically. 

Prognosis. — The disease is a very grave one, for out of 126 cases 88 died, 
a mortality of about 70 per cent. Sometimes the mortality is as high as 
90 per cent. Death usually ensues about the sixth to the twelfth day of 
the illness, but it may occur as early as the fourth day. Experience with 
cases which have occurred in Idaho, Wyoming, and Nevada shows that 
the mortality is far less in those States than in Montana. 

Treatment. — So far as is known quinine seems to act as a specific in this 
disease. Anderson thinks it should be given in the dose of 15 grains every 
six hours, hypodermically, and its use continued into convalescence. The 
heart must be supported by stimulants if it is feeble, and the kidneys flushed 
by copious draughts of water. The tick, if found, should be removed from 
the skin and the part cauterized with 95 per cent, carbolic acid to prevent 
infection, if possible. 



FOOT-AND-MOUTH DISEASE. 

Definition. — This is an acute infectious disease of herbivorous animals, 
which sometimes attacks omnivora and which spreads in epidemic form 
over large territories, causing great mortality in the animals affected. When 
the disease attacks the cow the animal becomes feverish, suffers from swell- 
ing of the mucous membranes of the mouth, and develops blisters on the 
edges of the tongue and on the lips. These blisters become discolored and 
rupture, leaving ulcers. At times similar lesions appear on the teats. The 
milk of such animals is discolored and seems to be thickened as if by mucus. 

The disease is rarely met with in England and America, and only possesses 
interest to us, because it is capable of being conveyed to man. This convey- 
ance occurs in the case of children by the use of the milk of the diseased cows, 
and in adults, as a rule, by this means or by cheese or butter. 

The symptoms in man are like those of severe stomatitis, associated with 
fever. Recovery in man usually occurs, but a mortality of about 10 per cent, 
is recorded. 

The cause of the disease has not been isolated. Even a porcelain filter 
does not arrest the organism, if organism it be, that causes the malady. 



MILIARY FEVER. 

Definition. — Miliary fever, sometimes called "the sweating sickness," is 
an acute epidemic disease characterized by fever, profuse sweating, an erup- 
tion, and a peculiar sense of constriction in the epigastrium. 

History. — The disease was far more prevalent in the seventeenth century 
than it has been since that time, but it still appears in certain parts of the 
world. Almost every country in Europe, including England, has suffered 
from its presence, but it has not, so far as I have been able to discover, ever 



JAPANESE RIVER FEVER 357 

appeared in the United States. The most recent epidemics have been in 
Austria in 1892 and in Styria in 1S93. 

Etiology. — The cause of the disease is unknown, but it is an acute infection, 
apparently resembling influenza in the manner of its spread, although it 
does not, as a rule, attack large numbers of people throughout a wide area, 
as does that disease. On the contrary, it is very often limited to the popula- 
tion of a single town or district. 

Symptoms. — The symptoms of miliary fever are ushered in, as they are in 
all the infectious diseases, by lassitude, headache, and anorexia. This pro- 
dromal stage may last a day or two or be so brief as not to be recognized. 
The patients go to bed well, and wake in the morning to find themselves 
ill and suffering from a drenching sweat, which persists throughout the 
illness. The bowels are usually confined, the tongue coated, and the pulse 
but little altered in character for the first few days of the illness. A symptom 
complained of by the patient is one of oppression, as if the air of the room 
were hot and vitiated. The fever is usually high, rising to 104° to 105°, and 
in fatal cases to 107°. On the third day there appears on the skin an out- 
break of red miliary papules, which often develop a white tip before they 
disappear, and between these are scattered large numbers of pearly vesicles, 
like sudamina, which seem filled with clear fluid. Prior to the appearance 
of this eruption a peculiar pricking or tingling sensation is felt in the skin. 
When the eruption has faded, desquamation sometimes occurs. The entire 
progress of the malady is usually completed in nine or ten days. 

The following facts are also noteworthy, viz. : The sweating is constant, 
but is characterized by paroxysms, in which it becomes still more profuse. 
The rash appears on the mucous membrane of the palate and cheeks. The 
sudamina, or pearly miliary vesicles, although they give the name to the dis- 
ease, are not a constant symptom in all cases. 

Abortion nearly always occurs if a pregnant woman is attacked. 

Miliary fever causes rapid emaciation. 

It is very prone to be followed by a relapse, but the relapse is rarely fatal. 

Prognosis. — Recovery usually occurs. In severe cases, in which the onset 
is fulminating, death may occur as early as the eighth hour after the attack 
begins. These cases have marked nervous symptoms, consisting of convul- 
sions, delirium, and coma. Evidently the patient is overwhelmed by tox- 
aemia. The mortality rate in various epidemics has varied from 5 to 25 per 
cent. The outlook in children is usually good. 

Treatment. — This consists of cold sponging to control excessive fever, the 
use of copious draughts of water to compensate for the loss of water by the 
skin, and for the purpose of flushing the kidneys, and in the administration 
of stimulants, if they are needed, to support the heart. 



JAPANESE RIVER FEVER. 

Definition. — Japanese river, or flood fever, is an acute, infectious disease, 
occurring in a very limited area in the island of Nippon, beginning with a 
necrotic ulcer, attended by an exanthem and continued fever. 



358 DISEASES DUE TO A SPECIFIC INFECTION 

The disease occurs in laborers who cultivate the inundated bottom lands 
of several rivers on the west coast of the island of Nippon. 

Etiology. — The etiology is obscure. The infection is evidently carried in 
the corn and hemp grown in these sections, and the primary eschar probably 
marks its point of entrance. The Japanese ascribe the disease to the bite of 
a small acarus. Baelz denies this. Given equal exposure, neither age nor 
sex shows any difference in susceptibility to the disease. 

Symptoms.— After several days of malaise and repeated rigors, the disease 
begins with the breaking out of a small, round eschar in the groin, axilla, 
or neck. The neighboring lymphatic trunks and glands become swollen, 
hard, and painful. A continued fever ranging between 103° and 104° 
develops, with bronchial cough and marked conjunctivitis. About the sixth 
day a coarse, red, papular eruption appears on the face, forearms, legs, and 
trunk. This eruption fades away in from one to seven days. The fever 
lasts a week longer, when it falls rather rapidly, and convalescence begins 
with a separation of the eschar from the primary sore. The mortality varies 
between 15 and 70 per cent, in different epidemics. No definite postmortem 
changes are found, beyond congestion of the bronchi, occasional hypostatic 
pneumonia, marked enlargement of the spleen, and swelling of the mesen- 
teric glands. 

Treatment. — Treatment is symptomatic. Baelz advises quinine and sali- 
cylates as antipyretics to be used with caution. 



FRAMBESIA (FRAMBCESIA TROPICA, YAWS). 

Definition. — Frambesia, or yaws, is a chronic contagious and infectious 
disease, characterized by the appearance of a diffuse granulomatous erup- 
tion on the skin. 

History. — The history of yaws begins with the historians of the Spanish 
conquest of America. It is a disease very closely confined to tropical coun- 
tries and very widely distributed in Africa, in the coast countries of trop- 
ical Asia, and in many of the Pacific islands. It also occurs in Central and 
tropical South America and the Antilles. The disease was exceedingly com- 
mon in Cuba and the southern United States during the first half of the 
nineteenth century, having been brought there during the slave-trading days. 
At one time it caused such a degree of disability among the negroes that the 
planters were forced to adopt stringent rules for its limitation. Most of the 
large plantations maintained isolation barracks, or "yaw houses, " for these 
cases. The disease still lingers in Cuba and the rest of the Antilles. It has 
all but disappeared from the United States. 

Etiology. — Many bacterial forms have been isolated from yaw lesions, but 
as yet the specific cause has not been determined. The disease can be, and 
frequently is, conveyed by direct inoculation, intentional or accidental. Such 
inoculation may take place in wounds, abrasions, and other injuries of the 
skin. In some yaw countries, notably in Fiji, it is a common practice for 
mothers to inoculate their children, under the same idea which prevails 
among our lower classes, who frequently expose their children to pertussis and 



I'RAMHUSIA 359 

eruptive diseases, on the theory that the illness must be gone through with 
some time, and the earlier the better. Heredity has no bearing on the etiology 
of yaws. Neither does a pregnant or nursing woman with yaws necessarily 
infect her child. Outside of direct inoculation the disease is conveyed by 
food, particularly by cooking utensils. In persons particularly susceptible, 
infection may take place by sleeping in a yaw house. All ages are attacked, 
but the majority of cases are seen in children. The black, yellow, and white 
races are susceptible in the order named. As a rule, one attack confers com- 
plete immunity. Frambesia is also seen in domestic fowls. 

Symptoms. — The incubation period of yaws is very variable. Generally 
speaking, in inoculation cases, it varies between fifteen and twenty days. In 
cases ordinarily acquired, the incubation is longer, ranging from fourteen to 
sixty days. In a small proportion of cases prodromal symptoms, languor, 
malaise, headache, and rheumatic fains are observed. This condition is 
followed by what is known as the primary eruption or the primary sore, con- 
cerning which there is some dispute among tropical practitioners. In experi- 
mental inoculation cases the primary sore is constant and occurs at the point 
of inoculation. It begins as a small papule, which, in the course of a w r eek, 
is converted into a shallow ulcer. In another week the ulcer heals, leaving a 
slight, thickened scar. In ordinary infection by yaws it is sometimes present 
and sometimes absent. 

The generalized eruption, the so-called secondary eruption, begins with 
the primary sore in exceptional cases, but, as a rule, is delayed for several 
weeks. Occasionally, in the period between the eruption of the primary and 
secondary lesions, a dry, scaly affection of the skin is seen. 

The secondary eruption begins as small papules, which itch intensely. They 
are scattered all over the body, but are most commonly seen, in order, on 
the face, neck, limbs, genitals, and trunk. The hairy scalp is not commonly 
invaded; the axilla very rarely. The lesions are particularly numerous at 
the mucocutaneous borders, the mouth, nose, anus, and vulva. The erup- 
tion is roughly symmetrical. The papules, at first the size of a pinhead and 
slightly prominent under the skin, gradually increase in size till they are as 
large as a pea or a hazelnut. Small, yellow spots of pustulation appear on 
the summit of the lesions; the skin cracks; a sticky, yellow, seropurulent fluid 
exudes, which hardens and forms rupia-like crusts or caps over the summit 
of the growths. The cap is tough and adherent. When it is pulled off it 
reveals a shiny, red papilloma underneath. This warty growth, the true 
yaw, resembles a berry in appearance, hence the name yaw, i.e., a straw T - 
berry; frambesia trom framboise, a raspberry. Indeed, most of the local 
native names for the disease are words which mean berry in their dialect. 

The growths resemble syphilitic condylomata in their appearance. They 
spring from the papillary layer of the skin, and the warty-like lobulations 
represent the greatly hypertrophied papillae. The uncovered yaw freely 
exudes the sticky, yellow pus, already mentioned, and in a little w r hile the cap 
is reproduced. As a rule, the lesions are painless, excepting where they occur 
under thick, dense skin, as in the palms and the soles, where tension may 
cause great pain. Itching is, however, very persistent and annoying. After 
persisting weeks and months, sometimes passing through recrudescences and 



360 DISEASES DUE TO A SPECIFIC INFECTION 

successive crops, the lesions gradually grow smaller, the papillomata dis- 
appear, and a dry eschar is left, which falls off, leaving a patch of thickened 
skin, bleached in the negro and pigmented in the light-skinned races. 

In old, long-standing, and neglected cases, severe bone and joint pains 
develop, and occasionally extensive periostitis and caries occur. These are 
the so-called tertiary lesions of frambesia. They are not constant; indeed, 
they never appear in properly treated cases. 

Diagnosis. — There are only two diseases with which typical yaws can be 
confused, syphilis and verruga. Hutchinson believes yaws and syphilis, if 
not the same disease, are descendents of the same parent stock; that originally 
they were identical and have become differentiated by thriving for long 
periods on different soils. Yaws undoubtedly suggests syphilis very strongly, 
but there can be no question of the duality of the diseases. Syphilis and 
yaws have frequently been observed in the same individual; syphilitics have 
been successfully inoculated with yaws, and vice versa. Finally, the histolog- 
ical differences are marked. No giant cells are seen in yaws and no thick- 
ened bloodvessels. 

Scheube believes yaws and verruga to be identical, but Glogner has 
recently drawn a careful distinction between the histology of the two 
diseases, and has clearly shown that they are not identical. 

Prognosis. — The prognosis is uniformly good. 

In patients reduced by disease and in infants the prognosis of yaws is 
not so favorable. 

Treatment. — Iodide of potash is the remedy for frambesia. Mercury not 
only does not do these patients good, but actually seems to do them harm. 
Stomatitis occurs with the greatest facility and is very severe. When the 
general condition is low, arsenic, iron, and the bitter tonics are indicated. 
Most tropical practitioners advise local treatment of the lesions. This 
includes antiseptic and stimulating applications and removal of old lesions 
with the curette. The prophylaxis of yaws consists in cleanliness and isola- 
tion of the infected. Great care must be taken of abrasions and cuts, and 
infected dwellings should be avoided. 



VERRUGA (VERRUGA PERUVIANA). 

Definition. Verruga (a w T art) is a chronic, infectious, and inoculable dis- 
ease, characterized by initial fever, rheumatic pains, anaemia, and the devel- 
opment of granulomatous lesions (warts) on the skin, mucous membranes, 
and internal organs. 

Distribution. — Verruga is limited to certain high valleys of Peru, on the 
Pacific slopes of the Andes. At present it is principally observed in the 
valleys of Huarochiri, Tanyos, Rimac, and Canta, at elevations varying 
from 3000 to 8000 feet above the sea. It is not observed at lower levels. 
Cases are also reported from the mountain districts of Ecuador, Bolivia, 
and Chile. The disease has existed since remote times in Peru, possibly in 
wider extension than at present. It occurred among the soldiers of Pizzaro's 
expedition, and is first mentioned by Zarate in his History of Peru (1543). 



VERRUGA 361 

Etiology. — Verruga occurs in small epidemics, but is not contagious. Car- 
rion, a medical student, in 1885, proved its inoculability on himself and died 
of the infection. As a rule, one attack of the disease confers immunity. The 
specific cause of verruga has not been established. The belief is prevalent 
among the population that the waters of certain springs are the cause of the 
disease. Moisture, heat, and elevation above the sea seem to be necessary 
factors. Malaria is apparently closely associated with the development of 
verruga: a particularly pernicious type, locally known as " Oroya Fever," 
being commonly observed with it. All ages and both sexes are equally liable. 
Natives of the verruga zone seem to suffer less severely than strangers com- 
ing to the valley. For a time this disease was believed to be a form of yaws, 
or frambesia, and, like it, was interpreted as a form of syphilis. Yaws, 
however, is not observed in the internal organs. Furthermore, verruga is 
observed in the domestic animals, including fowls, an observation contrary 
to any known manifestation of syphilis. 

Symptoms. — The incubation period is given as ten days to a year. Fifteen 
to forty days (according to Odriozola) seems a more reasonable figure. In 
the inoculation case of Carrion the incubation was twenty-three days. Clin- 
ically, two stages present themselves, the stage of invasion and the stage 
of eruption. The stage of invasion begins with prodromal symptoms. 
Lassitude, restlessness, and weariness of the legs, lasting for a few days, 
are followed by an evening fever. 

The fever gradually increases in severity, with marked rigors, and may 
be remittent or intermittent. In a few days joint pains develop. The joints 
invaded are the smaller articulations of the hands and feet, the knees, and 
the spine. The pain is severe, is worse at night, and is fugitive, passing 
rapidly from one joint to another. Painful contractions of particular muscle 
groups occur, most frequently in the calf-muscles and sternomastoids. Some- 
times large muscle groups are affected, so that in extreme cases opisthotonos 
may develop. As the disease progresses, anaemia and emaciation occur. 
The skin becomes pale and icteric; the liver and spleen become enlarged. 
Soft bruits are heard over the prsecordium. The fever persists from three to 
five weeks, when it gradually declines, and, with its disappearance, begins 
the stage of eruption. The eruption usually develops after twenty days, or 
it may be delayed as long as six or eight weeks. In rare instances it is 
observed at the very beginning of the disease. 

With the breaking out of the eruption, all the general symptoms are 
remarkably ameliorated. Beginning first as small, pinkish papides, the 
lesions become dark blue in color, and finally develop into warty excrescences. 
They appear on the face, particularly around the eyelids and nose, on the 
limbs, about the joints, and rarely on the trunk. The palms, soles, and 
hairy parts of the body are also attacked. In size the lesions vary from a 
millet-seed to growths as large as an apple. They may be few or many 
hundreds in number. These warty growths are exceedingly vascular and 
bleed freely, thus increasing the anaemia of the patient. When they develop 
on the mucous membranes and internal organs, dysphagia becomes a very 
common symptom, and hemorrhages occur from the various organs that are 
the seat of the lesions; haematemesis, haemoptysis, haematuria, metrorrhagia, 



362 DISEASES DUE TO A SPECIFIC INFECTION 

etc. After persisting from four to six months, perhaps passing through 
various recrudescences, the lesions subside by involution and desiccation 
or desquamation, or they may ulcerate, or the larger lesions may suppu- 
rate. 

Prognosis. — The prognosis is always grave, particularly so in white people, 
in whom 60 to 70 per cent, of all cases die. In natives the mortality is about 
10 to 15 per cent. The early and complete establishment of the eruption is 
a very favorable sign. In delayed or partial eruptions the prognosis is grave. 
Excessive anaemia is also an unfavorable sign. 

Treatment. — Treatment is symptomatic. On account of the very general 
association of this disease with malaria, quinine should always be freely 
administered. Sudorifics and hot drinks are usually employed with the idea 
of hastening or completing the eruption. Descent to lower altitudes not only 
diminishes the pain and abbreviates the disease, but also lessens the ten- 
dency to hemorrhages from the lesions. Odriozola recommends the removal 
of all ulcerated verrugas. 

KUBISAGARI. 

This disease occurs endemically in certain districts of northern Japan. 
It is very closely related to the endemic paralytic vertigo of Switzerland 
(Gerlier's disease). Kubisagari manifests itself by attacks characterized 
by dimness of vision, diplopia, and ptosis, associated with marked weakness 
of certain muscle groups. 

With respect to the etiology of the disease, very little is known. Like 
Gerlier's disease, it is observed among people who live under the same roof 
with their cattle. Miura attributes the disease to the effluvium from the 
cattle and notes that the endemic section is also particularly badly infected 
with cattle plague. 

Kubisagari is a disease of all ages and both sexes, and occurs principally 
in the warm months. 

The course of the disease is very chronic. The attacks come on at inter- 
vals of a few hours to several days and last from a few minutes to two to 
three hours. They are brought on by hunger, indigestion, muscular fatigue, 
and eye-strain. Ptosis and diplopia are constant symptoms. Paresis occurs 
in various muscle groups, most commonly in the posterior muscles of the 
neck, the head dropping forward in consequence (hence the name " kubisa- 
gari," i. e., one who hangs his head). Paresis of the muscles of mastication, 
deglutition, and locomotion may render chewing, swallowing, or walking 
difficult or impossible. Between attacks these symptoms all disappear, 
excepting the ptosis and head-hanging, which may be permanent. The 
superficial and deep reflexes are increased. The eye-grounds show conges- 
tion of the optic disk. 

The prognosis is favorable. Kubisagari never tends of itself to a fatal 
issue. 

Treatment. — Bromide of potassium has some effect in controlling the fre- 
quency of the attack. Miura reports the favorable action of the iodides and 
arsenic in some cases. 



DISEASES OF THE RESPIEATOKY SYSTEM 



DISEASES OF THE NOSE. 

ACUTE CORYZA. 

Definition. — Acute coryza is an inflammation of the nasal mucous mem- 
brane, characterized in its early stages by hyperemia, redness, and swelling, 
and followed by free secretion of mucus and serum. 

Etiology. — Without any doubt acute coryza is an infectious malady, 
although it usually follows exposure to cold or wet. The exposure produces 
a condition favorable to the growth of the micro-organisms which cause the 
disease. No single organism has been isolated, and in some cases several 
are probably active at once. Coryza is a conspicuous symptom of certain 
forms of influenza and may be produced by a number of micro-organisms, 
among which the pneumococcus should be mentioned. Hajek claims to 
have isolated an organism called the Diplococcus coryzce, which he believes 
is responsible for the malady. 

The disease can be transmitted from one person to another, probably by 
droplets of infected discharge, the susceptibility of an individual depending 
upon both a local and general lowering of vital resistance. The breathing 
of vitiated air, as in badly ventilated theatres and steam cars, and of dust- 
laden atmospheres, as in certain industries, is a frequent predisposing cause. 
The possibility of a diphtheritic origin in certain cases should not be over- 
looked. Damp cold, even if of moderate degree, is more provocative of the 
disease than dry cold. 

Pathology and Morbid Anatomy. — The pathology of acute coryza is that of 
an ordinary catarrhal inflammatory process affecting a mucous membrane. 
The bloodvessels of the submucosa become hypersemic, congested, and 
engorged, and from them an extravasation of white blood cells and red 
corpuscles takes place, accompanied by a transudation of serum, which 
increases the swelling, and finally escapes upon the surface of the mucous 
membrane, to be thrown off with the desquamated epithelium. The mucous 
glands secrete an excess of mucus laden with dead epithelial cells and leuko- 
cytes or pus corpuscles. As recovery takes place, the inflammatory exudate 
in the submucosa is absorbed, the dead epithelial cells are replaced by young 
cells, and in this manner the process of repair is completed. 

Symptoms. — The symptoms of acute coryza consist in primary chilliness 
and some restlessness and in a sensation of dryness of the nasal mucous mem- 

( 363 ) 



364 DISEASES OF THE NOSE 

brane of the part affected. This is accompanied by a loss of the sense of smell 
and by a dull frontal headache, probably due to congestion in the frontal sinus. 
There is frequently severe sneezing, due to the irritation of the nasal nerves 
by the inflammation and to the trickling of the serum over the angry mucous 
membrane. The voice sounds as if the nose was " stopped up." As the 
disease progresses, large amounts of mucopurulent material are discharged 
from the nostrils and find their way back into the nasopharynx. The consti- 
tutional symptoms are often quite severe, and consist in chilliness and flushes 
of heat, followed by relaxation of the capillaries of the skin and more or less 
perspiration. Aching in the head, in the muscles, and the small of the back 
are prominent symptoms, indicating that the local nasal process is not the 
only part disordered, but that other parts are indirectly affected. Without 
doubt, the two chief causes of these symptoms are the loss of large amounts 
of liquids by the nose, something like 1\ to 2 pints a day in some cases, and 
the absorption of toxic materials due to the infection. 

Diagnosis. — The acute rhinitis due to an oncoming attack of measles, or 
that due to an attack of hay fever, are the two states that most closely resem- 
ble true coryza. In infants the possibility of the attack being due to syphilis, 
" syphilitic snuffles," must be considered. 

Treatment. — The treatment of acute coryza consists, if the patient is seen 
in the stage of onset, of the use of a saline purgative to deplete the system 
and unload the bowels, and in the internal use of full doses, 20 to 30 grains 
every hour for five doses, of bicarbonate of sodium in water. At the same 
time the well-known combination called " rhinitis tablets " may be given. 
These consist of — 

R — Quininae sulph. . gr. j. 

Camphorae . . . . . . . . gr. \. 

Ext. belladonnae gr T \. — M 

Sig. — One or two every thirty minutes till six are taken. 

The nasal mucous membrane should be washed by a gentle spray of 
normal salt solution, followed by a spray of — 

R — Cocainae hydro chloratis . . . . . . gr v 

Chloretone . . . . . . . . gr. ij. 

Aquae destillat. . . . . q. s. ad f^j. — M 

Sig. — Apply as a spray. 

Followed by a spray of — 

R — Antipyrini gr. xv. 

Cocainae hydro chloratis . . . . . . gr. j. 

Aquae camphorae f 3 iij. 

Aquae destillat q. s. ad f^j. — M. 

This, in turn, should be followed by a spray of menthol in the proportion 
of 6 grains to the ounce of liquid albolene. 

In many instances a hot foot-bath and a dose of 5 to 10 grains of Dover's 
powder may be used to abort an attack. 

After the disease is well on its way, it is bound to run its course. We can 



CHRONIC NASAL CATARRH 365 

only give relief by using a type of nasal treatment like that just suggested 
and in cleansing the nasal chambers of mucus. 

When the attack has run its course the consequent debility is best con- 
trolled by the use of fresh air, arsenic, ammonium benzoate, and bitter tonics. 



CHRONIC NASAL CATARRH. 

Definition. — Chronic nasal catarrh, as its name implies, is a chronic inflam- 
matory state of the nasal mucous membranes, frequently due to repeated 
attacks of the acute variety, or occasionally coming on more insidiously. 
When it is well developed the tissues of the nasal chambers are relaxed and 
somewhat cedematous, the secretion is abnormal in character and in quantity, 
and this pathological condition is often subject to acute exacerbations due 
to exposure to the usual causes of coryza. 

Etiology. — The causes of chronic nasal catarrh are, as just stated, repeated 
attacks of acute coryza and continued exposure to the action of irritating 
dust or of cold, moist air, laden with infectious materials. The condition may 
be of syphilitic origin or arise from depleted vitality from constitutional dis- 
orders, such as Bright's disease. Foreign bodies should be searched for, 
particularly if the patient is a child, and nasal growths may be found as a 
cause, although, as a rule, the catarrh causes the formation of growths. 

Pathology. — An examination of the nasal mucous membrane in cases of 
this disease shows that the bloodvessels are distended and have lost their 
normal elasticity. They are unable to drive out any additional blood which 
may be sent to them because of the other parts being chilled. Exudation 
into the connective tissues takes place, and so this structure becomes thickened 
and enlarged. At this stage the condition is sometimes called hypertrophic 
rhinitis. 

Repeated or protracted irritation induces hyperplasia of the connective 
tissue of the submucosa, continued epithelial exfoliation, glandular atrophy, 
and sclerotic changes in all the layers of the mucous membrane. In the 
earlier stages these changes are those already mentioned when discussing 
acute coryza; later cell proliferation and leukocytic accumulation in the 
nasopharyngeal submucosa greatly thicken the membrane, particularly 
over the turbinates and the septum (hypertrophic rhinitis), while organiza- 
tion (fibroid change) increases the fibrous tissue in the areas involved, fol- 
lowed by contraction with atrophy of erectile, glandular, and even nerve 
tissues (atrophic rhinitis) . This lessens secretion, which tends to inspissate, 
form scabs, and decompose, causing the fetid emanations to which the name 
"ozsena" has been given. 

Extension to one or more of the facial sinuses, necrosis of bone, or 
involvement of the Eustachian orifice or tube are possibilities constantly to 
be remembered. 

Symptoms. — The symptoms of this stage of the disease consist in a con- 
stant secretion in excess of nasal mucus, which passes in large part into the 
postnasal and nasopharyngeal spaces. This secretion may be thin and 
liquid or thick and mucopurulent, and is apt to vary in quantity with exposure 



366 DISEASES OF THE NOSE 

to cold or dust. The secretion is so thick that it readily becomes inspissated 
and partly blocks the nasal passages, and, furthermore, becomes loaded with 
bacteria, so that it may be somewhat fetid. 

Treatment. — The treatment consists in maintaining nasal cleanliness by 
an ordinary nasal douche-cup, to be used night and morning, employing in 
it normal salt solution or Dobell's solution warmed to the temperature of the 
body. The physician should also cleanse the parts, when the patient visits 
him, by a mild alkaline wash, and when no acute exacerbation is present the 
hypertrophied mucous membrane over the middle turbinate should be 
cocainized and then lightly touched with a small electrocautery, a piece of 
oiled cotton being placed between the spot cauterized and the nasal septum, 
to prevent adhesions from forming during the period of acute swelling 
which follows the operation. Care should be taken to keep the parts clean 
for several days to prevent infection, if the patient is primarily anaemic or 
debilitated. This treatment should not be resorted to before the general 
health is improved by tonics. 



ATROPHIC NASAL CATARRH. 

Definition. — In this condition the nasal mucous membrane and the under- 
lying tissue undergo atrophy and contraction, with the result that the blood- 
vessels of the part are occluded or destroyed. 

Etiology. — Atrophic nasal catarrh follows the chronic type of ordinary 
nasal catarrh as a late condition. At times it seems to be due to some con- 
genital defect in the shape of the nasal chambers, and in some cases it begins 
to develop as the result of one of the acute infectious diseases. 

Pathology. — The chief change is an atrophy of the cells of the nasal mucous 
membrane and an overgrowth of the submucous connective tissue, which is 
prone to undergo contractile changes. This cuts off blood supply and 
increases the atrophic process. 

Symptoms. — These consist in the formation of scabs, or crusts of thickened, 
tenacious mucus, which are usually infected by many pathogenic germs. 
Some ulceration of the nasal septum may appear, and the patient may com- 
plain of a constant feeling of dryness and irritation, or occlusion of the nasal 
passages. 

The nasopharyngeal mucous membrane is often dry and shiny in appear- 
ance. When the condition is far advanced a state of fetid ozcena develops, 
in which the breath of the patient becomes fetid beyond the power of words 
to describe it. Nothing equals it, except the breath in a case of pulmonary 
gangrene. 

The sense of smell is practically destroyed by the process, and the patient 
is often ignorant of how disagreeable his breath has become. 

Prognosis. — The outlook for a cure of this condition is unfavorable. The 
bad odor can usually be relieved. 

Treatment. — The patient should be told to use a nasal douche-cup with 
warm Dobell's solution twice a day. Kyle recommends 1 drop of ordinary 
poal oil dropped into each nostril after this. The physician should see the 



HA Y FEVER 367 

patient every few days, cleanse the nasal chambers, and apply a 1:2000 
solution of trichloracetic acid on an applicator to the nasal passages, or 
1 : 500 solution of formaldehyde may be used. 



HAY FEVER. 

Definition. — Hay fever is an inflammation of the nasal mucous membrane 
which occurs periodically and usually at a time of the year when certain 
plants are in a certain stage of growth. Associated with the localized inflam- 
mation, there is often present an asthmatic condition, in which a sense of 
oppression is well developed. In other instances true asthmatic attacks 
ensue. Hay fever is often called " autumnal catarrh," " rose cold," " rag- 
weed fever," or " periodic rhinitis." 

Distribution. — The prevalence of hay fever depends largely upon the pres- 
ence in the air of the pollen of certain plants, and in those parts of the country 
where these plants do not grow the disease is unknown. It is more rare in 
England than in America, but much more common in these countries than 
elsewhere, being comparatively rare in France and Germany. Negroes and 
Indians are apparently immune, and the lower classes very frequently escape, 
the disease being chiefly a malady of the so-called upper classes. The dis- 
ease is rare after the fortieth year and affects males oftener than it affects 
females. 

Etiology. — There are two chief factors in the development of hay fever, 
namely, an idiosyncratic state of the patient and the presence of an exciting 
cause in the atmosphere. Much discussion has taken place as to what the 
condition is that renders the patient peculiarly liable to this affection. In 
some cases it seems to be a neurosis of the nasal cavities or a local disease; 
in others it is said to depend upon a "lithsemic state," whatever that may be. 
In every case, however, there is a condition of nasal hyperesthesia which 
renders the nasal mucous membrane extremely sensitive to irritants. Many 
sufferers from hay fever present irregularities in the nasal chambers which 
may aid in predisposing them to attacks of the malady. 

The second cause of hay fever in the great majority of cases is the presence 
in the air of pollen from some plant, chiefly "ragweed." Pollen is not the 
only cause, however, for typical attacks occur in certain persons at seasons 
of the year when no pollen is present, the condition being induced by some 
irritating dust or vapor which in no way influences the ordinary individual. 

Pathology and Morbid Anatomy. — In the state of the nasal mucous mem- 
brane there is nothing peculiar to hay fever, which presents on examination 
the evidences of an acute catarrhal inflammation with swelling and hyper- 
emia of the parts involved. 

Symptoms. — The symptoms of "hay cold" are usually sudden in onset 
and often appear on a certain day which the patient can foretell, and nearly 
always at a definite period in the year, for the reason already given. An 
acute rhinitis develops with irritation of the nasal mucous membrane, and 
the running of salty fluid from the nostrils irritates the nares and the upper 
lip. The conjunctival mucous membrane is irritated and inflamed, and 



368 DISEASES OF THE NOSE 

the eyes are tearful, partly because of this condition and partly because 
the tear ducts to the nose are stopped by the swelling of the mucous mem- 
brane. Photophobia and neuralgic pains in the head are often present 
and add greatly to the patient's misery. Frontal headache is constant and 
severe, and tinnitus and fulness of the head are also annoying symptoms. 
Some deafness may be present. Associated with these symptoms the patient 
often has marked systemic depression and wretchedness with great mental 
depression. 

On examining the mucous membrane of the nose there is found undue 
pallor in long-standing cases which is not to be expected when inflammation 
is present. If a probe is touched to the mucous membrane patches of 
hyperesthesia are discovered, as evidenced by sudden severe sneezing and 
other signs of acute irritation. 

The attack is prone to persist as long as the patient remains exposed to the 
cause, and upon his removal from exposure may cease almost as speedily as 
it came on. In cases in which a reflex asthma due to the nasal irritation 
ensues the patient may become a chronic asthmatic even if the hay cold 
disappears. 

Prognosis. — The outlook for cure in the affection is not good unless the 
patient can go away to a resort where the cause does not exist for a certain 
length of time each year. So far as life is concerned it never endangers 
it, but if the disease produces vital depression it undoubtedly increases 
the susceptibility to other diseases. The patient can be comforted by the 
statement that the attacks stop or diminish in many cases after forty years 
of age. 

Treatment. — A competent rhinologist should always be asked to correct 
all nasal irregularities during the period of quiescence, and the physician 
should correct any gouty or lithsemic state by the use of ordinary exercise, 
a good diet, and the use of the salicylates, or bitter tonics with arsenic to 
improve the state of the mucous membranes in general. Not infrequently 
good results follow the use of 30 grains of phosphate of sodium in a cup 
of hot water before breakfast, given to stimulate the gastroduodeno- 
hepatic glands. In other cases salicylate of sodium in 10 grain doses or 
salol may be used for this purpose. These measures and the resort to a 
region free of the exciting cause in the autumn months are the prophylactic 
measures. A sea voyage usually confers complete immunity if taken at the 
proper time of year, and sometimes residence at some mountain resort does 
likewise, particularly if the altitude is very great. 

In the way of local treatment for the attack the swollen mucous mem- 
branes may be constricted by the application of a solution of adrenalin 
chloride 1 : 5000, and after this is done the parts may be washed with a 
mild alkaline spray like Dobell's solution or normal salt solution which has 
been warmed. After this is done the cocaine solution and the antipyrin 
solution recommended for acute coryza may be employed and finally the 
parts coated by the use of the spray of menthol and camphor named in that 
article. 

Within the last few years several attempts to produce immunity to 
hay fever by the use of preparations of golden rod and ragweed have 



ACUTE CATARRHAL LARYNGITIS 369 

been attempted, the patients taking them for some time before the time of 
an attack in the hope that they would not suffer from the disease. This 
plan has not so far proved very successful. 

Still more recently Dunbar, of Hamburg, claims to have isolated a toxin 
from the pollen of certain plants, and by giving it to horses produced an 
antitoxic serum which, he states, will protect a susceptible person. This 
is not used hypodermically, but is dried, mixed with sugar of milk, and then 
finely triturated. A small part of this powder is to be snuffed up the nose. 
When it is desired to use the remedy in the eyes the fluid serum is employed. 
The value of this method is still undecided. 



EPISTAXIS. 

Etiology. — Nose-bleed is due to many different causes, chiefly traumatic. 
The condition only concerns us, from the medical standpoint, when it develops 
as a result of lesions in the nasal cavities or in the course of the infectious 
diseases, or in cases of heart disease in which there is cephalic congestion. 
Occasionally it occurs in very plethoric persons after severe exercise, and in 
them it may be a beneficial condition. 

Severe nasal hemorrhage usually arises from an ulcer on the nasal septum, 
from cardiac disease, the commonest lesion being mitral disease, and in 
typhoid fever as one of the prodromes. Occasionally it is a desperately 
persistent state in haemophilia, and even more rarely it seems to be of the 
nature of vicarious menstruation. Sometimes it is a manifestation of blood 
dyscrasia, as in leukaemia. 

Treatment. — The treatment consists in plugging the nostrils with cotton, 
if necessary saturating the cotton with adrenalin chloride 1 : 2000, and in 
compressing the artery on the upper lip near the nose by pushing it against 
the jaw-bone. Internal measures are usually unnecessary and useless. 



DISEASES OF THE LARYNX. 

ACUTE CATARRHAL LARYNGITIS. 

Definition. — Acute laryngitis, or acute catarrh of the larynx, is an inflam- 
mation of the mucous membrane lining the larynx, as a result of which 
there is more or less loss of voice, or aphonia, and perhaps a sense of con- 
striction or respiratory oppression. 

Etiology. — This condition arises as a result of any factor which directly 
causes irritation of the laryngeal mucous membrane, such as the inhalation 
of irritant vapors or dust. In some cases the inhalation of cool and damp 
24 



370 DISEASES OF THE LARYNX 

air produces like effects, particularly if the voice has been used much 
before the exposure. Indirectly it arises as the result of getting the body 
chilled in a cold wind after exercise, and in still other cases it seems to be, 
at least in part, due to some disorder of metabolism, whereby gouty con- 
ditions ensue, and these in turn cause laryngeal inflammation by some 
indirect effect when the voice is much used. Another cause, particularly in 
the case of children, is " mouth-breathing," which permits the air unmoistened 
by the nasal chambers to pass over the laryngeal surface. In still other 
instances it arises as a complication of one of the acute infectious dis- 
eases, as influenza and of hay fever. The possible diphtheritic origin of 
acute laryngitis, especially in children, should never be overlooked. 

Pathology. — The inflammation of the laryngeal mucous membrane is 
precisely like that of mucous membranes elsewhere, except for the fact that 
glandular tissue is quite scarce in these parts, and so there is but little 
mucus secreted even if a considerable amount of inflammatory exudate 
takes place in the tissues beneath the mucous membrane. The desquamation 
of epithelial cells and the presence of dead leukocytes cause the secretion 
to be white and tenacious, and the congestion of the bloodvessels gives 
rise to a sense of tightness in the laryngeal box which is distressing. As 
the congestion decreases the process of regeneration in the epithelial cells and 
submucous tissues takes place, secretion becomes more profuse, and per- 
fect recovery ensues. 

Symptoms. — The patient finds it difficult to develop the full resonance 
of his voice and often single words in a sentence, or all the words, are 
spoken somewhat huskily owing to failure to move the vocal bands as 
readily as in health. There is a sense of tightness in the larynx and even 
aching pain may be present. In some cases hoarseness is the only symptom, 
but in others the loss of voice is complete. Speech at this time is often so 
painful that the patient endeavors to avoid conversation. 

An examination of the laryngeal mucous niembrane at this time will 
reveal marked redness and hyperemia and even small punctiform hemor- 
rhages may be seen, particularly if the patient has repeatedly and violently 
endeavored to clear his throat by hawking or coughing. The ventricular 
bands are swollen, and this may be the chief cause of the loss of voice, for 
it often happens that the vocal cords escape the inflammatory process. In 
other cases the edges of the glottic opening, the epiglottis, and the mucous 
membrane over the arytenoids are inflamed. 

As the process proceeds secretion is begun and small particles of mucus 
are occasionally coughed up. This is particularly apt to occur after severe 
coughing in the morning in order to dislodge inspissated mucus. The 
masses expectorated are often distinctly purulent, and discolored with soot 
if the patient lives in a city. Secretion gradually becomes more profuse. 
Pain disappears and the voice, which has been whispering, becomes hoarse 
and coarse in character, certain words which require effort being sounded 
with difficulty. Finally the voice recovers its normal tone and the attack 
is over. 

Diagnosis. — Care should be taken that sudden attacks of hoarseness are 
not considered as due to simple catarrhal laryngitis until the possibility of 



CHRONIC CATARRHAL LARYNGITIS 371 

diphtheria is excluded by a thorough examination of the throat and larynx. 
This is particularly important in children. In adults the possibility of 
aneurysm, tuberculosis, papilloma, and syphilis should not be forgotten. 

Prognosis. — The prognosis is always good as to recovery if the exciting 
cause is removed. 

Treatment. — The treatment of acute laryngitis consists primarily in remov- 
ing the cause. If irritant dusts are present the patient must not be exposed 
to them, and if the outside atmosphere is raw and cold he must be kept 
in-doors until recovery takes place. When a gouty diathesis underlies the 
condition the salicylates should be freely used in the form of salicin, 5 grains 
three or four times a day, and the vegetable salts of potassium, such as the 
citrate, be given freely. About the neck may be fastened a capsicum draft, 
or, if this is not to be had, a folded handkerchief should be wrung in cold 
water and laid upon the larynx, being immediately covered by a cloth or 
piece of flannel, which is bound around the neck. The cold compress is 
promptly changed to a warm compress by the heat of the body, and this acts 
favorably upon the local inflammation beneath. The air of the room in 
which the patient is to sleep or rest during the day should be kept well 
moistened by steam disengaged by a bronchitis kettle or by adding pieces 
of unslaked lime to a tub of water. Into the water in the bronchitis kettle 
may be placed a few grains of menthol if it is desirable to exercise a very 
sedative effect, and the patient should be forbidden to go into any cold 
rooms or hallways. A hot mustard foot-bath and a hot lemonade with a 
drachm of sweet spirit of nitre at bedtime to produce sweating is also useful, 
or a dose of Dover's powder may be ordered if the patient is an adult. 
Kyle recommends the use of tablets of -j-J-q- grain of pilocarpine every hour 
for four doses, or if it is important to attempt to abort the disease he suggests 
the use of 5 to 10 drops of dilute nitric acid in water every hour for three 
doses, and then every two hours for two doses. This often gives temporary 
relief if it does no permanent good. 

If by any chance the inflammation involves the glottis and seems to 
endanger life, intubation or tracheotomy is necessary. 

For the hoarseness and thick secretion of the stage of convalescence 
benzoate of soda or of ammonia, in 10 grain doses three times a day, are 
useful, or 10 grains of ammonium chloride may be given thrice a day in 
licorice and water. In still other cases terpin hydrate in the dose of a 
teaspoonful of the elixir every three hours may be used. 



CHRONIC CATARRHAL LARYNGITIS. 

Symptoms. — Chronic catarrh of the larynx is characterized by chronic 
hoarseness, by constant clearing of the throat in an endeavor to speak 
clearly, and finally, in severe cases, by ulceration of the laryngeal mucous 
membrane. Not rarely after a period of rest the patient finds that after 
the first few words his voice forsakes him, or, instead, he may find that 
if speaking is difficult at the beginning it becomes more easy as exercise 
limbers up the infiltrated muscles and engorged mucous membrane. 



372 DISEASES OF THE LARYNX 

Pathology. — Pathologically the condition is characterized by chronic 
engorgement of the minute bloodvessels, thickening of the mucous mem- 
brane, and even infiltration of the submucous tissues and the laryngeal 
muscles. If this process persists for any length of time sufficient infiltration 
may be present to become unabsorbable and thus cause permanent alteration 
in the character of the voice. Not rarely there is thickening and swelling 
of the pharyngeal tissues as well, and the tonsils are the seat of chronic 
lymphoid changes. Spots of ulceration may develop between the arytenoid 
cartilages. 

Diagnosis. — As stated in the article on Tuberculosis, hoarseness which is 
persistent should always be carefully investigated, as it often is due to tuber- 
culosis or syphilis, or even papilloma. When it is due to aneurysm the laryn- 
goscope will usually reveal one cord paralyzed, and when due to syphilis 
the history of the patient and the benefit produced by specific treatment 
must be noted. In persons of advanced years the possibility of malignant 
growth must be considered. 

Treatment. — The treatment consists in the maintenance of cleanliness and 
free secretion in the upper respiratory tract by the use of alkaline sprays 
and nasal douches. To the larynx itself a spray of alumnol (3 per cent, 
solution) may be applied every second day. The use of tobacco and alcohol 
should be forbidden and the liver and kidneys kept active by mild alkaline 
purges and diuretics. Tonics to the general system, such as phosphorus, 
arsenic, and sometimes iron, particularly the syrup of the iodide are useful. 

« 

(EDEMATOUS LARYNGITIS. 

Definition. — (Edema of the larynx occurs as an acute affection, occasion- 
ally of such a severe degree that it endangers life. It is essentially an acute 
cellulitis of the laryngeal tissues, and when it involves the upper part of 
the larynx in particular it is called oedema of the glottis. 

Etiology. — (Edema of the larynx is far more frequently due to injury 
than to any other cause, and in many instances is produced by the inhalation 
of irritant vapors or fumes. The only cases I have seen have been due to 
the patient attempting to swallow ammonia water undiluted, which both by 
actual contact of the fluid with the pharynx and of the fumes with the larynx 
has caused serious respiratory distress. Another traumatic cause is fracture 
of the larynx, as by throttling or other injury. Of the non-traumatic 
causes we find that acute inflammations in other parts may be provocative of 
this state, as, for example, tonsillar abscess with inflammation of the adjacent 
tissue gradually extending to the larynx. Sometimes it ensues as a result 
of grave lesions in the cartilages of the larynx, as in the chondritis arising 
in typhoid fever, or even in scarlet fever in association with the develop- 
ment of the "collar of brawn." Infection by the staphylococcus or strepto- 
coccus of the perilaryngeal tissues, the floor of the mouth or pharynx (as in 
Ludwig's angina) may extend to the epiglottis and larynx. While often an 
infection, it may arise in the course of some affection characterized by wide- 
spread oedema, as Bright's disease or chronic heart disease, and so appear to 
have a dropsical origin. 



(EDEMATOUS LARYNGITIS 373 

Pathology. — The condition of oedema of the larynx, as its name implies, 
depends upon the extravasation of fluid into the submucous tissues, producing 
an oedema or hydrops of the part, which is practically always of an inflam- 
matory origin. This swelling may involve all the laryngeal structures 
equally and even extend well along the trachea. In mild cases the parts 
affected are not, however, seriously disorganized, and the swelling may 
disappear as rapidly as it came on, leaving behind it little trace of its exist- 
ence. In fatal cases the swelling is usually found at autopsy to have largely 
disappeared, although the parts may be red and inflamed and somewhat 
relaxed. In such cases the microscope commonly shows a serous, or sero- 
fibrinous, suffusion of the affected tissues, the exudate containing a varying 
number of leukocytes. In other cases the submucous and even the peri- 
laryngeal tissues may be infiltrated by pus, diffuse suppurative interstitial 
laryngitis, a most fatal disease. 

Symptoms. — With the onset of this condition several characteristic symp- 
toms at once develop, namely, impairment of the voice, stridulous or labored 
breathing, manifestly due to laryngeal obstruction, and increasing cyanosis. 
The patient is uncomfortable if lying down, and is more easy when sitting 
up and leaning forward. The tissues adjacent to the larynx may be swollen 
and the patient, if unable to speak, points appealingly to his larynx. 

In some instances a state of chronic oedema, due to heart or renal disease, 
may ensue, which is rarely so severe or as pressing for relief as is the acute 
malady. 

Diagnosis. — Difficult laryngeal breathing may be due to a laryngeal crisis 
in locomotor ataxia or to the lodgement of a foreign body in the larynx. 
These conditions should be excluded before the physician decides that 
oedema is the cause of the illness. Aneurysm of the aorta may produce 
severe laryngeal symptoms by pressure on the laryngeal nerves, and in 
children retropharyngeal abscess may, by rupture or pressure, produce some- 
what similar symptoms. 

Prognosis. — In the absence of virulent symptoms the prognosis is usually 
favorable even if the symptoms are severe, provided that when they appear 
the physician is ready to give relief by intubation or tracheotomy. If the 
oedema is due to the inhalation of irritating vapors and the lower respiratory 
tract is involved in the inflammatory process, the prognosis is, of course, 
very grave. 

Treatment. — The treatment consists in the administration of an active 
saline purge to deplete the vascular system, and the setting free of steam 
from a bronchitis kettle in the air of the room in which the patient lives. 
To the water in the kettle may be added a few grains of menthol for its 
soothing influence on the laryngeal mucous membrane. A 10 per cent, 
solution of alumnol may be sprayed into the larynx for its astringent effect. 
When the oedema arises as a complication of renal or cardiac disease and 
is part of a general tendency to anasarca, so active a purge as elaterium or 
colocynth is indicated to remove fluid from the body, and a hot pack may 
be used to cause sweating if the heart is strong enough to stand it. The 
use of pilocarpine for this purpose is unwise, because it is so prone to cause 
pulmonary oedema. When the laryngeal obstruction becomes marked it 



374 DISEASES OF THE LARYNX 

may be necessary for the physician to quickly perform intubation or trach- 
eotomy, but while he should be prepared to do so at any moment it is scarcely 
necessary to add that tracheotomy should only be done as a last resort. 



SPASMODIC LARYNGITIS. 

Definition. — Spasmodic laryngitis, sometimes called " spasmodic croup," or 
" false croup " in distinction from diphtheria or true croup, is a condition of 
acute laryngeal catarrh involving the mucous membrane in the region of 
the glottis, and resulting in swelling of those parts, so that the ingress and 
egress of air is difficult. The spasm of the laryngeal muscles, while it aids 
in producing the symptoms, is really of secondary importance as compared 
to this swelling. 

Etiology. — In the past it was customary to consider spasmodic croup a 
disease in itself. We now know that it is a symptom depending upon several 
causes, some of which are external, some internal. Appearing as it does 
almost always in children between one and six years, but sometimes persist- 
ing in its occurrence up to puberty, it depends chiefly upon rickets or mal- 
nutrition, the presence of postnasal adenoids, which make the child a mouth 
breather, or to some defect in the nose, which causes the same condition. 
In some instances errors in diet before retiring to bed seem to precipitate 
an attack. Of the external causes which, however, are only active in those 
who have a tendency to attacks of this affection, may be mentioned furnace- 
heated air, which is so dry and dusty that if the child is a mouth breather 
the larynx becomes rapidly dry and irritated. An acute coryza may also 
bring on an attack in that it causes mouth breathing. 

Treatment. — The treatment is evident from what has just been said. It 
may be divided into two parts, that for the relief of the attack and that 
for the cure of the underlying causes. 

When any sign of croup is manifested the nurse should place 1 or 2 grains 
of menthol in the bowl of a dry spoon and heat it over a gas jet or lamp. 
This sets free in the air of the room the menthol vapor and soothes the 
laryngeal mucous membrane. If the attack is well developed the nurse 
should, in addition, disengage from a bronchitis kettle steam laden with 
menthol, or with oil of pine and oil of eucalyptus, in the proportion of 15 
drops of each in the water in the kettle or on the sponge usually placed in 
its neck or spout. Internally a dose of 5 to 10 grains of bromide of sodium 
may be given in syrup, and over the larynx should be placed a compress 
wrung in hot or cold water. 

For the prevention of future attacks the child should be relieved of ade- 
noids or enlarged tonsils, should receive proper diet and tonics if rachitic, 
and should sleep in a bronchitis tent if the larynx is irritable. A sponge 
loaded with cold water may be sopped upon the skin over the larynx 
every morning to improve its vascular tone. 



TUBERCULOUS LARYNGITIS 375 



TUBERCULOUS LARYNGITIS. 

Definition. — As its name implies, tuberculous laryngitis is due to the 
presence of the Bacillus tuberculosis in the laryngeal tissues and the conse- 
quent development therein of miliary or larger tubercles. (See Tuberculosis.) 

Etiology. — In the vast majority of cases of laryngeal tuberculosis the 
infection is secondary to pulmonary disease, and is due to infection of the 
larynx by the sputum which the patient coughs up, or by direct extension 
from below upward. In rare instances it is undoubtedly a primary affection. 
I have had such a case under my care while writing this article. As in 
tuberculous infection in other parts there must be, in addition to the presence 
of the bacillus, a susceptibility to infection, or one acquired by general or 
local lowering of vitality. This disease occurs most commonly in males 
between twenty and thirty years of age. 

Pathology. — Here, as elsewhere in the body, the development of tubercles 
takes place by leukocytic migration and the proliferation of cells, and is 
accompanied by the closing of bloodvessels and the necrosis of the masses 
formed, followed by breaking down and escape of the cheesy material, and 
the production of ulcers in the laryngeal mucous membrane. As the process 
of infiltration proceeds the perichondrium is attacked and necrosis takes 
place in the laryngeal cartilages. 

In many other parts of the body the system makes efforts at repair, so that, 
even if the disease ultimately wins the battle, evidences of an active defence 
can be recognized ; but in the larynx it very commonly happens that no 
such reparative or protective process occurs, and this is one of the reasons 
why the malady is so rarely cured. In some cases the infectious process takes 
on some of the aspects of a tumor, a tuberculoma, manifesting a tendency 
to infiltration and induration, with but little inclination to ulceration. 

Symptoms. — There are few maladies which present such a distressing 
picture of suffering as does laryngeal tuberculosis. The loss of voice, which 
permits speech only with great effort, cuts off the patient from pleasant 
intercourse with friends and from expressing any but his most urgent 
needs, and then only with great pain and effort. The thickening of adjacent 
tissues nearly always makes swallowing most difficult and painful, and for 
this reason urgent thirst must be satisfied with but one swallow of water. 
The same dysphagia makes the use of solid food impossible and the taking 
of liquid nourishment almost so, yet the patient cannot combat the malady 
unless well nourished. Because of these factors and the constant pain and 
loss of sleep, the loss of weight in laryngeal tuberculosis is often extra- 
ordinary, almost equalling that seen in some cases of malignant growth 
elsewhere. 

In the earlier stages the loss of voice and constant discomfort in the larynx 
may be the only symptoms. Cough is present in all cases to some extent, 
and is often exceedingly painful. After all the muscles about these parts 
have had their action inco-ordinated by direct infiltration or disordered 
nerve supply, particles of food get into the larynx and cause spasm and pain 
which is insufferable. 



376 DISEASES OF THE LARYNX 

A careful examination of the chest wall will reveal in most cases some 
tuberculous focus. 

If the laryngoscope is used in the early stages, an acute hyperemia may 
be found, but in the chronic type the appearance will be that of marked 
local anaemia. A tuberculous lesion may be found in the epiglottis, from 
whence it gradually passes downward, or the disease may begin below the 
cords and work its way upward. These tuberculous areas are composed 
of small nodules or swellings which are hypersemic in the acute cases and 
anaemic in the chronic cases. As these nodules grow they may, by their 
mere mechanical presence, cause obstruction to free respiration. The 
infiltration of the epiglottis becomes marked, and the mucous membrane 
may become dotted by a multitude of small, yellow tubercles which are easily 
recognized. These break down and, having done so, form small ulcers which 
coalesce and form larger areas of ulceration. Comparatively rarely the vocal 
cords develop tiny vegetations. 

Diagnosis. — The discovery of a pulmonary tuberculous process in the 
presence of the hoarseness, which is persistent and does not clear up under 
the ordinary treatment for acute or chronic laryngitis, raises a suspicion 
of the tuberculous character of this malady at once. In syphilitic laryngitis 
the history of the patient, the reddened areola about the ulcers, and the 
presence of signs of syphilis elsewhere will aid the diagnosis. From carci- 
noma of the larynx we can separate tuberculous laryngitis by the fact that 
the former disease occurs as a single new-growth in a person who is usually 
past the period of life in which tuberculosis is prevalent. 

Prognosis. — The prognosis is most unfavorable even in cases seen in 
the early stages, because the ability to carry on repair in these tissues is so 
poor and because experience has taught us that these cases rarely recover. 

Treatment. — The treatment of laryngeal tuberculosis can be carried out 
only by a skilled and dexterous laryngologist. Even in his hands it may 
cause much distress and pain. In the hands of the tyro clumsy handling 
is probably worse than useless. For the palliation of the condition and of 
the suffering the parts may be sprayed with peroxide of hydrogen followed 
by a mild alkaline solution, and these in turn by a spray containing menthol 
5 grains, oil of sandal-wood 5 minims, and liquid albolene 1 ounce. General 
tonic treatment such as is used in all cases of tuberculosis, with careful 
feeding, is essential. As a rule, the patient should avoid high altitudes, 
particularly if they are windy, as the drying of the mucous membrane 
increases discomfort in the larynx. 



SYPHILITIC LARYNGITIS. 

Etiology. — Syphilis of the larynx appears during the secondary and ter- 
tiary stages of the disease. In the secondary stage it may amount to nothing 
more severe than hyperemia or erythema, such as is usually met with in 
ordinary acute catarrhal laryngitis, but in other instances mucous patches 
develop, which are most numerous about the aryepiglottic folds, the region 
of the vocal cords, the arytenoid cartilages, and on the edges of the epiglottis. 



ACUTE CATARRHAL BRONCHITIS 377 

If active treatment is instituted they usually readily yield, but they may 
become distinct ulcers. When these heal there may be sufficient thickening 
of the parts to cause permanent hoarseness. 

Tertiary syphilis appears in the larynx as a diffuse or circumscribed 
gummatous growth, which usually attacks the epiglottis, the cords, and 
the posterior wall of the larynx, causing thickening and infiltration of the 
tissues, and finally ulceration of the surface in some instances. The cicatri- 
zation of the ulcers, or sclerosis of areas by infiltration, may cause stenosis 
and distortion of the laryngeal wall. 

Symptoms. — The symptoms are hoarseness and loss o] voice, but pain is 
rarely present. 

Diagnosis. — The diagnosis is based on a history of syphilitic infection or 
by the finding of evidences of syphilis and by the relief which follows specific 
treatment. Tuberculous ulceration is not so rapid in its development and 
the patient reacts to tuberculin. Further than this, in syphilis the upper 
surface and in tuberculosis the lower surface of the epiglottis is usually 
affected. From malignant growth of the larynx syphilis is separated by 
the fact that the ulcer is solitary in epithelioma. 

Prognosis. — The prognosis is good if treatment is used early, before the 
stage of ulceration is well developed. After ulcers have become deep and 
severe they may be healed by treatment, but cicatricial contractions neces- 
sarily appear as healing goes on. 

Treatment. — The treatment consists of iodide of potassium and the mer- 
curials, as in other cases of syphilis. (See Syphilis.) 



DISEASES OF THE BRONCHI. 

ACUTE CATARRHAL BRONCHITIS. 

Definition. — Acute bronchitis is an inflammation of the bronchial tubes 
which is usually confined almost entirely to the mucous membrane lining 
them. 

History. — Bronchitis has been recognized as a distinct condition for many 
centuries. It was not, however, until the early part of the nineteenth cen- 
tury that this term was used to describe the condition now under discussion, 
when Badham, in England, and Franck, in Germany, first employed this 
term. As with many other diseases involving the thoracic organs, a clear 
description of the pathological condition was first given to us by the French 
physician Laennec. 

Distribution. — Acute bronchitis is a disease which occurs in all parts of 
the world, but it affects chiefly the inhabitants of those regions in which 
the climate is moderately cold and raw, and where the degree of humidity 
in the atmosphere is high. On the other hand, hot and dry portions of the 



378 DISEASES OF THE BRONCHI 

earth's surface are usually free from this disease. Another important factor 
in its prevalence is sudden changes of temperature and the prevalence of 
cold winds laden with moisture. For these reasons the disease is most fre- 
quent at those times of the year when sudden changes of temperature are 
apt to occur, and therefore is commonly met with in the late winter and 
early spring months. 

Etiology. — The etiology of acute bronchitis, so far as external influences 
are concerned, has just been described. In a goodly number of cases, 
practically in all, it is probable that micro-organisms have much to do with 
the development of the disease, and that the primary hyperemia and con- 
gestion of the bronchial mucous membrane is due to the exposure of the 
surface of the body to external influences and, to a slight degree, to the 
passage over the bronchial mucous membrane of an atmosphere which, 
because of its physical condition, is irritating to these parts. It is a well- 
known clinical fact that exposure of the surface of the body to cold seems 
to be followed by congestion of the bronchial mucous membrane, and that 
this actually takes place has been proved, first, by experiments upon animals, 
and, second, by observations upon man. Thus, it is possible by the external 
application, alternately, of heat and cold to the upper portions of the thorax 
to produce great changes in the capillary circulation of the larynx and 
trachea and probably the bronchial mucous membrane as well. 

Much depends, too, upon the general health of the patient who is exposed 
to the provoking causes which have just been named. Strong, hearty, or 
robust individuals who have a well-balanced circulation and elastic blood- 
vessels frequently suffer from no pulmonary inconvenience from exposure, 
but persons who have been enfeebled by disease, or by advancing years, or 
those who are very young frequently suffer from such a severe congestion, 
and it may produce fatal consequences. Bronchitis is also not rarely the 
result of an inflammatory process which begins higher up in the respiratory 
tract and extends to the tubes. Practically all acute infections of the lung 
also produce some bronchial inflammation. 

So, too, any condition of cardiac or renal disease which impairs circula- 
tory activity is exceedingly prone to render the patient susceptible to this 
form of inflammation. We find, therefore, that acute bronchitis is a disease 
which is most prevalent in infancy and old age, and it is entirely competent, 
at these two periods of life, to produce death if it is present in a severe form. 
Those who have been attached to the departments for children in large 
hospitals cannot fail to have been impressed with the very great frequency 
of this disease in the winter months, and also with its rarity among the 
adults who come to the same institution for various ailments. 

Both sexes are equally prone to suffer from acute bronchitis, but it is 
more frequently met with in males because males are more exposed to the 
provoking causes than females. 

Certain of the acute infectious diseases very strongly predispose to this 
malady. Thus, it is nearly always present in a well-developed form in a 
case of measles, even when that disease is present in a mild form. Again, 
there are but few cases of tvphoid fever which do not have a certain amount 
of bronchitis. 



ACUTE CATARRHAL BRONCHITIS 379 

The reason that bronchitis so frequently complicates cardiac disease 
depends upon the intimate relationship between the circulation in the 
lungs and the right side of the heart, for the bronchial veins open into the 
venae azygos and the superior intercostals, and so are intimately connected 
with the right side of the heart. These bronchial veins also anastomose 
closely with the pulmonary veins, and so valvular disease which results 
in congestion of the right side of the heart naturally tends to produce a 
disturbance of the circulation in the bronchial mucous membrane. 

When emphysema of the lungs is present the coincident bronchitis is 
really due to two causes : first, the congestion of the right side of the heart 
which is so apt to ensue in emphysema, and, second, the pathological 
changes in the heart result in impairment of the bronchial circulation. 
On the other hand, bronchitis sometimes leads to emphysema. These 
affections are therefore interactive. 

There are three other important etiological factors in the production of 
bronchitis which must also be considered. The first of these is the inhala- 
tion of irritant gases or vapors, producing what is known as acute traumatic 
bronchitis. The second is the inhalation of dust. These dusts may be 
vegetable, animal, or mineral in their origin. Sometimes all three forms 
are combined. Finally there can be no doubt that the inhalation of various 
micro-organisms may result in bronchial infection. 

Of the forms of dust which produce bronchitis we find that vegetable 
dust seems to be the most frequent cause. 

That form of bronchitis which most frequently follows the inhalation 
of irritant vapors or gases is seen in persons who have been exposed to 
ammonia fumes, irritating smoke, or to chlorine gas. Another form of 
local irritation producing bronchitis is that which is seen in large cities 
which are heavily veiled with smoke and fog. Thus, in the city of London 
the particles of moisture in the air become coated with the sooty materials, 
and so evaporation, even in houses which are fairly well heated, is greatly 
impaired, and the fog penetrates in-doors. As a result the frequency of 
acute bronchitis is greatly increased in London in those seasons of the year 
in which these fogs are prevalent, and the mortality of chronic bronchitis 
is wonderfully increased at these times. So powerful an influence do these 
deleterious factors exercise that it is a well-known fact that the mortality in 
the city of London may be doubled in those weeks in which the fog is present. 
Thus, on some occasions the mortality is as high as 46 per cent, as against 
an ordinary death rate of about 18 per cent. The deaths from diseases of the 
respiratory organs rose on one occasion from 415 per week to 994 per week 
during the prevalence of a dense fog. Of these, 694 were due to bronchitis 
and 185 to pneumonia. That this increase was due to the fog and not to 
the other conditions of the climate is proved by the fact that a similar 
increase in mortality did not take place in surrounding provincial cities 
and towns. These facts are well emphasized by West in his well-known 
book upon Diseases of the Organs of Respiration. 

The micro-organisms infecting the bronchial mucosa are the pneumo- 
coccus, which is most common; Friedlander's bacillus > the Streptococcus 
pyogenes, and the pyogenic staphylococci. The Klebs-Loeffler bacillus is 



380 DISEASES OF THE BRONCHI 

usually present in the bronchitis which complicates diphtheria. In some 
cases of bronchitis additional micro-organisms have been found, such as 
the Bacillus typhosus, Bacillus coli communis, and various forms of fungi. 
In most instances, however, bronchitis is polymicrobic in origin, and it is 
often impossible to decide what organism is the primary infecting agent. 

Prevention. — Acute bronchitis can only be prevented by proper care of 
the general health, by proper clothing, and by the avoidance of climatic 
influences which are known to be deleterious. Persons who have learned 
by experience that they are peculiarly susceptible to the various provoking 
causes named, should, by change in climate or occupation, avoid these 
various causes of irritation. 

Pathology and Morbid Anatomy. — Acute bronchitis is characterized by 
hyperemia and swelling of the mucous membrane lining the bronchial 
tubes, accompanied by some infiltration of the submucous tissues. At first 
there may be an almost total absence of secretion or undue dryness of the 
surface involved, but very soon the engorged mucous glands begin to pour 
out into the lumen of the tubes considerable quantities of mucus, which also 
soon contains epithelial cells coming from the lining of the glands them- 
selves and from the surface of the mucous membrane as well. Leukocytes, 
which have undergone diapedesis, as they do in all acute inflammatory 
processes, are also present, and even red blood cells may be seen. A 
similar extravasation of red cells may also take place into the submucosa, 
and, escaping on the surface tinge the sputum. In the smaller bronchi 
the lining epithelium may be cast off in shreds, and if the inflamma- 
tion is intense, we may find the tubes almost or completely closed, with 
resulting capillary bronchitis or suffocative catarrh. By the extension of 
the inflammation to the peribronchial tissues and the pulmonary alveoli 
there is developed a bronchopneumonia. (See Bronchopneumonia.) As 
recovery takes place the dead epithelium and extravasated cells are expelled 
from the tubes by coughing, and new epithelium is developed from deeper 
layers of cells. Sometimes, particularly when a large number of infecting 
micro-organisms are present, the sputum is distinctly purulent. When 
bronchial inflammation persists for any length of time, or the attacks are 
frequently recurrent, permanent thickening of the submucosa results. This 
fibrosis may extend to adjacent structures (peribronchitis) or be continuous 
with the increased fibrous tissue of chronic interstitial pneumonia. 

Symptoms. — The symptoms of acute bronchitis can be divided into three 
stages, namely, that of onset, the stage of profuse secretion, and the stage 
of convalescence. 

In the stage of onset there may be a chill, which usually is not 
severe; a short, dry cough which may, by its persistance, be annoying, 
and, owing to the dry and inflamed state of the mucous membrane of the 
bronchial tubes, be distressing because of the soreness or pain it produces 
under the sternum. If the degree of swelling of the mucous membrane 
is marked, there may be a sense of oppression, and the breathing may be a 
little quickened. The temperature of the body is usually not much above 
normal in the adult, but in children it is often as high as 102° or even 103°. 
and the pulse is apt to be rapid in direct proportion to the degree of fever. 



ACUTE CATARRHAL BRONCHITIS 381 

Auscultation at this time reveals an increased roughness of the inspiratory 
or expiratory bronchial sounds, and perhaps a few dry rales between the 
shoulder-blades. 

In the second stage there is a disappearance of the soreness in the 
chest, but the cough may be persistent, and is more or less productive 
of expectoration of mucopurulent material. Febrile movement continues 
if that symptom has been present earlier. The pulse is but slightly 
quickened and auscultation reveals, particularly over the bronchial tubes 
posteriorly, large, moist rales and rhonchi. 

The duration of an attack of acute bronchitis rarely exceeds ten days 
to two weeks, and is often shorter than this. 

Treatment. — The treatment of acute bronchitis divides itself into two 
parts: that part which is devoted to allaying the inflammation in its early 
stages, and that which is directed toward the dissipation of the results of 
the inflammation after it has peen present for some days. In the early stage 
no better remedy can be administered internally than a prescription which 
contains in each dose J a drachm of syrup of ipecac and 1 teaspoonful to 
2 teaspoonfuls of the official liquor potassii citratis of the United States 
Pharmacopoeia. This should be administered every three or four hours. 

If cough is an annoying symptom, and there is much pain in the chest, 
Dover's powder may be given to an adult in the dose of 2 or 3 grains every 
three or four hours until 10 grains have been taken. A mustard plaster may 
be applied to the chest, back and front, or the thorax may be rubbed with 
ammonia liniment or with chloroform liniment. In children a very useful 
counterirritant application to the chest is 1 drachm of the oil of amber in 
2 tablespoonfuls of sweet oil. If the patient be a child, and if the air of 
the bed-room is particularly dry and irritating, because it is furnace-heated, 
much relief can be obtained by disengaging a small quantity of steam. 
This may be given off from a tea-kettle which is kept boiling constantly, 
or may be obtained by dropping large pieces of unslaked lime into a tub of 
water. It is probable that when the latter procedure is resorted to the air 
of the room not only contains an extra amount of moisture, but fine particles 
of lime, which act advantageously upon the bronchial mucous membrane. 

If the evidences of bronchial irritation are very marked, the patient, 
whether he be an adult or a child, should sleep in a bronchitis tent. A 
bronchitis tent, it will be remembered, consists in a tent-like arrangement 
of sheets spread over the bed, and resting upon four corner sticks, one of 
which is tied to each corner of the bed. Under this canopy the patient will 
have plenty of air, and the steam from a kettle can be disengaged within its 
confines. If necessary, 1 or 2 grains of menthol may be added to the hot 
water every two or three hours. In other instances the bronchial irritation 
will be greatly soothed by pouring into the boiling water a tablespoonful of 
a mixture composed of equal parts of compound tincture of benzoin, oil 
of eucalyptus, and oil of pine. 

After secretion has begun to form in the secondary stage of acute bron- 
chitis it then becomes necessary to administer not sedatives, but stimulant 
expectorants, and of these chloride of ammonium, without any doubt, is 
usually followed by the best results. From 5 to 10 grains of this drug may 



382 DISEASES OF THE BRONCHI 

be given with equal parts of the fluid extract of licorice and water every 
four or five hours to an adult, and, if cough is excessive, \ of a grain of 
sulphate of codeine or 20 drops of paregoric may be added to each dose. 
Under the influence of this remedy the expectoration of yellow or muco- 
purulent sputum is at first increased, but at the end of twenty-four or forty- 
eight hours the quantity diminishes. 

When there seems to be lack of secretion, the compound licorice mixture 
of the United States Pharmacopoeia, which contains a small quantity of 
tartar-emetic, may be used in place of the plain extract of licorice just 
named. If for any reason the cough and expectoration persist and do not 
diminish under the use of the chloride of ammonium, we may give with 
advantage 5 to 10 minims of the oil of sandal-wood in capsules, three or four 
times a day. Other patients do well at this time if they receive 5 minims 
of the oil of eucalyptus in capsules three times a day. The latter remedy, 
however, is quite apt to disorder the stomach. Another very valuable 
remedy in the secondary stage of bronchitis, to promote expectoration, is 
terpin hydrate, which is best given in the form of an elixir, dose, a tea- 
spoonful, and which may be much increased in its efficiency if to each 
dose is added yj of a grain of heroin, or \ of a grain of codeine sulphate. 
The dose of terpin hydrate is from 2 to 5 grains four times a day, but 
in obstinate cases larger doses may be administered. Terebene may also 
be given in capsules in the dose of 5 minims three or four times a day. 

If the general nutrition of the patient is not good and he seems somewhat 
debilitated, the employment of cod-liver oil, or syrup of iodide of iron, in 
moderate doses, will often produce the most advantageous results at this stage 
of the illness. 

CHRONIC CATARRHAL BRONCHITIS. 

Definition and Symptoms. — By chronic bronchitis is meant a condition in 
which there exists a chronic inflammatory process in the bronchial mucous 
membrane, as a result of which the patient suffers from cough and the 
expectoration of thick, mucopurulent sputum. When uncomplicated there 
is no febrile movement in association with this condition, nor is there, as 
a rule, any loss of flesh or impairment of the general health. It may be 
regarded as a subacute continuation of an acute cold. The chief objection 
to the term " chronic bronchitis " is that it so often is applied by the careless 
or ignorant, or by those who wish to use an euphemism, to designate a far 
more serious condition, such as pulmonary tuberculosis or bronchiectasis. 

Treatment. — The treatment of chronic bronchitis is practically identical 
with that of the later stages of the acute form, which has just been described, 
but the most important thing for the physician to do, to whom is presented 
a so-called case of chronic bronchitis, is to carefully exclude tuberculosis or 
renal disease as causative factors in the case. Many cases of so-called chronic 
bronchitis are treated for weeks with ordinary expectorants when tuberculosis 
is present or Bright's disease is the real cause of the disorder. 



BRONCHIECTASIS 383 



BRONCHIECTASIS. 

Definition. — Bronchiectasis, as its name implies, is a condition in which 
the bronchial tubes are dilated. This dilatation may occur in three forms, 
namely, the cylindrical or fusiform, the saccular, and the trabecular or 
moniliform. The first of these is the only true type of bronchiectasis, but 
the other forms are those most commonly met with. 

The disease is not common in its well-developed form. If we combine 
the statistics of the Brompton Hospital, of London, with those of Biermer 
and Willigk, we find that in SI 44 autopsies bronchiectasis was found in about 
4 per cent. These are, however, postmortem figures, and do not represent 
a certain proportion of cases which do not come to autopsy because of a 
respiratory ailment. 

Etiology, Pathology, and Morbid Anatomy. — The saccular form is common 
in adults, and when it is present, the lung, at autopsy, contains one or 
more saccules, or globular cavities, which usually are not very large, but may 
be the size of a small lemon. These cavities or open spaces, when large, 
are due not only to simple dilatation of the bronchi, but to involvement of 
the surrounding tissues as well, and their walls are composed of parts of 
the bronchial tubes and thick connective tissue which has been formed in 
part as the result of chronic inflammatory changes, the lung tissue having 
undergone fibroid change. Sometimes these spaces are filled with thickened, 
inspissated secretion, and seem like closed cavities. It is readily seen, 
therefore, that the differentiation between this state and fibroid phthisis 
(see Tuberculosis of the Lung), so called, may be by no means easy, par- 
ticularly as these pouches may become infected, ulcerate, and really form 
small abscesses. 

The trabecular form is still less a true bronchiectasis, and yet it is the 
condition most commonly met with, and to which the term bronchiectasis 
is most frequently applied. It consists in irregular cavities with smooth 
linings, which cavities are surrounded by dense walls of overgrown con- 
nective tissue which do not contain any signs of remnants of the tissues of 
the bronchial tubes. On the contrary, the only relation borne by the bron- 
chial tube to such a cavity is that it forms the trabecular with the atrophied 
bloodvessels. These cavities are often joined one to another by openings, 
so that the lung may be thoroughly riddled with spaces more or less well 
filled with secretion. 

Cylindrical bronchiectasis (Figs. 51 and 52) is usually developed in children 
as the result of strain upon the bronchial tubes produced by the violent 
efforts in whooping-cough or measles. It probably depends primarily upon 
inherent weakness of the muscular and elastic coats of the tubes. The 
affected bronchus is uniformly dilated in its entire circumference for a con- 
siderable distance, and this dilatation may be so great that its calibre is 
increased to twice or thrice the normal. In other instances it is dilated in 
sections, with a normal or nearly normal calibre between. 

When bronchiectasis occurs in the saccular and trabecular type it is a 
subacute or chronic disorder, and results from chronic inflammation of the 



384 



DISEASES OF THE BRONCHI 



bronchial tubes, with resulting atrophy of the elastic and muscular coats. 
Of the provoking causes influenza is an important factor. Another cause is 
the progress of cicatricial or cirrhotic change in the pulmonary parenchyma, 
which, as it proceeds, distorts the bronchial tubes, narrowing them in some 
places and widening them in others. In other instances it can be readily 
understood how chronic thickening of the visceral layer of the pleura may 
so result. In still others a localized bronchiectasis may be caused by the 
entrance of a foreign body. 



Fig. 51 




Bronchiectasis, originating in acute lobar pneumonia. Marked saccular and cylindrical dilatations 
with a large gangrenous cavity in the middle lobe. Duration eleven months. From a case under the 
care of Dr. Maguire. Dr. Barty King. (Brompton Hospital Museum. Scottish Medical and Surgical 
Journal.) 



The influence of age in the development of the various types of bronchi- 
ectasis is quite noteworthy. Cylindrical dilatation is largely a condition 
limited to childhood, and the saccular and trabecular types are chiefly met 
with in adults. It has been thought by some physicians that the latter forms 
occur with increasing frequency as old age is approached, but the statistics of 
Barty King indicate that the age incidence of the pure type is from thirty 
to forty years. Thus, 53.1 per cent, of his cases occurred between twenty 



BRONCHIECTASIS 385 

and forty years. The same observer places the proportions of the two sexes 
as 77 per cent, in males and 23 per cent, in females. 

Symptoms. — The symptoms of bronchiectasis naturally vary greatly with 
the form of the disease which is present. Cough of severe degree may be 
considered the most constant of them all. This cough is peculiar in that 
in many cases it is particularly severe in the morning, persisting until the 
patient has rid his dilated and feeble bronchi of the secretions which have 
accumulated in them during the night. Not only is this cough peculiar in 
this respect, but it not infrequently happens that the patient, after a pro- 

Fig. 52 




Cylindrical bronchiectasis. A typical case. Dr. Barty King. (St. Thomas' Hospital Museum. 
Scottish Medical and Surgical Journal.) 

longed attack of coughing which is unproductive, is enabled to get rid of 
a large quantity of sputum, which may come away in a gush or which 
may not be dislodged until by some change in posture drainage from the 
bronchiectatic area can take place. 

The sputum is also somewhat characteristic, for it is often grayish- 
brown in appearance, somewhat fetid in odor, and separates when placed 
in a glass into three layers, the upper one brownish and thin, the second 
one mucoid, and the third granular and filled with dead epithelial cells and 
pus corpuscles. This lower layer also contains large crystals of the fatty 
25 



386 DISEASES OF THE BRONCHI 

acids and crystals of hamiatoidin. The sputum is so distinctly purulent 
that it may closely resemble that expectorated in cases of pulmonary 
abscess, a resemblance still further increased by the fact that it may be 
extremely fetid. It is not nummular, as in many cases of phthisis, and it 
rarely contains elastic-tissue fibres, which is of some importance in dif- 
ferential diagnosis. Fever is usually not present unless the purulent process 
in the bronchi is marked and septic absorption results. An additional symp- 
tom, sometimes met with, is hcemoplysis from ulceration of a bloodvessel. 

The physical signs of bronchiectasis have little about them that is distinctly 
characteristic, and for this reason an absolute diagnosis may be difficult or 
impossible unless the lesions are so far advanced as to have affected the 
whole lung and caused alteration in the configuration of the chest. When 
the bronchiectatic spaces or cavities are large the physical signs are prac- 
tically identical with those of pulmonary tuberculosis with cavity forma- 
tion { but there is this important difference, namely, that the cavities in 
tuberculosis are commonly apical while the cavernous breathing of bron- 
chiectasis is usually most marked near the base. The physical signs of 
cavity formation also vary with the condition of the cavity — that is, whether 
it is full of secretion or empty, and therefore change in the patient's posi- 
tion, and cough with expectoration, may cause very great differences both 
in examination by auscultation and percussion. Loud, moist rales and 
amphoric breathing may be present. 

Diagnosis. — -It is manifest from what has just been said that the differ- 
ential diagnosis of bronchiectasis from pulmonary tuberculosis may be quite 
difficult and, indeed, impossible in certain cases, for it not uncommonly 
happens that a superficial dilated and sacculated area in the lung gives, on 
auscultation and percussion, physical signs which are identical with those 
which are produced in pulmonary tuberculosis with cavity. The presence of 
tubercle bacilli and of yellow elastic tissue in the sputum, of hectic fever, of 
rapid loss of flesh, and of night-sweats point to tuberculous infection. Another 
useful differential point is the fact that in tuberculosis the cavity is usually 
at the apex, whereas in bronchiectasis it is lower down in the lung. Still 
another point is that the patient is rarely as ill as in tuberculosis, and can 
get about year after year unless some acute intercurrent pulmonary malady 
intervenes. 

Further than this, bronchiectasis and pulmonary tuberculosis may exist 
simultaneously. Thus, in 68 cases of bronchiectasis observed by Trajan- 
owski, 21 occurred in individuals who were affected with phthisis, and in 
75 autopsies on individuals who died from phthisis Wilson Fox found 
bronchiectasis in 27 cases. Twenty-one (21) were of the fusiform variety 
and six (6) were saccular. 

Complications. — Haemoptysis, as a complication of bronchiectasis, is rarely 
severe and occurred in Barthez's cases 16 times out of 39 cases. Grainger 
Stewart met with it 3 times in 8 cases, and Fowler met with it 14 times 
in 35 cases. Three of these cases were tuberculous. 1 

Another complication is rheumatoid arthritis. I have recently had a case 

1 For some of the cases in French literature see Devic and Bertier, Lyon medical, January, 1904. 



BRON CH1ECTAS1S 387 

under my care in which, after many years of chronic bronchiectasis, a maiden 
lady developed multiple arthritis, and in the course of a few weeks became 
completely disabled. Sometimes no more serious joint difficulties arise than 
swelling of the finger-joints and clubbing of the finger-tips, with incurvation 
of the nails, or the case develops true pulmonary osteoarthropathy. The 
joint complications are probably septic in origin. Pulmonary gangrene may 
also develop, and Duret has operated on such cases with success. 

Brain abscess may arise from a septic focus in bronchiectasis. 

Cyanosis and dyspnoea on exertion are such constant symptoms that they 
can scarcely be considered as complications. 

'When we consider the state of the tissues involved we can readily under- 
stand how readily a septic bronchopneumonia may be developed in these 
cases, either as a result of direct extension of the inflammatory process from 
the area primarily involved, or by the inspiration into other parts of the 
lung of septic material during paroxysms of coughing. 

Prognosis. — This depends upon the state of the patient's health, the 
presence or absence of sepsis, and the presence or absence of tuberculous 
infection. In severe forms the health is greatly impaired. Recovery from 
the condition itself, if it be well developed, is manifestly impossible. Never- 
theless, life may continue for many years. 

Treatment. — The treatment of well-developed bronchiectasis can be only 
palliative. Once the condition of dilatation of the bronchial tubes has 
been established, it is evident that they cannot be brought back to their 
normal calibre. On the other hand, in the early stages of bronchiectasis, 
much can be done in the way of palliative treatment. It is a mistake, how- 
ever, to give sedatives to control the cough unless the cough is so excessive 
that it materially interferes with sleeping and eating, for cough is a measure 
designed by nature to rid the dilated tubes of the secretions which certainly 
do harm if they are retained. Ordinarily, expectorant remedies cannot be 
expected to do as much good as they do in ordinary cases of bronchitis. 
The best to be employed are creosote in doses of 3 to 5 minims three or 
four times a day; guaiacol in the dose of 3 minims three times a day, or 
guaiacol carbonate in the dose of 3 grains three times a day. In some 
instances much- good follows the administration of a mixture containing 
iodide of ammonium. Still other cases are benefited by the chloride of 
ammonium. 

It must not be forgotten that many cases of bronchiectasis which 
have lasted for some years suffer as w T ell from feebleness and dilatation 
of the right side of the heart, and the degree of cyanosis and dyspnoea on 
exertion can be much decreased by the administration of small and con- 
tinuous doses of digitalis or strophanthus, and, in some instances, by the 
proper use of strychnine. A certain amount of rest in bed or on a couch 
every day is very advisable; and if the patient seems to have great difficulty 
in expectorating the contents of certain cavities, experiments should be 
made with different postures to determine that in which the cavity is most 
easily drained, and he should be instructed to take this posture in order 
to avoid prolonged and exhausting spells of coughing. 

Within the last few years a number of clinicians have warmly advocated 



388 DISEASES OF THE BRONCHI 

the employment of intratracheal injections of medicaments in cases of 
bronchiectasis. Various mixtures have been employed, of which perhaps 
the most popular have contained menthol, guaiacol, olive oil, or albolene. 
They do little good. In other instances, asserted good results, so far as 
elimination of the symptoms are concerned, have followed the inhalation 
of various drugs, such as the vapor of chloride of ammonium, creosote, 
and tar. 

So far as climatic treatment is concerned, these patients should carefully 
avoid high, dry altitudes, and should resort to hill altitudes or the seaside 
resorts, unless the latter are too damp, in which case the drier places must 
be sought, as, for example, Thomasville, Georgia; Lakewood, New Jersey, 
or some similar spot not too near the sea, where there is a sandy soil and 
a heavy pine growth. Such patients, too, should be warned of the danger 
of complications which may follow exposure to sudden changes of temper- 
ature and to wet, and should wear flannels next to the skin all the year 
round, if possible, to avoid chilling the surface. If these precautions are 
taken, the greater amount of time spent in the fresh air the better, as in-door 
life for these patients is disadvantageous if the climate is at all suitable to 
their condition. 



FIBRINOUS BRONCHITIS. 

Definition. — Fibrinous bronchitis is an exceedingly rare affection, char- 
acterized by the formation of a fibrinous exudate which makes a cast of the 
bronchial tubes. As ordinarily observed it is in no way related to diphtheria, 
in which disease, however, casts of the larynx and trachea and even of the 
bronchial tubes sometimes form. 

Etiology. — The cause of this strange affection is practically unknown. 
When it occurs as a complication or sequel of other diseases, it seems to 
bear no relation to them save that of coincidence. The condition is much 
more frequent in males than in females, and is not particularly prone to 
occur at any particular age. West states the youngest case recorded is 
four years of age, and the oldest seventy-two years. It has occurred more 
frequently after acute croupous pneumonia and during the progress of 
pulmonary tuberculosis and ordinary chronic bronchitis than in other 
maladies, but its occurrence in these affections is not sufficiently constant 
to justify us in considering that these relationships are direct. In some 
instances it is associated with the presence of mitral disease of the 
heart. 

Pathology. — The casts when expelled are found to be composed of masses 
of gelatinous or pulpy-looking material which, when "floated in water or 
carefully spread upon a glass surface, are found to be in the form of the 
bronchial tubes; sometimes even of the smaller tubes. The casts are tough 
and yellowish-white in appearance, and many are composed of fibrin in 
which may be found white blood cells and epithelium from the bronchial 
mucous membrane. Other casts contain no demonstrable fibrin, but are 
rich in mucin. Whether they are distinct forms or altered fibrinous casts 



FIBRIXOUS BRONCHITIS 389 

is not known. The cast may be hollow or filled with gelatinous mucus. 
It is a curious fact that these casts may form without resulting in serious 
lesions of the lining membrane of the tubes, for even the epithelial lining 
of the bronchial tubes may not be found seriously impaired after a cast is 
thrown off (Fig. 53). 

As the affection is very rare, and still more rarely causes death, we know 
comparatively little of its true morbid anatomy. Sometimes casts have been 
found at autopsy when the condition was not suspected to be present, and 
in other cases in which casts had been thrown off in life none have been 
found at the postmortem. 

Fig. 53 




2cm. 

Cast from a case of fibrinous bronchitis. 

Symptoms. — The symptoms of fibrinous bronchitis chiefly consist in 
severe attacks of cough and dyspnoea, the cough being an effort to dislodge 
the membrane and the dyspnoea the result of the obstruction to the respi- 
ration. Sometimes the dyspnoea has been quite urgent, but it has usually 
been almost completely relieved after the cast is expelled. This expulsion 
of a cast may occur once in a lifetime, once in several weeks, once in several 
days, or several casts may be expelled in one day. Rarely the formation of 
a cast suggests periodicity. While the cough is usually severe in the effort 
to dislodge the exudate, the expulsion may be readily accomplished. Occa- 
sionally hoemo'ptysis complicates the case, usually amounting to nothing more 



390 DISEASES OF THE BRONCHI 

than slight streaking of the expelled membrane, but in other instances 
the bleeding is quite profuse. The blood comes from the bronchial, not from 
the pulmonary, vessels. Fever may be present in the acute cases, but is 
usually absent in the more chronic ones. 

Diagnosis. — This condition must be separated from diphtheria, which can 
be done by the absence of false membrane in the fauces and larynx; from 
croupous pneumonia, which is possible by reason of the absence of the 
fever and other signs of that disease; and from foreign bodies in the air- 
passages, which cause dyspnoea and violent attacks of cough, by the history 
of the patient. 

Prognosis. — The prognosis as to return of the disorder is bad, as most 
cases suffer from recurrence, although acute cases in which complete recovery 
has occurred have been reported. In regard to the effect of the disease on life 
it may be said that this varies greatly with the general state of the patient's 
health and upon the gravity of the diseases which are associated with it. 

In cases with no grave complications recovery may be expected in a 
majority, both as to complete temporary recovery and recurrence. 

Treatment. — The only plan of treatment which has proved itself of value 
in a sufficient number of cases to be regarded with any confidence is 
the use of iodide of potassium in full doses. Some patients seem to be 
made more comfortable by the inhalation of steam. Climatic change is 
often essential, and Southern California, or Florida, or Madeira, may be 
resorted to. 

BRONCHIAL ASTHMA. 

Definition. — Strictly speaking, the word " asthma " may be applied to any 
condition in which the respiration is labored and difficult, but in medicine 
it is most commonly used to describe a condition of difficult breathing due to 
constriction of the bronchial tubes and further narrowing of their calibre by 
swelling of the mucous membrane lining them. This state of spasm of the 
bronchial muscle fibres and hyperaemia of the mucous membrane depends 
upon a neurosis. This neurosis may arise in turn from a large number of 
causes, all of which probably exercise their influence through the pneumo- 
gastric nerves. 

It is unfortunate that the term "asthma" has also been applied to labored 
breathing due to various toxaemias, such as uraemia and the coma of diabetes. 
Renal disease may, it is true, indirectly produce true asthma, but this word 
ought not to be applied to that form of labored breathing in which there is 
no swelling or spasm of the sort described in the preceding paragraph. The 
term asthma is, therefore, used in this article to mean bronchial asthma. 

Etiology. — The cause of asthma in many cases cannot be determined, and 
in some persons it is evidently due to some lack of stability in the nervous 
control of the bronchial tubes. In others the asthmatic attack arises 
because of the inhalation of bad air, which acts as an irritant to the respiratory 
tract, either because of the state of the atmosphere itself or because the air is 
laden with dust. The influence exercised by the atmosphere in producing 
asthmatic attacks is very great and varies in different cases to an extraor- 



BRONCHIAL ASTHMA 391 

dinary degree. Mere impurity of the air has little to do with this influence in 
some cases. Thus, I had under my care an old man, from a healthy country 
district in Pennsylvania, who came to Philadelphia to get relief from nightly 
attacks of asthma. Without any treatment the severity of the attacks dimin- 
ished when he breathed city air on the level of the street, dust laden though 
it was, and his attacks ceased entirely so long as he remained in a private 
room of the fifth floor of the Jefferson Hospital, where there was less dust, 
but, perhaps, more smoke and gas from the neighboring chimneys. In other 
instances gases or fumes, as from coal or arsenic, produce an attack, and in 
still others the patient only suffers at that season of the year when the pollen 
of certain plants or flowers is set free. For this reason, sufferers from "hay 
fever'' often suffer from asthma, since the exciting causes of both states are 
present, namely, a respiratory neurosis and the irritants in the air. 

In still other cases the cause lies in the system of the patient and does not 
come from outside. Thus certain persons who are sufferers from gout will occa- 
sionally have attacks of asthma, just as they have pain in the toe or soreness 
in the voluntary muscles ; and, again, it not uncommonly happens that persons 
who have an unstable nerve supply to the bronchial tubes have an attack of 
asthma if exposed to great cold or if they have a slight bronchial congestion 
due to this cause. So, too, such persons may be seized with an attack as the 
result of great physical weariness or of nervous excitement, and it by no 
means rarely happens that feebleness of the heart, which results in poor cir- 
culation in the lungs, produces a seizure in susceptible persons. Such a case 
is called one of " cardiac asthma" In other instances deficient activity of the 
kidneys produces indirectly a similar seizure or so-called "renal asthma." 
In some cases great acidity of the stomach, and the various forms of indigestion, 
reflexly provoke an attack through the gastric fibres of the vagus nerves. 

The nervous mechanism whereby an asthmatic seizure is produced is sup- 
posed to be as follows: The control of the circulation in the bronchial 
mucous membrane, and of the muscular fibres controlling the bronchial tubes, 
resides in the vagus nerves, which possess efferent and afferent fibres, not only 
connected with the lungs, but with the stomach and heart as well. There are 
also, in all probability, fibres which indirectly connect the nasal mucous mem- 
brane with the vagus. Certain causes of irritation acting upon the respiratory 
and gastric and cardiac fibres of the vagus give rise to an afferent impulse sent 
to the vagus centre, and this in turn results in the irradiation of an efferent 
impulse to the bloodvessels in the bronchial mucosa and to the bronchial 
muscular fibres, whereby the tubes are constricted, the mucous membrane 
becomes swollen, and, in addition, secretion takes place, which aids in ob- 
structing still further the smaller tubes. 

Pathology and Morbid Anatomy. — The pathology of this condition has 
been described in part in the preceding paragraph. The morbid change 
which is manifest is the engorgement of the mucous membrane, the thick, 
viscid, bronchial secretion, and the spasm of bronchial tubes. About this 
subject many earnest discussions have taken place and the profession are 
not in accord. Brodie and Dixon speak of four theories as to the cause of 
the attack, but believe that the spasm of the bronchial muscle is the essential 
factor. The other possible factors, in their opinion, are swelling of the 



392 DISEASES OF THE BRONCHI 

bronchial mucosa, the so-called reactionary hyperemia of Traube or vaso- 
motor turgescence of Weber, bronchiolitis exudativa of Curschmann, and, 
lastly, a reflex spasm of the respiratory muscles. 

The morbid anatomy, unless secondary conditions arise, is nil, for with 
the disappearance of the attack the lungs attain their normal state within 
a short time. It is only when repeated attacks of asthma occur that the 
patient as a consequence suffers from chronic bronchitis, emphysema, or 
bronchiectasis, although, if a single attack is very severe, he may develop 
bronchopneumonia, particularly if exposed to cold and dampness. 

The chest of the asthmatic patient, who has suffered from this disease for 
many years, is usually like that of pulmonary emphysema in its configura- 
tion, and if the disease be present in early life, when the chest is very pliable, 
a "pigeon-breast" may be developed, or a well-marked Harrison's groove 
may be seen. 1 

In most instances in which asthma has been present for years the heart 
undergoes dilatation and hypertrophy, particularly on the right side, and 
its beat may be quite feeble if hypertrophy has not fully compensated for 
the dilatation. Secondarily, these cardiac changes may result in hepatic and 
renal congestion. 

The scanty sputum which is expelled by asthmatic patients possesses in 
many instances peculiarities which are pathognomonic. This sputum, if 
examined, is found to contain little lumps or balls, which, if they are teased 
out on a plate of glass placed on a black background, are found to consist 
of minute curls or twisted fibres, in form not unlike the curls of hair on a 
child's head. These curls are called " Curschmann' s spirals," and in their 
folds are found crystals of the fatty acids, the so-called " Char cot-Ley den 
crystals." That fatty acids are present, however, is denied by many. Thus, 
Goodhart and Taslett think these curls are related to the casts of fibrinous 
bronchitis, and they point out that such casts frequently show twists or 
spiral terminations. Hoffmann thinks the terminal bronchioles are spiral 
in form. 

Before and during an attack of pure bronchial asthma there is an 
extraordinary increase in the number of eosinophiles in the blood. This 
eosinophilia is said not to occur in cases of renal and cardiac asthma. 

Symptoms. — The symptoms of spasmodic or bronchial asthma, in well- 
developed cases, are very typical. The patient usually retires to bed per- 
fectly well and wakes at midnight or in the early morning with a sense of 
intense dyspnoea and oppression, which may be so severe as to seem to threaten 
death from asphyxia, but death never occurs in an attack from this cause. 
The attitude of the patient suffering from asthma is most characteristic. If 
he is in bed he sits up and places his hands back of him on the mattress, so as 
to support himself in that posture which will enable him to use his auxiliary 
muscles of respiration to the greatest possible extent. His respirations are 
labored, his brow is covered with sweat, and his face is at first anxious and 
pale, and then cyanosed and livid. The efforts at inspiration and expiration 
are forcible, but the chest has the appearance of distention, since the inter- 

1 "Harrison's groove" is that depression which begins at the sternum at the attachment of the seventh 
or eighth rib, and extends backward in the line of the ribs toward the axilla. 



BRONCHIAL ASTHMA 393 

costal spaces are often unduly full, and the anterior portion of the thorax 
is elevated. The difficulty under which the patient labors is that he retains 
in his chest an excess of air which has become vitiated, but which he cannot 
expel, and therefore he has no room for fresh air. The condition is rather 
one of difficult expiration than of difficult inspiration. Owing to the great 
shortness of breath the patient is often unable to speak except in a whisper, 
and speaks but a word or two with each breath. The superficial veins are 
engorged. The urine during an attack is often scanty and heavily loaded 
with urates, but after the attack it is often passed in large quantities, and 
is clear and limpid. 

The attack may last from half an hour to several hours, and leaves the 
patient quite exhausted. In some instances, with the passing of the seizure, 
almost total respiratory relief follows, but in most cases some dyspnoea per- 
sists for several hours, and cyanosis may be present till all respiratory diffi- 
culty is relieved. If the degree of relief is sufficient to permit sleep, the patient 
may be sufficiently rested to attend to business the following day, but in the 
majority of cases this is impossible, or at least inadvisable, because of the 
fatigue, the weak condition of the heart and lungs from the effects of the 
attack, and the presence of the bronchitis and bronchial secretion, which may 
result in fatal bronchopneumonia if the patient is not very prudent as to 
exposure. 

Diagnosis. — The history of the attack, in its mode of onset and subsequent 
development, renders a diagnosis easy. The duty of the physician is to dis- 
cover, if possible, the cause of the attack and remove it, resting confident 
that asthma is always a symptom and not a disease. The physical signs present 
in an attack are very characteristic. In the early stages auscultation reveals 
harsh bronchial breathing, with musical rales,which may be scattered here and 
there through the chest, and owing to the disturbed respiratory cycle it may 
seem as if one part of the lung does not expand simultaneously with the other 
parts. When the attack is well developed the difficult passage of air 
through the narrow tubes results in the still greater development of musical 
sounds, which may be described as resembling those made by a litter of mew- 
ing kittens or crying puppies. These to-and-fro, loud, musical rales, widely 
diffused through both lungs, are so characteristic of the asthmatic patient as 
to make the diagnosis certain in many cases. 

There is one condition from which asthma in the later stages must be care- 
fully separated, namely, that of pulmonary oedema. Aside from the fact that 
the underlying cause of pulmonary oedema is often serious renal disease, and 
therefore a dangerous state deserving recognition, the history is often given 
of previous attacks of shortness of breath, or even of wheezing respirations; 
and the physical signs in the later stage of bronchial asthma, when widely 
diffused and musical moist rales are heard, may not differ materially from 
those of pulmonary oedema, since musical moist rales and some impairment of 
resonance on percussion may be present in this condition as well. In spas- 
modic croup the obstruction to respiration is so clearly laryngeal and the 
chest is so free from widely diffused rales that the diagnosis is not difficult, 
and in laryngeal spasm due to locomotor ataxia the same freedom from 
musical rales in the chest again enables us to make a differentiation. 



394 DISEASES OF THE BRONCHI 

Sometimes labored respiration resembling that of spasmodic asthma occurs 
in acute pneumothorax, but the physical signs are so different that no 
difficulty is experienced in separating these two conditions. 

Prognosis. — The prognosis as to recovery from an individual attack of 
asthma is very favorable, even if it be exceedingly severe, provided that no 
acute complication arises. The prognosis as to recovery from the tendency 
to asthma is very bad, for the history of the vast majority of cases is that 
they have recurrences. It is only in those cases in which there is a manifest 
exciting cause, external or internal, which can be removed, that a favorable 
prognosis as to the future can be advanced. The tendency of spasmodic 
asthma to produce bronchopneumonia, emphysema, dilatation of the right 
side of the heart, and secondary circulatory feebleness must never be for- 
gotten ; but, on the other hand, it is remarkable that very many asthmatics 
live to moderate old age without being invalided. 

Treatment. — The treatment of spasmodic asthma may be divided into three 
parts : that devoted to the prevention of the attack, the relief of a paroxysm 
which is present, the removal of the underlying causes and of the sequelae 
which are produced by the attack. It has already been pointed out that cer- 
tain conditions of the atmosphere and the presence of certain kinds of dust 
in the air strongly predispose certain individuals to attacks of asthma. On 
the principle that an ounce of prevention is worth a pound of cure, it is 
evident that asthmatic patients should be exposed as little as possible to such 
provoking causes, and if they must of necessity sleep in a room the air of 
which has been heated by a furnace, steam should be disengaged in the air 
of this room, so that it will not be unduly dry. Such patients should be sub- 
jected to a careful examination of the nasal, pharyngeal, and tracheal mucous 
membranes, with the object of discovering whether they suffer from any 
localized spot of hyperesthesia in these mucous membranes, for it not infre- 
quently happens that foreign bodies or dry air may irritate these spots and 
so reflexly produce an attack. Indeed, in some cases of so-called "nasal 
asthma " it is possible by touching a hypersesthetic spot on the nasal mucous 
membrane to precipitate an attack of spasmodic asthma. Such hyper- 
sesthetic spots should be removed by the application of the cautery where it 
can be employed. 

For the relief of the attack of asthma itself when it is threatened, the inhala- 
tion of nitrite of amyl and the drinking of strong, black coffee may be resorted 
to, or a hypodermic injection of morphine and atropine may be given. 

When the attack is developed, an innumerable number of drugs have 
been recommended by various practitioners and by a still greater number 
of sufferers. Among the older remedies, without doubt, belladonna and 
its sister drugs possess the confidence of a large number of the profession; 
but none really exercise a powerful curative influence, unless they are given 
in doses which are so large as to be almost capable of producing moderate 
poisoning. These drugs probably act by their depressant influence upon 
the vagus nerve, and by altering the circulation in the capillaries supplying 
the bronchial mucous membrane. They are particularly useful in those 
cases of asthma in which, during the attack, there is formed a considerable 
quantity of bronchial secretion, and they are the chief ingredients, with 



BRONCHIAL ASTHMA 395 

nitrate of potassium, of most of the proprietary cigarettes and powders which 
are burned in the patient's room. 

Of the so-called depressant remedies for asthma, we have lobelia, which 
is very highly thought of by many practitioners, particularly in England. 
On the other hand, some physicians are afraid of this drug, because of 
the depressant influence upon the heart. It is not to be employed when 
the heart is feeble. When the heart is strong, it should be given in full 
doses, if given at all. As much as J to 1 drachm of the tincture should 
be given in one dose, and repeated in the dose of 10 minims every 
half-hour or hour until the patient's circulation is markedly depressed 
and the skin is relaxed and perspiring. These doses may produce nausea 
and even vomiting, but the associated relaxation often will abort an 
attack, whereas smaller doses which do not produce vomiting may pro- 
duce more profound circulatory symptoms, since all of the drug is 
absorbed and none lost by emesis. Pilocarpine may also be employed in 
those cases of spasmodic asthma in which there seems to be an excessive 
dryness of the bronchial mucous membranes. But the fact that this drug 
in some cases seems to depress the heart seriously, and in others cause an 
excessively profuse outpouring of bronchial secretion, has properly prevented 
its general employment. Many patients experience great relief in the 
early stages of .an attack if they receive a hypodermic injection of \ grain 
of morphine with -^jro g ram °f atropine. In a disease which recurs fre- 
quently, as does asthma, this use of morphine is always dangerous, in view 
of the possibility of establishing the morphine habit. Furthermore, the after- 
depressant effects of the drug upon the following day often renders the 
remedy almost as bad as the disease. 

For internal administration in the treatment of asthma, there is no 
drug which meets as many indications in as many cases as nitroglycerin. If 
the attack is threatened y^ or even -^ of a grain should be given hypo- 
dermically, and the same dose may be repeated every hour or two, particu- 
larly if the patient is one of advanced years and has a somewhat high arterial 
tension. In some cases the inhalation of a few minims of nitrite of amyl, 
poured upon a handkerchief, will serve to abort a threatened attack or to 
modify the severity of one which is already well developed. 

In those cases where there is great irritability of the nervous system 
underlying the asthmatic attack, the occasional use of the bromides may be 
advantageous, but they are of little value for the prevention of an individual 
attack, and their continued use between attacks is obviously unwise. The 
same opinion may be expressed in regard to the employment of chloral, which 
has the additional disadvantage that the chloral habit may be instituted, or 
that the heart may be depressed to an undue degree. 

For many years the author has employed a compound in tablet or elixir 
in the treatment of asthma, both as a preventive remedy and as a cure for 
individual attacks, and has gotten results from it which cause him to regard 
this formula with considerable favor. It is now placed on the market by 
all large manufacturing druggists. 



396 



DISEASES OF THE BRONCHI 



& . — Sodii iodidl .... 


. gr. ij. 


Potas. bromidi .... 


• gr- ij- 


Ext. euphorbiae piluliferae . 


• TTLiij- 


Nitroglycerin! .... 


• gr- ?&<>• 


Tinct. lobeliae .... 


. mu.-M 


Ft. in tabel. vel capsul. No. i. 




S. — One every four to six hours. 





It must never be forgotten, however, that asthma is a symptom rather than 
a disease, and that the remedies which prove useful in one case may in 
another prove entirely useless, because in each instance the underlying cause 
of the malady is quite different. It is this fact which has probably caused 
some physicians to speak in high praise of certain remedies in the treat- 
ment of spasmodic asthma, while others with equal experience assert that 
they have gotten no good results from the employment of such drugs. 

Reference has already been made to the value of supplying asthmatic 
patients with moist air, particularly when they live in furnace-heated houses. 
It is the author's constant habit, when cases of asthma come under his 
care to place them in a bronchitis tent. To the air of this tent is sup- 
plied a small quantity of steam, with the result that the patient has a great 
diminution in the degree of dyspnoea, and frequently gets some hours of 
refreshing sleep. An additional advantage in putting these patients in a 
bronchitis tent is that it requires them to remain in bed, and so gives rest 
to the heart, which organ is often sadly in need of relief, since the difficulty 
of breathing and the lack of sleep throws upon it, day after day, in some 
patients, a very severe strain. In some instances the addition of a few 
grains of menthol to the boiling water seems to increase the efficiency of 
the bronchitis tent. In still others equal parts of oil of pine, oil of euca- 
lyptus, and compound tincture of benzoin may be added, in the quantity 
of a tablespoonful or two to the boiling water, with benefit to the patient. 

In all cases of asthma the physician should carefully examine the heart, 
and if there are any evidences of feebleness and dilatation of the right side 
of the heart, as manifested by venous engorgement, and the extension of 
cardiac dulness downward and to the right, small doses of strophanthus 
or digitalis should be given. In some cases in which the cardiac difficulty is 
marked during the attack, full doses of Hoffmann's anodyne are advisable. 
These drugs may be assisted in their stimulating influence by one or two 
hypodermic injections of strychnine. 

It is also the duty of the physician in all these cases to carefully and 
repeatedly examine the urine, since renal disease sometimes produces true 
asthmatic seizures, and still more commonly produces attacks of dyspnoea, 
which the patient may call asthma, but which are really those of true 
ursemic poisoning. Then, too, if asthma is present with a moderate degree 
of albuminuria without casts, this albuminuria may aid the physician in de- 
termining that the heart is yielding under the strain, since this albuminuria 
is frequently due to renal congestion, resulting from a feeble circulation. 
The albuminuria disappears, the urinary flow becomes more profuse, and 
the heart's action gets better under the administration of digitalis or stro- 
phanthus, combined with rest, as already indicated. 



BRONCHOPNEUMONIA 397 

DISEASES OF THE LUNGS. 

BRONCHOPNEUMONIA. 

Definition. — Catarrhal pneumonia, lobular pneumonia, or bronchopneu- 
monia is an acute inflammation of the small bronchioles and of the tissues 
immediately surrounding them and their attached lobules, and primarily 
involves the lobules, rather than the lobes as does the croupous type of 
pulmonary consolidation. It is called bronchopneumonia because of this 
primary inflammation of the smaller bronchi, and it is called lobular 
pneumonia because it affects the lung by lobules rather than by lobes. 
More commonly still it is designated catarrhal pneumonia, since it usually 
follows inflammatory changes in the mucous membrane of the bronchial 
tubes. No single or specific micro-organism is the cause of bronchopneu- 
monia, but it is due to infection of the bronchi and adjacent tissues by 
many pathogenic germs. 

As with typhoid fever, so with bronchopneumonia: Gerhard, a Phil- 
adelphia student of Louis, in Paris, was the first person to clearly differ- 
entiate bronchopneumonia from croupous pneumonia (1834), although as 
early as 1823 Seger had separated the pneumonia of adults from this form 
which is that which commonly affects children. 

Distribution. — Bronchopneumonia, because of its various causes, is found 
everywhere throughout the world. 

Etiology. — Frequently bronchopneumonia is due to the micrococcus of 
croupous pneumonia, which for some unknown reason fails to produce a 
croupous exudate in a single lobe or in several lobes, as is usual when that 
organism enters the lung in an adult. In other instances pyogenic organisms 
such as the streptococcus or staphylococcus are responsible for the disease. 
Thus, in 103 cases of bronchopneumonia examined by Netter, Weichsel- 
baum, and Pearce, the streptococcus was found in about 30 and the pneu- 
mococcus in 29. When associated with other organisms the number of 
instances in which these cocci were found was much greater. Primary 
bronchopneumonia is usually due to the pneumococcus, and secondary 
bronchopneumonia to the streptococcus. 

When such a specific malady as diphtheria is the primary cause of the 
illness the Klebs-Loeffler bacillus is the most frequent cause of the pneu- 
monic lesions. Thus, in 62 cases of bronchopneumonia following diphtheria 
examined by Pearce, this organism was found 52 times and the strepto- 
coccus 27 times. In still others the bacillus of Pfeiffer (that of epidemic 
influenza) brings on an attack. The tubercle bacillus not rarely is respon- 
sible for the inflammatory process, and almost any pathogenic organism 
entering the lower bronchial tubes may act as an exciting cause. Doubtless 
these organisms often gain access to the bronchioles in periods of good 
health without producing evil effects, but if by chance there is present a 
general or local impairment of vital resistance pathological changes ensue. 

Bronchopneumonia is usually said to be capable of division into two 



398 DISEASES OF THE LUNGS 

types, namely, the primary and secondary. The primary form is met with 
in children and adults who are usually in poor health with diminished 
vitality, and seems to have its onset with the development of an acute "cold." 
It is most commonly met with in infants, and in them, as has just been stated, 
is usually a pneumococcus infection, although true croupous pneumonia at 
this age is not common. The secondary type is much the more frequent of 
the two; indeed, it may be considered the rule that bronchopneumonia 
occurs as a secondary affection in the vast majority of cases, for nearly 
always there is a history of a previous acute or subacute bronchitis, or of 
some disease which predisposes to such a condition, as whooping-cough, 
measles, or influenza. 

In adults there is usually the history of a severe cold affecting the upper 
respiratory tract, or of the use of an anaesthetic drug by inhalation, 
which has at one and the same time irritated the air-passages arid per- 
mitted the entrance of saliva or particles of mucus or food containing 
many micro-organisms which produce infection. A similar result may 
accrue in instances in which no such drug is employed. Thus, in some 
asthmatics during the progress of an attack there may be drawn into the 
air-passages micro-organisms from the mouth or tiny particles of food. 
In individuals suffering from the coma of alcoholism, cerebral congestion, 
uraemia, or apoplexy, with stertorous breathing, the same accident may 
ensue. Such a form of infection may occur in the coma following an epileptic 
seizure. In some instances the presence of an ulcerative laryngitis, due to 
syphilis, tuberculosis, or malignant disease produces an infection in this 
manner. Bulbar paralysis, or that due to diphtheria, may also provoke 
this type of pneumonia. In many cases of severe illness, as in typhoid 
fever, with foul secretions in the nose and mouth, this method of infection 
ensues because the ordinary sensitiveness of the glottic mucous membrane, 
and that of the trachea, is obtunded by the dryness of these parts or by 
the benumbing effects of the disease. This form of the disease is called 
aspiration pneumonia, or the " Schluck-pneumonie " of the Germans. Old 
age and debility are also predisposing causes. 

Prevention. — From what has been said it is evident that the secondary 
forms of bronchopneumonia are capable of prevention, at least to some 
extent. Perfect cleanliness of the mouth is one of the methods of prophy- 
laxis, in that it prevents the inhalation from the oral cavity of infecting 
micro-organisms. So, too, during the course of measles and whooping- 
cough careful avoidance of exposure and the use of a bronchitis tent to 
allay bronchial irritation is preventive in its influence. If local lesions 
in the upper respiratory tract exist, they should be modified or removed by 
proper treatment. 

Frequency. — Bronchopneumonia is an exceedingly common disease 
probably outranking in frequency its sister malady, croupous pneumonia. 
As a terminal infection it causes death in many maladies otherwise almost 
never fatal in themselves, such, for example, as whooping-cough and measles, 
both of which have a high mortality in very young children from this very 
cause. Thus, out of 446 cases of bronchopneumonia in children cited by 
Holt, it followed or complicated whooping-cough 66 times and measles 



BRONCHOPNEUMONIA 1 399 

89 times. It is a noteworthy fact that bronchopneumonia is the type 
which is particularly common in infancy, while croupous pneumonia 
is generally a disease of later life. In the child under five years it is very 
common, and fatal in direct proportion to the youth of the patient, whereas 
croupous pneumonia is rare in this period of life, and very rarely is fatal 
at this time. Out of Holt's 426 cases, 53 per cent, occurred in the first year 
of life and 33 per cent, in the second year. 

Pathology and Morbid Anatomy. — This form of pneumonia, at least in its 
earlier stages, occurs in patches which cause the lung to present during life 
physical signs, and, after death, macroscopic appearances, ordinarily quite 
distinct from those of the solidified or hepatized lung of croupous pneumonia. 
Macroscopically the lung presents a mottled appearance because its surface 
represents three conditions of the pulmonary parenchyma, namely, (a) areas 
of consolidation, (b) areas of atelectasis or collapse, and (c) areas of emphy- 
sema, or enlargement, of groups of vesicles due to overdistention, resulting 
from collapse of adjacent lobules. The consolidated areas are pinkish, 
reddish, or grayish-yellow in hue, the emphysematous patches are paler 
and crepitate when touched, while the collapsed portions are bluish or 
mahogany in color and depressed below the rest of the cut surface of the 
lung. 

The inflammatory process usually begins in the smaller bronchi and 
extends from them to the tissues immediately adjoining, forming patches of 
consolidation, which are deep red in hue, and which extend farther and 
farther from their original site, until perchance they coalesce and form 
fairly large airless consolidations. As the margin of the inflammatory zone 
extends, the primary area of inflammation undergoes necrotic degenerative 
changes, loses its red appearance, and may become grayish, through granular 
and fatty degeneration of the exudate. This inflammatory exudate not only 
invades the peribronchial tissues, but the vesicles as well, so that they are 
rendered airless. If the lung be cut across these patches of consolidation 
will project slightly, and in the centre of each can be seen the cross-section 
of the primarily involved bronchus, which looks whitish, and from which 
mucopus may exude. In some instances in which the infection is severe 
and the inflammatory process rapid, the mucopurulent character of the 
exudate into the bronchial tubes is very well developed, and this purulent 
process may extend into the peribronchial spaces and, in septic cases, cause 
small pyogenic foci. The exudate itself is composed, as would be expected 
from the character of the lesions, of serum, red cells, epithelial cells which 
have separated from the bronchial and vesicular walls, and a large number 
of leukocytes, and in varying numbers the associated bacteria. 

The exudate contains much less fibrin than it does in croupous pneu- 
monia, and a copious fibrinous deposit on the pleura is exceptional. 

If the inflammation of the walls of the bronchial tubes is severe they 
become thickened and swollen, and therefore their lumen is greatly decreased 
or even occluded. This result is greatly aided by their becoming plugged 
with the mucus and dead cells, and so it not infrequently happens that a cer- 
tain area, or several areas, of the vesicular portion of the lung is deprived 
of air and undergoes collapse or atelectasis. 



400 DISEASES OF THE LUNGS 

It is worthy of note that catarrhal pneumonia is in the great majority 
of instances present in both lungs, and that it is not usually conspicuous in 
the bases posteriorly. The anterior portions of the lungs and particularly 
the apices, except in tuberculous cases, show little involvement unless the 
lesions are well developed elsewhere. 

The exudate in bronchopneumonia undergoes resolution, as do most 
inflammatory exudates, by the degeneration of the extravasated and des- 
quamated elements and their speedy absorption or expectoration. With 
this process the material plugging the bronchial tubes disappears and the 
collapsed vesicles, upon receiving their normal supply of air, expand so 
that complete recovery ensues. 

When this does not take place we find the development of dense con- 
nective tissue about the air tubes and between the air spaces, which, as 
it increases in degree, causes thickening and induration. As this process 
increases the connective tissue distorts the lung so that the bronchi are 
twisted or bent, patches of vesicular tissue collapse, secretion is retained in 
the bronchial tubes, and as a result chronic bronchial inflammation, dila- 
tation, or sacculation of these tubes occurs, and the patient becomes a 
sufferer from chronic bronchitis, with bronchiectasis or a chronic broncho- 
pneumonia. 

In other instances old tuberculous lesions are rendered active by the 
acute bronchopneumonia, or a new tuberculous infection is superadded, 
so that the case speedily passes into a well-developed pulmonary tuber- 
culosis. In still other instances the whole process from the very beginning 
is really due to the Bacillus tuberculosis, and the patient rapidly develops 
unmistakable evidences of tuberculous infection, the microscope showing, 
sooner or later, the presence of these organisms in the sputum. In such 
cases the exudate in the air cells goes on to caseation, and may become 
encapsulated or disseminated, depending upon the virulence of the organ- 
ism and the resistance of the patient. 

Symptoms. — The symptomatology of bronchopneumonia varies with the 
'primary cause. If it be primary it naturally presents symptoms which 
differ somewhat from those which it presents when it is secondary, and 
follows some more or less prolonged and exhausting malady. Then, too, 
the symptoms naturally vary with the age of the patient attacked, with the 
areas of the lungs which are involved, and with the severity of the illness 
which has preceded it. 

For the ready study of the symptoms of bronchopneumonia we may 
therefore form at least three classes of cases: those which are distinctly 
primary, those that are clearly secondary, and those which involve the 
small bronchioles very early in the attack, producing what is known as 
acute, suffocative catarrh. 

When the child is attacked with the primary form of bronchopneumonia 
there is usually a chill at onset, which varies greatly in its severity, in some 
cases being so slight that it is scarcely noted, and in others amounting to a 
true rigor. Commonly there is a history that the child has been exposed 
to cold and wet. As in all inflammatory conditions in childhood, there is 
a sharp rise in temperature, almost from the very first an increase in the 



BRONCHOPNEUMONIA 



401 



respiratory rate, and, it may be, very considerable evidence of respiratory 
difficulty. 

It is curious to note how the severity of the symptoms of catarrhal pneu- 
monia vary in different children. Some become dyspnceic very early, and 
others suffer very little respiratory embarrassment through the whole course 
of the malady. 

So sudden may be the onset in this primary form of bronchopneumonia 
that it may be practically impossible for the physician to separate it from 
croupous pneumonia, particularly as children suffering from the latter dis- 
ease rarely bring up rusty sputum, and also because they frequently have a 
pulse rate which is higher in proportion to the respirations than that ratio 
which is common in croupous pneumonia in adults. Cerebral symptoms 
may also be present, just as they are in croupous pneumonia; and this is not 



Fig. 54 




Lung of a child. Catarrhal pneumonia following measles. In the upper left quadrant is part of the 
wall of a small bronchus, the epithelium of which is desquamating (A) ; several air vesicles contain- 
ing catarrhal exudate are shown (B). The connective tissue of the bronchus and the intervesicular 
structure are slightly cedematous and the seat of considerable leukocytic infiltration (C). 

surprising in view of the fact already pointed out, that the pneumococcus 
is the micro-organism most frequently responsible for both forms of pneu- 
monia in children. For this reason, probably, primary catarrhal pneu- 
monia in children not infrequently ends by crisis, and recovery may speedily 
take place after a very few days of illness. Indeed, the outlook in a case of 
this kind in an otherwise healthy child, which is not very young, is usually 
favorable. 

The symptoms of the onset of secondary bronchopneumonia vary greatly 
from those just described. Instead of having a sharp onset the onset is 
insidious. A child having been ailing from some other malady for a number 
of days or weeks, is found to have an accession of fever, to be languid, to 
have a rapid pulse, to have a very marked increase in respiratory rate, and 
26 



402 DISEASES OF THE LUNGS 

the skin is found to be hot and dry. The speed of the pulse is often exces- 
sive, reaching 150 to 200 a minute; but in this disease, as in all others, its 
quality is of as great importance as its speed. An' irregular pulse is of evil 
import. The cough is fairly constant and sometimes produces pain, and if 
the area involved is at all large respiratory embarrassment is early mani- 
fested-. This is shown by the increased number of respirations, by the fact 
that they are somewhat labored, and also by the fact that the intercostal 
spaces are frequently drawn in by the suddenness of the inspiratory move- 
ment. Auscultation will probably reveal in the smaller bronchial tubes 
some fine rales, with exaggerated inspiratory and somewhat prolonged 
expiratory sounds. The breathing is of the exaggerated, puerile type; the 
cough is unproductive. Percussion for the first twenty-four hours of the 
attack may reveal practically nothing. This is in part due in children to 
the resiliency of the entire chest, so that, unless very gentle percussion is 
exercised, the resonance of neighboring parts may cover the impaired 
resonance of the consolidated area. Again, those areas which have under- 
gone compensatory dilatation possess a hyperresonance which may cover 
the impairment. If, however, the pathological lesion is well developed, at 
the end of twenty-four or forty-eight hours careful percussion will usually 
reveal distinct impairment of resonance, particularly if the lesions are, as 
is common, chiefly at the bases posteriorly. 

If the disease is severe the symptoms of dyspna?a may become distressingly 
well marked, and cyanosis may become constant, the child being so short of 
breath that it ceases to cry, and, indeed, may have difficulty in taking liquids 
because of its dyspnoea; that is to say, it is so short of breath that it cannot 
take time to swallow. Usually at this time the expression is somewhat 
anxious. If the dyspnoea has been prolonged enough to exhaust the child, 
and the accumulation of carbon dioxide in the blood has been sufficient to 
benumb its sensibilities, it is markedly apathetic. These symptoms last a 
variable number of days, but usually a change for the better in a mild case 
begins to be noted by the end of the fifth, sixth, or seventh day, and with 
the beginning of improvement in the general symptoms auscultation will 
reveal that the rales in the chest are more moist, that on coughing they 
alter in quality more than before, and, further, air will be found passing 
through portions of the lung which heretofore have seemed devoid of it. 

In other instances the disease runs a much longer course, and the child, 
after hovering between life and death for a number of days, slowly emerges 
from its illness, and the physical signs in the lungs equally slowly disap- 
pear. 

In young children it is by no means an uncommon occurrence for the dis- 
ease to spread in a violent form into the smaller bronchioles, and by the 
swelling of the mucous membrane, the copiousness of the exudate, and 
the wide area involved, produce what is known as acute suffocative catarrh, 
a condition which at one time was considered as a separate entity from 
bronchopneumonia, but which is now recognized as being simply a malig- 
nant form of the disease involving a large number of the smaller bronchi- 
oles, and so greatly interfering with respiration. Another term which has 
also been used to describe this condition is "capillary bronchitis;" in other 



BRONCHOPNE UMOX J A 403 

words, this name is meant to bring out the fact that the finer bronchioles are 
involved. A very excellent term to describe this form of the disease is "acute 
disseminated bronchopneumonia." 

Capillary bronchitis, or acute suffocative catarrh, is one of the most dis- 
tressing acute maladies which affect young children. Its onset is usually 
very rapid, and within twelve or twenty-four hours the child may be 
suffering intensely from dyspnoea. At first, the dyspnoea and inability to get a 
sufficient quantity of oxygen render it fretful and restless ; but very soon it 
becomes weary, and with the weariness of the general system there develops 
a weariness of the respiratory centre, which fails to send out sufficiently 
powerful influences to cause the remaining healthy portion of the lung to 
be completely filled at each inspiration. Very speedily, too, carbonic acid 
gas accumulates in the blood and benumbs the respiratory centre, so that 
within twenty-four or thirty-six hours after the beginning of the malady 
the child may lie in its .mother's arms limp and motionless except for the 
rapid respirations which are required to maintain life. I have not infre- 
quently seen a child in this condition as limp as it is when under the influ- 
ence of ether or chloroform, and only semi-conscious. The finger-nails are 
livid, the lips much darker than normal. The mouth is apt to be excessively 
dry, owing to rapid evaporation of moisture from the high fever and rapid 
breathing. 

During a portion of the attack the respiratory rate may become as high 
as 60 or even 70 a minute, and not infrequently death comes on 
as a combined result of the infection, of the dilatation of the right side of 
the heart, of the accumulation of carbon dioxide in the blood, and of general 
nervous exhaustion. 

Probably the most characteristic symptom of capillary bronchitis is the 
intense dyspnoea, w T hich is quite as acute in some cases as it is in diph- 
theria w T ith laryngeal obstruction. Indeed, I have known intubation to be 
done in a case of capillary bronchitis, it being thought that the child had 
laryngeal trouble in addition to its pulmonary difficulties, although no 
laryngeal lesion was actually present. 

The temperature in cases of capillary bronchitis varies very greatly. In 
some patients it is very high, rising, it may be, to 107°; in other instances 
it rarely passes above 101° or 102°. In the latter type, however, there 
may be a sharp rise a few hours before death. At the time of death the 
temperature may, superficially at least, be subnormal, although the rectal 
temperature may be high. The general run of the temperature pursues 
no definite course as it is wont to do in croupous pneumonia, but progresses 
very irregularly. 

The degree of fever in bronchopneumonia of the secondary type is of 
little value for the purpose of determining the severity of the disease. Some- 
times when the infection is quite severe the temperature may not rise above 
101° or 102°; whereas in other cases which are really less ill, it may reach 
105° or 106°. 

Duration. — The duration of bronchopneumonia varies very greatly with 
the condition of the child at the onset of the disease. In primary broncho- 
pneumonia, occurring in an otherwise healthy child, the malady may last for 



404 DISEASES OF THE LUNGS 

but a few days, and it is a noteworthy fact that it may be arrested in any 
stage of its development, so that recovery may speedily take place. 

In secondary bronchopneumonia the duration is apt to be very much 
longer than in the primary form. Under these circumstances it commonly 
runs a course of from ten days to two weeks, and if the condition of the 
patient is seriously impaired at the time of its onset, it may last for three or 
four weeks. Usually, however, during the last ten days or two weeks of a 
prolonged attack of this character, the symptoms are much modified and 
the temperature is but a little above normal. Whooping-cough, which is a 
very frequent cause of bronchopneumonia, runs a course of from six to 
twelve weeks, and if bronchopneumonia develops early in the attack of 
whooping-cough the persistency of the spasmodic seizures, with their accom- 
panying bronchitis, naturally prolongs the duration of the pulmonary dis- 
order; whereas, in another disease like measles, which runs a much shorter 
course, the pulmonary disorder may disappear almost as soon as the erup- 
tive disease, although very often it persists for a week or ten days, and con- 
valescence from measles is well established. Much depends, too, as to the 
duration of the malady, upon the size of the areas of consolidation and the 
presence of more slowly liquidated exudates. Commonly, the greater 
the area infected, the greater the length of the disease. 

Complications. — The complications of bronchopneumonia are not numer- 
ous. As already pointed out, it occasionally happens that tuberculosis 
develops in the area which is diseased. More rarely still the infection 
of the peribronchial tissues is so severe that pulmonary abscess results. 
Pleuritis is rare unless there happens to be a patch of consolidation close to 
the pleura, in which case a small area may be involved. This rarely spreads 
and still more rarely is accompanied by marked effusion, but it sometimes 
results in empyema. 

Diagnosis. — Bronchopneumonia is to be differentiated from ordinary severe 
bronchitis by the presence of patches of impaired resonance on percussion, 
and by the fact that during the course of an acute bronchitis an exacer- 
bation of temperature and of the general symptoms of severe illness ensue. 
Beyond these points it may be practically impossible to separate the two 
maladies. It is not to be forgotten that bronchitis is not associated with 
hyperresonance in any portion of the chest as a rule, but catarrhal pneu- 
monia is frequently associated with this physical sign. Percussion in capil- 
lary bronchitis may therefore give exaggerated resonance owing to the 
emphysematous state of the vesicular parts of the lung, for, as in asthma, 
the difficulty, which often exists, is an inability to expire some of the air 
which has been taken in by forced inspiration. As has already been stated, 
hyperresonance may completely take the place of impaired resonance due 
to consolidation. 

From croupous pneumonia bronchopneumonia is to be separated by the 
fact that its onset is more gradual or insidious, by the intermittent character 
of the fever, and by the irregular distribution of the physical signs in the 
chest. Another important differential point is the fact that catarrhal pneu- 
monia is usually bilateral and joined at the bases, whereas croupous 
pneumonia is not; that bronchopneumonia is usually well diffused, and in 



BRONCHOPNEUMONIA 405 

both lungs, whereas the croupous type is usually but not always unilateral, 
and commonly limited to one lobe. Croupous pneumonia usually ends by 
crisis, whereas bronchopneumonia may end by lysis. The predominance of 
severe cerebral or meningeal symptoms is rather in favor of the croupous 
type of the disease. 

In many cases it is impossible to determine whether the bronchopneu- 
monia is due to the pneumococcus or some other coccus, or is the result of 
the infection by the tubercle bacilli. In the absence of enlargement of the 
mesenteric glands and of other signs of tuberculous infection, the differential 
diagnosis between bronchopneumonia of tuberculous origin and that due to 
ordinary causes is practically impossible, until the disease has advanced so 
far that other systemic manifestations of tuberculous infection are manifest. 

Sometimes the intermittent and irregular temperature curves of broncho- 
pneumonia suggest the possibility of malarial infection. The differential 
diagnosis in a case of malarial infection, with bronchial symptoms like those 
of bronchopneumonia, can of course only be made by careful examination 
of the blood, and by a more careful study of the temperature chart than is 
usual in the ordinary case. Then, too, in the malarial forms of the disease 
the symptoms will be modified or arrested by the use of quinine. 

As already pointed out, the symptoms of bronchopneumonia, in children 
in particular, vary to an extraordinary degree with the primary illness from 
which the patient has been suffering. Thus, in whooping-cough the onset 
of the disease is often so insidious as to be easily overlooked because the 
rales are mistaken for those of the usual mild bronchitis. In other instances 
the symptoms may be those of tuberculous or acute meningitis, particularly 
in rachitic infants. 

Not rarely an acute diarrhoea may be present, the stools being green and 
containing much mucus, some of which is due to a coincident gastrointestinal 
catarrh, and some of it being from the bronchial tubes, for a child rarely 
expectorates, and usually swallows what he coughs up from his chest. Be- 
cause of the associated indigestion there may be vomiting and distention of 
the abdomen by gas, which factors all aid in increasing the adynamia, and in 
interfering with the cardiac and pulmonary activity. These facts emphasize 
a fact too frequently overlooked, namely, that the condition of the lungs 
should always be carefully investigated in all cases which present signs of 
illness elsewhere, since it may be found, to the physician's surprise, that 
the pulmonary condition is not rarely the primary underlying cause. 

Prognosis. — The prognosis of bronchopneumonia varies very greatly 
with the underlying cause of the disease and with the age of the patient. 
In young infants it is an exceedingly fatal malady, whether it is primary or 
secondary, and during the first year of life, if the disease is well marked, 
the prognosis is always unfavorable. The favorableness of the prognosis 
increases with each year of age. Another important factor in the prognosis 
of these cases is the general vitality of the patient. Children who are natu- 
rally strong and healthy, and are provided with good air and sunshine, have 
a better opportunity than those who live in poorly constructed dwellings 
with bad ventilation, and whose primary vitality is necessarily limited. 
This question of the vitality of the patient is a most important factor from 



406 DISEASES OF THE LUNGS 

a prognostic standpoint, and therefore if the child has been much weakened 
and devitalized by prolonged illness, or has had its heart seriously weakened 
by the prolonged strain of severe whooping-cough, the outlook is much less 
favorable than if the disease attacks the child who is suffering from a mild 
attack of measles. 

The mortality of bronchopneumonia in very young children in private 
practice is probably about 30 per cent.; whereas in asylum practice, where 
it is impossible to provide them with the same amount of fresh air and 
careful nursing, and where the health is often previously impaired, it is not 
infrequently as high as 65 or 70 per cent. While it is true that poorly 
nourished, rachitic children are very apt to fall victims to the disease, it is 
also a fact that well-nourished, stout, fat children sometimes have marked 
difficulty in surviving its attack; and this is particularly true if they are 
"condensed-milk babies," for such children usually have low vital resist- 
ance. The complicating maladies, as, for example, active diarrhoea and 
indigestion or vomiting, of course make the prognosis very uncertain, 
and if they resist treatment are still more cause for anxiety. 

Treatment. — In the treatment of bronchopneumonia it is of the greatest 
importance that the child should be in a well- ventilated room which receives 
as much sunshine as possible, for bronchopneumonia is essentially a disease 
of bad ventilation. The temperature of the room should be kept constant, 
and every care should be exercised that it is not damp. If possible, it should 
be heated by a stove, or by an open fire, rather than by furnace-heated air, 
and if it is necessary to heat it by means of a furnace, care should be taken 
that the air of the room should not be allowed to become unduly dry. This 
may be prevented by having the air from the furnace flue pass over the 
surface of a pan of water, and if the air is very hot and thoroughly dried it 
is better to set free in the air of the room a certain amount of steam from 
a tea-kettle, a pan of boiling water, or by occasionally immersing a large 
piece of quicklime in a bucket of water. 

There can be no doubt that the influence of dusty, impure, or dry air upon 
the bronchial mucous membrane in cases of this disease is most deleterious, 
and I believe that in many instances much better results can be obtained if 
it is possible to place the child in a bronchitis tent, or to provide the air of 
the room with a sufficient degree of moisture to make the apartment the 
equivalent of a bronchitis tent. This can readily be accomplished in the 
way just suggested, or by the use of what is known as a "croup kettle," 
which continually sets free a small quantity of steam. To the water which 
is placed in the croup kettle 1 or 2 grains of menthol may be added every 
two or three hours, and in some instances, for their soothing influence, a 
few drops of oil of eucalyptus and compound tincture of benzoin may be 
so employed. As far as possible the patient should be kept quiet in bed, 
or, in the case of little children, should be moved as little as is consistent with 
comfort; but if the child is very ill, it should not be allowed to lie in one 
posture hour after hour, but occasionally be changed, lest hypostatic 
congestion occur. Easily digested, nutritious food should be given in small 
quantities every two hours. No medicine which may disturb digestion 
should be given to a child in its food. 



BRONCHOPNEUMONIA 407 

In the way of external applications to the chest, the child's back, sides, 
and front may be rubbed with a mixture of a teaspoonful of turpentine 
and three tablespoonfuls of sweet oil. In other instances a weak ammonia 
liniment may be used, or in still other cases oil of amber, in the strength of a 
teaspoonful to two tablespoonfuls of sweet oil. These methods of treatment 
provide sufficient counterirritation and do not maintain the febrile tempera- 
ture as do the poultice or cotton jacket, both of which forms of application 
have now deservedly gone out of use, as it is inconceivable that they can 
favorably affect the lesion in the lung, and they certainly increase the dis- 
comfort, the fever, and the irritation of the child's nervous system. 

Stimulants are not needed in all cases of bronchopneumonia, but are 
used wisely in a larger proportion of patients than in those who suffer from 
the croupous variety of the disease, because bronchopneumonia, as has 
already been pointed out, usually attacks the feeble and therefore those 
who commonly need stimulation. The quantity of stimulant which is 
given varies of course with the feebleness of the heart sounds, the condition 
of arterial tension, and the degree of general nervous prostration. One of 
the best stimulants which can be used is the carbonate of ammonium in 
the dose of 2 or 3 grains every three or four hours to a child of a year or 
two, usually giving it in the syrup of acacia and water. Carbonate of ammo- 
nium, however, acts best when it is given for comparatively short periods of 
time, and for a constant stimulant during the greater portion of the disease 
it is probable that brandy occupies the first place. Care should be exercised 
that the brandy is at least five years old, and that it is as bland as possible. 
It should be given very well diluted by water, and a child of a year may 
take as much as half an ounce to an ounce in twenty-four hours with 
advantage, 30 drops being given every two or three hours. 

As a rapidly acting diffusible stimulant to meet critical periods of depres- 
sion Hoffmann's anodyne in the dose of 5, 10, or 15 drops maybe employed 
in young children. In other instances y^- grain of strychnine may be used, 
or a larger dose than this, it being always borne in mind that the nervous 
system of a child is exceedingly susceptible to this drug. Like the carbon- 
ate of ammonium, strychnine is only to be used when it is necessary to 
bridge an exceedingly 'critical period. If the dose of strychnine is to be 
repeated, -g-J-g- of a grain is a sufficiently large amount. This quantity may 
be given twice, thrice, or four times in twenty-four hours, but, as a rule, it is 
unwise to continue its use for a longer period than this. 

Where the quantity of bronchial secretion is considerable, particularly 
in many cases of suffocative bronchitis, a critical period may be weathered 
by the use of small doses of atropine; from yroo" to -g-g-g- of a grain may be 
given every two or three hours by the mouth, or, if need be, -g-g-g- to -g-^-g- 
may be given hypodermically, if there seems to be danger of the child 
drowning in its own secretions. Oxygen may be taken by inhalation • in 
some cases with advantage. 

The use of antipyretic drugs is to be absolutely condemned. They are 
even more dangerous in this disease than in croupous pneumonia. If the 
temperature is so high as to be dangerous in itself, it may be controlled by 
cool or tepid spongings, with gentle friction; by the use of cool cloths to 



408 DISEASES OF THE LUNGS 

the forehead, or an ice-bag applied to the head if cerebral symptoms are 
marked. Sometimes, too, placing the child in a tepid bath for a few 
moments will act as an excellent antipyretic. 

When the symptoms of respiratory oppression are marked and the fever 
is high, it is often advantageous at a critical period to dip the child alter- 
nately in cool and hot water, the water being hot enough to produce distinct 
counterirritation on the skin, and, reflexly, to arouse the dormant nervous 
system. Under these circumstances the child often rallies, takes deep 
inspirations, dislodges the mucus which is otherwise obstructing its breath- 
ing, and at the same time has a reduction in its temperature. Such an 
alternate hot and cold plunge bath should only be resorted to when condi- 
tions are desperate, and should not be repeated too frequently. A tepid bath, 
the patient being immersed or simply sponged, will also very frequently allay 
restlessness and permit quiet sleep. 

In the protracted cases it is exceedingly important that pure air and good 
food should be provided. Not infrequently the child which fails to improve 
in the city may, when carried in its nurse's arms to the sea-shore or the 
mountains, change for the better to a remarkable degree within a very short 
period of time. This is particularly true if the weather is oppressively hot. 
Such patients also may be benefited in some instances, particularly during 
the winter months, by cod-liver oil inunctions, and, if the digestion will 
stand it, by the administration of small quantities of cod-liver oil or the 
syrup of iodide of iron by the mouth. Sometimes such patients are also 
greatly benefited by the administration of the hypophosphites. 

During the acute stage of bronchopneumonia there is little use in employ- 
ing the ordinary expectorants. During the stage of resolution, if the secretion 
is profuse, small doses, such as 1 or 2 grains of chloride of ammonium, 
with fluid extract of licorice and water, may be given twice or thrice a day. 
Rarely in young children is there much expectoration, either in the sense 
of expelling mucus from the mouth or coughing it up into the pharynx. 
The younger the child the less chance there is of freeing its bronchial tubes 
of secretion by coughing, and care should always be taken that the admin- 
istration of an expectorant, which is not of very great importance, does not 
disorder the digestion, which is of far greater importance to the maintenance 
of the child's health and strength than any medicine can be. 

The bronchopneumonia of adults usually follows asthma or the inspira- 
tion of irritant materials, and must be treated in much the same manner as 
that just described for bronchopneumonia in children, except that the doses 
should be larger in proportion to the age and size of the individual. In 
nearly all cases active stimulation is required, and digitalis and strychnine 
are particularly useful. Counterirritation, freely applied to the chest, seems 
to be of advantage in some instances, but here again the cotton jacket or 
the poultice ought not to be resorted to, as they simply oppress the patient 
and do little good. 

METASTATIC PNEUMONIA. 

Definition. — By the term metastatic pneumonia is meant a condition of 
consolidation of part of one lung, or more rarely parts of both lungs, as 



METASTATIC PNEUMONIA 409 

the result of the plugging of one or more of the pulmonary vessels by an 
embolus which is of septic origin. 

Etiology and Pathology. — As elsewhere, emboli reaching the lung may be 
(1) simple or bland, (2) septic or infective; either of these may be massive 
or small. A large mass thrown into the pulmonary artery at once arrests 
the flow of blood, the patient gives a few gasps, possibly has a convulsion, 
or at least convulsive movements, and dies. Smaller emboli, if numerous 
(an embolic shower), may induce similar phenomena. The simple or bland 
embolus occludes one or more vessels, and leads to the formation of a hemor- 
rhagic infarct. These irregularly shaped or conical areas vary in size, 
depending upon the magnitude of the occluded vessel and the efficiency of 
the collateral circulation. They may be central or peripheral, massive or 
small, single or multiple. 

The question of autochthonous embolism is of pathological rather than 
clinical interest. 

The affected area is airless, denser than the uninvolved pulmonary tissues, 
and near the centre it is dark purple or almost black in recent infarcts, black 
or brownish-black in older areas, and it may be surrounded by a zone of 
reactionary inflammation. If the lesion is peripheral the indurated area 
rises above the level of the pleura and is frequently covered by a delicate 
stratum of fibrin. Certain pleurisies, particularly those following operations, 
have been attributed to pulmonary infarction. Histologically such areas 
when recent show air vesicles occupied by blood cells and fibrin and more 
or less interstitial extravasation. Later the erythrocytes are fragmented, the 
leukocytes increased, phagocytes abundant, and evident reparative processes 
in progress. 

The sputum is more or less blood-stained, and when the infarcts are 
large or numerous it may be intensely so. In fat embolism, such as may 
accompany fractures of the long bones, oil globules may be demonstrable 
in the sputum. 

^Yhether the process arises to the dignity of a pneumonia depends, of 
course, upon the amount of accompanying inflammation. It is evident 
that a few small infarcts irregularly distributed may give rise to no symp- 
toms because of the insignificant lesions induced; or, on the other hand, 
large, or multiple, areas may be accompanied by evident lung symptoms. 
Whether inflammation be marked or slight is so largely dependent upon the 
presence of infection that in the absence of bacteria the name metastatic 
pneumonia is scarcely applicable. 

Embolism due to fragments of neoplasms entering the lungs usually 
escapes notice until the proliferating cells give rise to metastatic tumors. 

The most important and gravest type of metastatic pneumonia is that 
seen in pyaemia. 

During the course of a septic process in any part of the body, even though 
it may be so minute as to escape notice unless carefully sought, it is possible 
for a small clot (embolus) infected by micro-organisms to enter the circula- 
tion and, being carried to the lung, to plug one of the vessels. The difference 
between the infarct resulting from an ordinary embolus and the lesion 
ensuing from one of septic origin is very marked, for in the latter condition 



410 DISEASES OF THE LUNGS 

there speedily develops an acute local process due to the rapid extension 
of the infection from the embolus. In this way the immediate neighborhood 
of the closed vessel becomes engorged ; polymorphonuclear leukocytes accum- 
ulate in the infected area, which rapidly undergoes liquefaction, necrosis, and 
an abscess is formed. As such emboli are rarely solitary, multiple foci are 
prone to develop; these may, by extension, become confluent or successive 
embolic showers may cause closely approximated lesions of different 
ages. 

As the quantity of infective material and its distribution constantly varies, 
the anatomical result of such conditions can rarely be the same in any two 
cases. There may be a single area of infection, or the lung may be riddled 
by abscesses, the "pyyemic pneumonia' ' of old writers. 

The area of solidification in the lung may resemble the patchy state seen 
in bronchopneumonia or the hepatized appearance of croupous pneumonia. 
There is, however, this important difference in the further progress of the 
local lesions between the two diseases named and that under discussion, for 
in metastatic pneumonia the inflammatory process usually goes on to suppu- 
ration, the entire infected area becoming crowded with pus cells and cocci, 
the walls of the vesicles and the connective tissue of the lung breaking down 
instead of remaining intact as in most cases of ordinary pneumonia. As 
a result we find one or more abscesses of the lung which may rupture into 
a bronchus, into the pleural cavity, or even through the diaphragm, and are 
practically always accompanied by marked septic fever. 

The pleura rarely escapes, and empyema, in patients surviving sufficiently 
long, is not uncommon. As the abscesses open into the bronchi and eroded 
vessels give way, pulmonary hemorrhage is prone to occur. Large areas of 
pulmonary tissue may undergo necrosis and further complicate the case by 
the addition of pulmonary gangrene. 

Symptoms. — The symptoms of metastatic or septic pneumonia present so 
little that is characteristic that they are often overlooked. This is because 
the lesion in the lung is secondary to some inflammatory process already 
present, which is responsible for much of the fever and other signs of an 
infection. In the midst of these symptoms, if they are severe, the slight 
exacerbation produced by the embolism is not recognized. It is only in 
those cases in which the area of the lung involved is very considerable that 
pulmonary signs are forced upon the physician, projecting themselves, as it 
were, above those already present. When the pulmonary symptoms are 
marked they so closely resemble those of an acute pneumonia that not 
infrequently the diagnosis of an intercurrent pneumonia is made, only to be 
modified when repeated chills, sweats, and a temperature chart indicative of 
sepsis show that the process in the lung is septic. (See Pyaemia.) 

When the embolus is a large one and plugs the pulmonary artery at its 
bifurcation, death suddenly ensues. 

The physical signs of metastatic pneumonia are practically identical in the 
early stage of the affection with those of bronchopneumonia or croupous 
pneumonia, for the consolidated portion of the lung produces dulriess on 
percussion, bronchial breathing, and increased vocal fremitus and resonance. 
Later, when the consolidated area breaks down and begins to undergo sup- 



PNBUMONOCONIOSIS 411 

puration, the physical signs may be those met with in beginning resolu- 
tion in ordinary croupous pneumonia. 

Prognosis. — The prognosis in metastatic pneumonia is bad because it is a 
septic process and also because it is a serious complication added to a 
process which is already more or less severe. It usually ends in abscess or 
gangrene, and these affections, particularly the latter, are fatal in the great 
majority of cases. ■ In the rare instances in which recovery takes place the 
health of the patient is, as a rule, permanently impaired. I have, however, 
seen two instances followed by abscess end in complete restoration to health. 

Treatment. — There is no specific treatment of this condition unless it be 
known that the streptococcus is the cause of the infection, in which case 
antistreptococcic serum may be employed. Even in these instances, how- 
ever, it cannot do much good because, after the pulmonary vessel is mechan- 
ically closed by an embolus, no treatment can bring about its relief. The 
most that the serum can do is to limit the degree of general toxaemia. 

Ordinarily the treatment must consist in the use of as much easily assimi- 
lated food as the patient can take without disordering his digestion, the 
administration of proper quantities of stimulants, and the careful control 
of such symptoms as may become excessive, as, for example, the reduction 
of high temperature, if it is persistent, 



PNEUMONOCONIOSIS. 

Definition. — This term is applied to a state of the lungs in which, by 
reason of exposure to, and inhalation of, various kinds of dust a deposit of 
the foreign body takes place in the pulmonary tissues and produces secondary 
changes. When the individual is exposed to coal-dust in sufficient amount 
and for a long-enough period to cause its accumulation in the lung, the 
state of the lung is called " antliracosis;" when the dust is derived from the 
grinding of iron or steel, it is called "siderosis ;" when the dust arises from 
stones, the term "lithiasis" or "chalicosis" is employed. Still another type 
of foreign body capable of causing pneumonoconiosis affects those who work 
in large textile industries and shoddy mills. The minute particles of wool 
and cotton, and of the clay used for "sizing," often cause bronchitis and 
favor the occurrence of phthisis. The dust can often be found in the sputum 
of such patients. Reference to this type of the disease is made in the author's 
Fiske Fund Prize Essay for 1885. Still another form of exposure gives rise 
to "grain-shovellers' disease/' and to "potters' rot." 

Etiology. — Under ordinary circumstances the respiratory tract is able to 
get rid of minute foreign bodies which may enter it. This is accomplished 
by the arrest of the dust in the nasal and pharyngeal mucus, and by the 
action of ciliated epithelium lining the larynx, trachea, and bronchial tubes, 
which continually passes along toward the mouth for expectoration any 
dust particles which may enter. If these protective measures are insufficient 
because of the great quantity of dust inhaled, or where after a time this 
ciliated epithelium is destroyed, some of the particles are carried through 
the mucous membrane and are arrested in the nearby connective tissue; 



412 DISEASES OF THE LUNGS 

but if the amount of dust is so large that even this third barrier is passed, 
then the dust particles are taken up by the lymphatics and carried to the 
bronchial lymph nodes, or to the interlobular pulmonary septa under the 
visceral layer of the pleura, or to the substernal lymph glands, where they 
are deposited and remain fixed. Very rarely the fine particles may enter 
the circulation and be deposited in the liver and spleen, as in a case 
reported by Welch, or they may be even excreted in the urine. 

Pathology. — Up to this stage these results may possess no pathological 
significance, but in some instances the presence of large quantities of these 
foreign bodies produce a low-grade inflammatory process in the lung tissues 
which results in overgrowth of connective tissue; that is, a chronic pro- 
ductive interstitial pneumonia or pulmonary sclerosis. Occurring inde- 
pendently of the interstitial change, or associated with it, there is quite 
constantly a subacute or chronic bronchitis and emphysema, and finally 
areas of softening take place, in the fibroid portions of the lungs, which are 
small in size and filled with dust-stained fluid. Sometimes these com- 
municate with a bronchial tube and may then become infected and ulcerate. 
These ulcerated patches or spots of softening may or may not be due to 
infection by the Bacillus tuberculosis. It is by this process that we have 
established "miners' phthisis" or "grindstone consumption" and "gold- 
dust complaint" of the lung. So common is this condition in Sheffield, 
England, that it has been called " knife-grinders' rot." 

Symptoms. — As a rule symptoms of pulmonary trouble do not come on 
in serious form until the individual has been exposed for some months or 
years, when chronic cough, dyspnoea, and loss of flesh call attention to the 
insidious changes in the lungs. A macroscopic or, when this fails, a micro- 
scopic examination will usually reveal the dust in the sputum, and the his- 
tory of the case renders the diagnosis easy. 

Prognosis. — In an investigation carried on at Solingen, Germany, by 
Moritz, it was found that there were no fork-grinders above forty-five 
years of age and no sword-grinders above fifty. Of the total number 
of knife-grinders employed, only 5.5 per cent, were over forty years of age. 
Of the scissors-grinders there were 8.4 per cent, above forty. The fork- and 
sword -grinders work with dry grinding stones, while the knife- and scissors- 
grinders work with grinding stones which are constantly kept moist. The 
relatively greater number of scissors-grinders who live to be over forty is 
explained by the fact that the knife-grinders sit closer to their machines 
than the scissors-grinders, and thus inhale more dust. 

Peabody, in some investigations made at Sheffield, England, found that 
the average period of knife-grinders who are able to continue their work is 
thirteen years. In South Africa, Fox states that the duration of life in 
gold mines where there is much dust from blasting is only four years. Out 
of 1377 rock-drill miners, 225, or 16.34 per cent., died in two and a half 
years. 

Treatment. — The treatment is removal from exposure and the use of the 
medicinal measures advised in the articles on Chronic Bronchitis and 
Emphysema. It is the duty of all employers of labor in dusty places to 
provide free ventilation, both to dissipate the dust and to diminish the 



EMPHYSEMA OF THE LUXGS 413 

chance of tuberculous infection. In many industries the employees should 
use moist respirators to catch the dust in the respired air. Moist or wet 
grinding should be used instead of dry grinding to prevent dust, and 
workmen known to be tuberculous should be excluded from the workshop. 



EMPHYSEMA OF THE LUNGS. 

Definition. — The term emphysema, as applied to disease of the lung, signifies 
a condition in which the air content of the organ, in a large or small area, 
is in excess of the normal. Systematic writers ordinarily make it include 
(1) essential, hypertrophic or large-lunged emphysema; (2) atrophic or 
senile emphysema; (3) compensatory emphysema, a form of vesicular over- 
distention due to inexpansion, or absence, of pulmonary parenchyma in 
some juxtaposed or, less commonly, a distant area, and (4) a form of what 
occurring elsewhere is ordinarily termed "surgical emphysema/' but in the 
lung is called "interstitial," " interlobular," or " intervesicular " — names that 
indicate the location of the air and differentiate the condition from the first 
named states or those forms in which the abnormal air content is intravesicular 

Emphysema has also been divided into an acute and chronic form. In 
point of time the interstitial is always acute, the essential and atrophic 
always chronic, while the compensatory may be either. Some writers 
apply the term "acute" to that condition in which rapid overdistention of 
relatively large areas occurs as a result of violent inspiratory efforts, or 
obstructed expiration, such as occurs in cardiac asthma, bronchial obstruc- 
tion, and allied conditions. 

Briefly described, vesicular emphysema is a state in which there is atrophy 
of the septa between the air cells so that a number of vesicles coalesce. 
As a result we find in the lung many small, bladder-like spaces containing 
air. Associated with this minute change the entire lung increases in bulk 
and the thoracic cavity is usually much increased in all its diameters, 
especially the anteroposterior and the vertical, producing the so-called 
"barrel-shaped chest." 

Etiology. — Much difference of opinion exists as to the primary cause of 
pulmonary emphysema. It is universally acknowledged that the condition 
develops as a result of inadequacy, either congenital or acquired, of the 
supporting elastic tissue between the vesicles; but one school of pathologists 
maintains that the giving way of the vesicular walls depends upon mechanical 
stress, while another school asserts that such a result ensues only when the 
normal support is removed through failure of nutrition in these parts so 
that atrophy results. The author is convinced of the correctness of the 
latter view, namely, that the coalescence of the vesicles takes place only 
after the elastic connective tissue has become wasted as the result of im- 
paired circulatory supply. It is perfectly true that great pulmonary stress 
tends to produce emphysema of the lung, but it only produces this state 
when the connective tissue is unable to provide proper vesicular support. 

Probably in a large proportion of cases the tendency is hereditary, the 
defect is congenital, and the tissues succumb as soon as any great stress is 



414 DISEASES OF THE LUNGS 

put upon them. If this primary nutritional feebleness be admitted as the 
fundamental cause of the condition, it is easy to understand how it is that 
persons so affected fall victims to emphysema when attacked by spasmodic 
asthma, or when following occupations which produce pulmonary stress, 
and it also makes manifest why it is that other persons exposed to equally 
severe exciting causes escape. 

Frequency. — The frequency of true pulmonary emphysema is difficult to 
determine because many of the mild cases are overlooked, and patients do 
not present themselves for treatment until the disease is far advanced. 
To show how widely statistics may vary according to the method of their 
collection, it is interesting to note that Lebert states that pulmonary emphy- 
sema forms about 5 per cent, of all diseases, while Virchow found in nearly 
200,000 cases, admitted to the Charite* in Berlin, that the percentage of 
emphysema was only 0.3, a result confirmed by West at St. Bartholomew's 
in London. The disease is met with three times as frequently in men as 
in women, probably because they are exposed to its secondary causes more 
constantly, and it occurs chiefly between the ages of thirty and sixty years. 
It occurs in children, but rarely before they are ten years of age, although 
cases as young as two years of age have been recorded. 

Pathology and Morbid Anatomy. — It has already been stated that the 
essential characteristic of pulmonary emphysema is the wasting of the inter- 
alveolar tissues so that coalescence of the vesicles takes place. As a result 
small, bladder-like spaces are formed, the lung loses its elasticity, and so 
fails to expel the air on expiration, with the result that the quantity of 
residual air is greatly increased. This results in dyspnoea in two ways: 
first, there is an impaired circulation of fresh air in the lung, and, second, 
there is a decrease in the area of the vesicular tissues, so that a much 
smaller surface is afforded for the absorption of oxygen. 

When the thorax of a case of essential emphysema is opened the lungs do 
not retract as do healthy lungs. Indeed, they may project into the opening 
which has been made. The left lung extends so far forward as to cover 
the heart, and the right lung may overlap the edge of the left. Often the 
epiclavicular spaces are distended by lung tissue, and if the disease be 
marked the convexity of the diaphragm is reduced, with consequent dis- 
placement downward of the adjacent abdominal viscera, particularly the 
liver. 

The chest is changed in appearance because with the increase in the size 
of the lungs the ribs become more horizontal and the intercostal spaces more 
bulging, the sternum and costal cartilages are projected forward, and the 
normal dorsal curvature of the spine is exaggerated. 

When the lungs are removed from the chest it is found that they possess 
four peculiarities aside from their great size: they are pale gray in color, 
unusually free from blood, dry, and when pressed between the fingers they 
lack the crepitation met with in normal lung-tissue. A noteworthy change 
is the presence of dilated pouches or bladder-like protuberances on the 
surface of the lung, and particularly at its margins. If the lung be cut, 
somewhat smaller spaces will be found scattered through it. It is note- 
worthy that in emphysema these open spaces are surrounded by thin walls 



EMPHYSEMA OF THE LUNGS 415 

which readily collapse, whereas the sacculations of saccular bronchiectasis 
are surrounded by areas of thickening and inflammatory change. 

With the coalescence of the air spaces the capillaries which usually 
pass between the vesicular walls disappear, and this in turn diminishes the 
number of pathways by which the blood can pass from the right to the left 
side of the heart. As a result three chief circulatory changes ensue. 
Some of the blood finds its way by large anastomotic channels from one 
side to the other, and so is imperfectly oxidized. The increased obstruc- 
tion to the flow results in distention and arteriosclerotic changes in the 
pulmonary artery, in dilatation, with more or less hypertrophy, of the 
right ventricle and finally in dilatation of the right auricle. Eventually, 

Fig. 55 




Section of anterior margin of the lung from a case of essential emphysema, showing the wasting 
and absorption of the vesicular walls. 

when the pathological process is far advanced we find that the liver is 
greatly engorged with blood, ascites may develop, the cardiac failure 
rapidly progresses, and death results from the various sequences of the 
primary lesions. 

Associated with emphysema there is usually more or less well-developed 
chronic bronchitis. 

Symptoms. — The symptoms of emphysema may be best divided into the 
objective, or those that can be seen by the physician, and the subjective, or 
those described by the patient. 

Physical Signs. — The most noteworthy objective signs are the increase in 
the diameter of the chest, so that the anteroposterior diameter equals the 
lateral; the fulness or bulging of the intercostal spaces; the impaired respir- 
atory movement of the thorax, which may seem quite fixed; the well-filled 



416 



DISEASES OF THE LUNGS 



or distended cervical vessels, and the presence in the epigastrium of the apex 
beat of the heart. If the case is severe we see in addition to these signs 
pulsations of the jugular veins, labored breathing, cyanosis of the lips, 
fidness of the abdomen, due to the displaced and engorged liver, and the 
accumulation of fluid in the peritoneum. Not infrequently inspection of the 
upper part of the epigastrium reveals a network of enlarged capillaries in 
the skin. These are the chief signs on inspection. 

Fig. 56 




Zcm. 



Lung, anterior aspect, from a case of essential emphysema. The large bullae on the anterior margin 
of the middle lobe are nearly two centimetres in diameter. Smaller vesicles are present on the 
anterior margin of the upper lobe and along the diaphragmatic border of the lower lobe. The apex is 
but slightly involved, but in some cases it is markedly affected. 



On further careful physical examination we find on palpation that the 
apex beat cannot be felt at the normal area near the nipple because it is 
displaced and covered by the enlarged lung. The lower margin of the liver 
may be felt as low as the navel. Palpation of the chest while the patient 
speaks reveals a marked decrease in vocal fremitus. Percussion gives a 
high-pitched resonant note all over the chest, particularly over the upper 
lobes; reveals a decrease of the normal area of cardiac dulness; shows the 
liver to be as low as palpation indicated it to be, and gives flatness in the 



EMPHYSEMA OF THE LUNGS 417 

flanks and in the suprapubic area if ascites is present. Auscultation reveals 
a feeble vesicular murmur, marked prolongation of expiration because of the 
inelastic state of the lung, and sometimes there can be heard rales, which 
are due to the associated bronchitis. A curious crackling sound, the 
cause of which is not certain, is also heard sometimes. It is not due to 
pleurisy and is probably produced by the air in the bladder-like dilata- 
tions in the margins of the lungs. This sound is usually best heard at the 
apices. 

Subjective Signs. — The symptoms from which the patient complains 
are chiefly those connected with respiration. The shortness of breath varies 
greatly in different cases. In some it is constant. In others it is only devel- 
oped when exercise is taken, and the difference in its degree on exertion 
varies widely in different individuals. Often dyspnoea is only felt on warm, 
oppressive, or humid days, while in other cases any exertion whatever 
produces such severe dyspnoea that the patient is forced to rest. This 
dyspnoea, as already . stated, depends upon deficient oxygenation of the 
blood, upon the interference with the action of the right side of the heart, 
and upon the inability of patient to take fresh air into his lungs in large 
quantity because of the excess of residual air which is present. 

The cough in some cases is so constant as to greatly annoy the patient. In 
other instances it is almost entirely absent. The development of this symptom 
largely depends upon the degree of bronchitis which is associated with the 
emphysematous change. If marked bronchial irritation is present, the cough 
is not only annoying because of its persistency, but also exhausts the patient, 
and aids in the dilatation and fatigue of the right side of the heart. The 
sputum which results from the cough varies in quantity with the severity 
of the bronchitis which is present, and is not peculiar in appearance unless 
by chance the patient is also a sufferer from asthma, when the characteristics 
of asthmatic sputum may be manifest. The digestive disorders sometimes 
complained of by the patient depend chiefly upon the impairment of the 
circulation in the liver, stomach, and intestines, produced by the secondary 
cardiac lesions. Sometimes, too, the urine is scanty, owing to congestion 
of the kidneys from the same cause. 

Diagnosis — From what has just been said of the symptoms and typical 
signs of pulmonary emphysema it is evident that the diagnosis is not difficult. 
Indeed, in a well-developed case there is probably no pulmonary condition 
so easily recognized. The bilateral increase in the size of the chest, the 
narrowing of the intercostal spaces, the dyspnoea, the cyanosis, the prolonga- 
tion of expiration, the hyper resonance on percussion are all to be noted in 
forming a positive conclusion as to the character of a case. It is not necessary 
for the diagnosis of emphysema that deformity of the chest be present 
Sometimes a marked degree of pulmonary change exists without any change 
in the shape of the thorax. 

Emphysema of one lung is practically never seen, and therefore pneumo- 
thorax can be easily separated from emphysema. 

Prognosis. — The prognosis of emphysema is always unfavorable; at least, 
so far as complete recovery is concerned. In many cases, however, the 
progress of the disease is so slow that the patient may live for years with a 
27 



418 DISEASES OF THE LUNGS 

fair degree of comfort. Indeed, in some instances the pathological process 
becomes stationary. Patients with well-developed emphysema are, however, 
rarely fortunate enough to develop this arrest of the disease, and equally 
rarely live until advanced old age, usually because with advancing years 
the muscle fibre of the right side of the heart becomes less and less able to 
stand the strain which is thrown upon it. 

It is vitally important, so far as prognosis is concerned, for patients suf- 
fering from pulmonary emphysema, to avoid exposure to sudden changes 
of temperature; for such changes may produce a severe bronchitis or pneu- 
monia, conditions which the patient is ill able to withstand. The presence 
of a persistent chronic bronchitis renders the prognosis more grave than if 
this complication does not exist. Death rarely comes on suddenly in these 
patients, but slowly, as a result of constantly increasing circulatory failure. 
Lebert asserts that one-third of these cases die from cardiac dropsy, and the 
rest from pulmonary congestion and gradual feebleness, with slow suffocation, 
increasing cyanosis, and constantly developing bronchitis. 

Treatment. — The treatment of pulmonary emphysema is, unfortunately, 
very limited. There is no curative treatment. The most that the physician 
can do is to improve the condition of the circulation and the nutrition of the 
patient, and to prevent him from throwing severe strain upon his pulmonary 
tissues and his circulatory apparatus. Where the patient follows an occupa- 
tion which is manifestly injurious, he must be advised to give it up, and, for 
that matter, to avoid all violent muscular effort which will throw a strain 
upon his heart and lungs. Incipient attacks of acute bronchitis should be 
treated at the earliest possible moment, and, if chronic bronchitis is present, 
the remedies which are commonly given for that disorder should be em- 
ployed, care being taken, however, that no drug is given which tends, on the 
one hand, to act as a circulatory depressant, and, on the other, to promote 
too free bronchial secretion, for it must always be borne in mind that drugs 
of this character may precipitate an attack of profuse bronchial secretion, 
in which the patient may drown in his own fluids. 

Many of these patients will be benefited by the administration of 5 grains 
of carbonate of ammonium and 5 grains of chloride of ammonium given in 
a cachet, or capsule, or in fluid extract of licorice and water, three or four 
times a day. In other instances, if the bronchitis is chronic and well 
marked, creosote or guaiacol may be used; but care must be exercised that 
they do not disorder the stomach. If the secretion is thick and tenacious, 
iodide of ammonium, or iodide of sodium, in the dose of 5 grains three 
times a day, is useful, care being taken, however, that the administration 
of this remedy does not produce too free bronchial secretion. It must also be 
borne in mind that bronchitis complicating emphysema is not infrequently 
the result of impaired cardiac action, and, therefore, that the best treatment 
for the bronchitis is the administration of cardiac tonics, such as small doses 
of digitalis, 3 to 5 minims twice or thrice a day, or the tincture of strophan- 
thus, or, in other cases, the administration, for a few days, of moderately 
large doses of strychnine or nux vomica. 

When the patient's means permit him, it is important that he should avoid 
extreme climatic changes. High altitudes are, of course, not only disadvan- 



EMPHYSEMA OE THE LUNGS 419 

tageous, but even dangerous to patients suffering from pulmonary emphy- 
sema, because of the dyspnoea which such altitudes produce and because of 
the strain which is thrown upon the dilated right heart. 

In cases of emphysema suffering from an unusually severe attack of 
dyspnoea, with great congestion and engorgement of the venous system, it is 
often advantageous to resort to venesection, removing as much as 20 to 30 
ounces of blood ; but it is manifest that this method of treatment can only 
be resorted to on a few occasions, and when the symptoms of dilatation and 
distention of the right side of the heart and of the liver are very well devel- 
oped. Sometimes in these cases, if there is evidence of hypostatic congestion 
of the lungs, the application of wet or dry cups, posteriorly, near the bases 
is advantageous. 

For many years various text-books have recommended the employment 
of the iodides in their various forms in the treatment of pulmonary emphy- 
sema, with the idea that they distinctly modify the pathological process 
going on in the lungs, and to a certain extent arrest the destruction of the 
elastic tissue which, by its failure, results in the coalescence of the vesicles. 
It must be manifest that even that wonderful drug, iodide of potassium, 
must be quite useless for this purpose in many instances. Any advantage 
which follows its employment probably depends upon its influence upon the 
associated bronchitis, or upon the effect which it produces upon the vascular 
system by diminishing the tendency to atheromatous change, and by reducing 
high arterial tension if it is present, and so relieving the heart of unnecessary 
burden. Still another advantage in the iodides may be that in some cases 
they act as a diuretic and so help to relieve the tissues of an undue quantity 
of fluid if dropsy be threatened. 

Compensatory or Acute Emphysema. — This is an unfortunate use of 
the word emphysema, as the condition is not a true emphysema, but simply 
an abnormal distention of each individual air vesicle by active efforts at 
forced respiration, so that the entire lung may be increased in size and the 
areas of pulmonary resonance greatly increased. Usually in this state some 
high-pitched rales are audible in the chest. The condition may be seen in 
cases which have suffered from stridor due to laryngeal obstruction, or more 
commonly in those who are recovering from an acute asthmatic attack. It 
is also found in those parts of the lungs which have endeavored to compen- 
sate for other parts affected, as, for example, by pneumonia. 

Interstitial Emphysema. — In interstitial emphysema the pathological con- 
dition is not like that of ordinary pulmonary emphysema, for the lung is 
riddled with tiny globules of air which find their way between the lobules 
and underneath the visceral layer of the pleura, where they may form quite 
large blebs. The condition arises whenever air escapes into the pulmonary 
tissues, as after tracheotomy, when it extends down along the trachea into 
the lung itself; fractures of the ribs with puncture of the lung; other wounds 
of the lung; rupture of air vesicles by great thoracic compression, as in sand 
crushes, even without injury to the skeleton, and occasionally results from 
violent abnormal respiratory action, as in whooping-cough, strangling, and 
sneezing. It has been observed after severe convulsions in epileptics and 
eclamptics. 



420 DISEASES OF THE LUNGS 

Small-lunged Emphysema. — Small-lunged emphysema is sometimes 
called senile or atrophic emphysema, or senile atrophy of the lung. It resem- 
bles ordinary emphysema, as just described, in the fact that there is a wast- 
ing of the walls of the air vesicles, so that several vesicles form a larger 
cavity; but instead of the lung being larger and more voluminous than normal, 
it is shrunken and small, so that the heart is uncovered, the diaphragm 
raised in well-marked cases, and the whole thorax distinctly decreased in 
size. The expansion of the vesicles, as in large-lunged emphysema, is most 
marked at the apices and the edges of the lung. Inspection of the chest in 
such a case shows the intercostal spaces obliterated by the drawing together 
of the ribs, while the epiclavicular and episternal spaces are exaggerated and 
the respiratory movement is feeble and very shallow. On percussion the 
chest is found to be hyperresonant everywhere, but there is a great increase 
in the area of cardiac dulness, due to the retraction of the lung. On 
auscultation little that is abnormal is heard, save that expiration may be 
prolonged. 

Except there be an associated bronchitis, the patient with this type of 
emphysema rarely suffers from much inconvenience as a result of the pul- 
monary disease, and life is not materially shortened. 

Treatment. — There is no curative treatment for this type. The physician 
can only order rest, good food, proper clothing, and the avoidance of 
exposure. 

GANGRENE OF THE LUNG. 

Etiology. — This condition arises in individuals whose general vitality is 
greatly impaired by some primary disease, with the result that various micro- 
organisms, putrefactive and otherwise, produce death of part of the 
pulmonary parenchyma, and so a slough is formed. Manifestly, the causes 
of gangrene and abscess must be nearly related, and why gangrene rather 
than abscess should develop in any particular case is difficult to determine. 
Infarction of the lung, or pulmonary hemorrhage, may, by affording a nidus 
for the development of putrefactive germs, result in this state, and so may 
croupous pneumonia; yet it is a curious fact that bronchopneumonia, which 
is often due to profound debility and secondary infection, rarely so results. 
Equally curious it is to note that pulmonary tuberculosis in all its forms is 
rarely complicated in this manner. 

The most common cause of pulmonary gangrene is embolism and 
thrombosis, after this croupous pneumonia, and, thirdly, injuries to the lung 
through the chest wall, as in gunshot injuries. It may also arise from 
foreign bodies in the bronchi. It may also be due to pressure produced by 
an aneurysm, or tumor, or by an extension of an infective process to the 
lung from the oesophagus, pleura, vertebra?, mediastinum, or ribs. It may 
also follow the inspiration of particles of food. Rarely it is due to pressure 
of an aneurysm or to perforation of the oesophagus when that tube is affected 
by cancer. 

Frequency. — Pulmonary gangrene most frequently attacks males in middle 
life — that is, from twenty to forty years of age — and is undoubtedly a very rare 



GANGRENE OF THE LUNG 421 

affection. In a large hospital service only a single case may be met with in 
many years. 

Pathology and Morbid Anatomy. — No description of pulmonary gangrene 
is better than that given by Laennec, who, nevertheless, in an experience of 
twenty-four years, saw only 2 cases. He divides the condition into three 
stages: (1) that of early mortification, in which the pulmonary tissue is 
cedematous and of dark-brown or greenish hue, the sloughing area looking 
shreddy and water-soaked; (2) that of deliquescence or liquefaction, the 
part of the lung affected becoming still more soft and flabby ; and (3) that 
of excavation or abscess formation, in which the lung undergoes the separa- 
tion of the slough and the formation of a line of demarcation to limit the 
pathological process. At this line of separation a consolidation takes place, 
the sphacelus breaks down, and suppuration rapidly results in the coughing 
up of the dead tissues. As a matter of fact, it is incorrect to speak of a single 
sphacelus, for the cavity usually contains separate masses of shred-like 
tissue. 

Finally the limiting wall may undergo fibroid contraction, as it does 
in abscess, and the area be more or less closed, a focus usually remaining, 
from which more or less foul pus is constantly discharged. In the majority 
of cases this reparative process does not occur, and the patient dies. Over 
the seat of the process the pleural membrane is usually thickened and may 
be covered by a fibrinopurulent exudate, while if the pleura be perforated a 
putrid empyema may develop. In such cases pyopneumothorax may also 
manifest itself. Extensive suppuration of the bronchial glands may occur. 

Pulmonary gangrene affects the lower lobes oftener than the upper. 

Symptoms. — The symptoms of pulmonary gangrene in the early stages are 
not very definite. They depend, to some extent, upon the severity of the 
lesions and upon the micro-organisms which produce it. The patient is 
markedly prostrated, the heart's action is feeble and rapid, the skin leaky, 
the face anxious and thin, and the tongue dry and coated. The temperature 
runs the typical course of hectic fever, and it is a noteworthy fact that the 
exhaustion seems out of proportion in its severity to the febrile movement. 
Sometimes these symptoms are ushered in with severe chills, which recur at 
irregular intervals. The respirations are quickened, and there may be cough 
and expectoration, but until the break-down goes on so far as to result in 
suppuration there may be but little material expectorated. If a cavity forms, 
the ordinary signs of excavation, with those of surrounding consolidation, 
may be developed upon auscultation and percussion. 

One of the most characteristic symptoms of pulmonary gangrene is the 
odor of the patient's breath and of the materials which he expectorates. 
There is probably no discharge from the human body the odor of which is 
so penetrating and disgusting as is that of pulmonary gangrene. Not only 
does it render the patient disgusting to everyone who comes near him, 
but it penetrates every part of the room in which he exists, and often can 
be smelled throughout the whole house. On some davs it is worse than 
others, but the variation of the quantity of expectoration does not neces- 
sarily mean a variation in its fetid character. The quantity of material which 
is expectorated does not give any very definite conception of the size of the 



422 DISEASES OF THE LUNGS 

lesion of the lungs. West quotes a case of God lee and Williams in which 
the patient expectorated a quart daily, and yet the autopsy revealed a 
gangrenous cavity which was not large enough to contain more than an 
ounce of fluid. 

The sputum is peculiar, in that on standing it separates into three 
layers. The upper layer is apt to be yellowish-green and opaque; the middle 
layer is opalescent and turbid, and resembles saliva when a considerable 
quantity is gathered in a glass. The lowest layer consists in a mass of 
greenish or brown-looking material, which contains considerable quantities 
of pus, altered red blood cells, and fragments of connective tissue. A careful 
microscopic examination of this sputum will show that it is filled with an 
immense number of micro-organisms, and crystals of leucin and tyrosin can 
be seen in large numbers. Various fatty acid crystals are also present. 
The sputum, at first alkaline, becomes acid, and seems to exercise a peculiar 
digestant or disintegrating influence upon the shreds of connective tissue 
which it contains. 

The cough in a case of pulmonary gangrene varies greatly according to the 
amount of material which is expectorated, and also with the degree of bronchial 
irritation which coexists. Sometimes, after a prolonged spell of coughing, 
a considerable amount of material from the gangrenous area comes away in 
a gush. Sometimes, too, the fluid which is expectorated is distinctly blood- 
tinged, due to the ulceration of small bloodvessels in the part surrounding 
the affected part. Not only may free haemoptysis develop, but septic emboli 
may be carried elsewhere, as, for example, to the brain or liver, and so cause 
secondary abscesses. 

If by chance the patient swallows any of the sputum, septic diarrhoea may 
be established and the stools may also become excessively offensive. The 
degree of exhaustion gradually increases, the heart becomes more and more 
feeble, the patient more and more emaciated, and, finally, dies of asthenia. 

Diagnosis. — The diagnosis between a moderate degree of pulmonary 
gangrene, pulmonary abscess, and bronchiectasis may be almost impossible, 
since, if bronchiectasis exists, the fetor of the sputum may be very marked. 
If the sputum under the microscope shows a large amount of connective 
tissue, the diagnosis is largely in favor of gangrene. The absence of tubercle 
bacilli in the sputum and the presence of the various bodies already named 
as appearing in this fluid will also aid in differentiation of the case. When 
the gangrene cavity is small, a positive antemortem diagnosis may not be 
possible, the more so because of the presence of acid-resisting bacilli, which 
may be mistaken by the novice for tubercle bacilli. 

Treatment.— The treatment of pulmonary gangrene is not promising. It 
is the duty of the physician to maintain the strength of the patient, as far as 
possible, by the administration of nutritious food given at frequent intervals, 
in small quantities, so that the digestion will not be overloaded; to give 
stimulants, as alcohol; and occasionally, if the circulation becomes feeble, 
to administer strychnine hypodermically, or by the mouth. Bitter tonics 
may also be prescribed for the purpose of maintaining digestive activity. 
The employment of antiseptic inhalations, as suggested in the treatment of 
pulmonary abscess, may also be resorted to, but at most only do good by 



PULMONARY ABSCESS 423 

soothing the irritation of the bronchial mucous membranes and cannot, of 
course, influence the pulmonary parenchyma where the disease exists. 

If the evidences of sepsis are marked and anaemia is present, the tincture 
of chloride of iron is to be administered, and the heart supported by alcohol, 
digitalis, and occasionally by caffeine. The internal use of creosote, car- 
bolic acid, and similar substances, with the idea that they exercise a 
beneficial influence upon the gangrenous portion of the lung, is futile. 

A few cases of gangrene of the lung have been treated surgically, with 
success, by incision and drainage. For these methods the reader is referred 
to surgical treatises. 



PULMONARY ABSCESS. 

Etiology. — Abscess of the lung is always due to invasion of its tissues by 
one or more forms of pyogenic micro-organisms. Single large abscess occurs 
very rarely, but it is met with as a sequel of lobar pneumonia, broncho- 
pneumonia, and as a result of injury to the lung by the entrance of foreign 
bodies through the chest wall or by the respiratory passages. Most commonly 
small abscesses are the result of septic emboli. Abscess may be due to the 
extension of a septic process from the mediastinal tissues or of the liver. 
So, too, a suppurative process in the deep tissues of the neck may result 
in secondary infection of the lung. 

When pulmonary abscess ensues after an attack of croupous pneumonia 
or bronchopneumonia, it is usually not single, but multiple, the area of con- 
solidation being the seat of several foci of purulent material. These forma- 
tions are not by any means so rare as in the larger variety. Holt states that 
he found them in about 7 per cent, of the autopsies of young children dying 
of pneumonia. Such foci are really not true abscesses; that is to say, they 
have no true abscess wall. When these formations are numerous, as they 
usually are, and of considerable size, the patient may maintain a high tem- 
perature for a long time after the acute primary disease has passed away, 
and may, by causing septic absorption, ultimately produce the patient's 
death. It may be difficult, even at autopsy, to state positively whether the 
purulent infiltration of the later stages of both forms of pneumonia is 
present, or if there is a true suppurative abscess in the lung. In both cases 
the areas of softening are found to be infected by the streptococcus, 
staphylococcus, or other pyogenic organism. 

When the foci are of large size, and are multiple, the prognosis is bad, for 
widespread suppuration in the lung is always fatal when the breaking-down 
process involves the exudation of pneumonia. If there be a single, large, 
localized abscess involving the area of pneumonic exudate, the prognosis is 
less grave, but it is exceedingly bad, nevertheless. To sum up, therefore, 
we find that suppuration takes place in the lung in three degrees or forms 
after pneumonia: (1) as a mild suppurative process, which is really nothing 
more than a rapid breaking down of the exudate of the disease; (2) as a 
more severe process, partaking more of the character of true suppuration, 
in which multiple and large foci of pus form; and (3) of a single large sup- 



424 DISEASES OF THE LUNGS 

purative process; in other words, a single abscess of the lung. As already 
stated, these so-called " abscesses" rarely have a true abscess wall. 

Abscess, multiple or single, when it arises from the entrance of a foreign 
body, only occurs if that body enables infecting micro-organisms to enter 
the surrounding tissues. Thus, a marble, or small stone, entering a bronchus 
may be there for a long time without causing abscess; whereas, the entrance 
of a piece of food, a straw, or a fragment of cork, or other organic matter 
may speedily cause a septic suppurative pneumonia and death. Such an 
abscess may follow a septic infection in a gunshot injury. 

If by chance the patient recovers from the acute illness, there may be left 
a constantly discharging focus of pus. 

Again, we find pulmonary abscess forming as the result of a septic embolus 
entering the lung. About the site of its lodgement an inflammatory exudate 
rapidly forms, and this speedily proceeds to suppuration. Pus and yellow 
elastic tissue are expectorated, and the patient dies of septic poisoning and 
exhausion, or if recovery takes place there is formed around the zone of 
necrotic tissue a wall of inflammatory exudate, which prevents further 
destruction of the parts, and, with recovery, proceeds to organization, finally 
developing into more or less well-formed fibrous tissue, which gradually 
contracts until the cavity disappears or is greatly decreased in size. We 
have in this type what may be called the true form of abscess as it occurs in 
other tissues; whereas, the ordinary suppurative foci hitherto described 
are hardly to be regarded as true abscesses. Occasionally the abscess 
cavity persists for months, and we have then a chronic pulmonary 
abscess. 

When abscesses elsewhere than in the lung break into its tissues the result 
is not always a pulmonary abscess by any means. It is often extraordinary 
how much foul pus may pass from an empyema or hepatic abscess through 
the lung, and be expectorated, without causing any severe lesions in these 
organs. 

Sometimes suppuration takes place in an echinococcus cyst in the lung. 

Symptoms and Diagnosis. —The diagnosis of pulmonary abscess in its early 
stages may be practically impossible, for there may be present no other 
signs than cough, fever, and scanty expectoration, with patches of impaired 
resonance on percussion. In unresolved pneumonia the physical signs may 
be identical, but the leukocyte count is rarely above 15,000 or 20,000, 
whereas in abscess from 30,000 to 50,000 white cells may be present. As 
the pus is freely formed, much aid may be gained from the temperature 
chart, which may show the long sweeps of septic absorption. There may be 
sweats, chills, and some hectic flushing ; but these do not necessarily point 
to abscess of the lung, for they may be due to empyema or an abscess else- 
where, or be a result of tuberculosis. If the sputum becomes distinctly puru- 
lent, and the microscope shows abundant pus and masses of connective 
tissue without tubercle bacilli, the diagnosis is readily made. About this 
time it may be possible, too, to discover the physical signs of cavity. 

When a single large abscess is present the positive diagnosis may be 
made evident by the sudden rupture of its contents into a bronchus, and 
the expelling through the mouth of a considerable quantity of pus. I had 



CONGESTION OF THE LUNGS 425 

under my care recently a young woman, aged twenty years, who, after an 
attack of typical croupous pneumonia, developed a more and more septic 
temperature, and, finally, expelled at one time nearly a pint of pus from the 
right lung. Constant expectoration of pus persisted for several days, and 
then an equally large amount was expelled, nearly causing death by strangu- 
lation. After a long convalescence she reached perfect health. In this case 
the fluoroscope revealed the site of the abscess very clearly. Care must be 
taken that the purulent expectoration and fetid breath of a case of bron- 
chiectasis is not considered an indication of true pulmonary abscess. 

Prognosis. — The prognosis in these cases is always very grave. Death may 
ensue, not only from septic absorption, but from the gradual exhaustion 
due to prolonged suppuration or from the ulceration of the wall of a blood- 
vessel with consequent severe haemoptysis. Again, a secondary pneumonia 
may develop from the primary suppurative process. 

Treatment. — The treatment of abscess of the lung divides itself into three 
parts : the support of the patient's strength by good food and the moderate 
use of stimulants ; the resort to as much fresh air and sunshine as possible ; 
the inhalation of gentle antiseptic balsams which do not really influence 
the abscess, but perhaps benefit the associated bronchitis; and, lastly, 
by the use of the knife, bone forceps, and the actual cautery, to open the 
abscess through the chest wall and lung. 

As supporting drugs, iron and arsenic, whiskey and port wine, are par- 
ticularly valuable. Easily digested semi-liquid foods, with digestants to aid 
their speedy absorption, are valuable, and in the way of an inhalation equal 
parts of oil of eucalyptus, oil of pine, and compound tincture of benzoin 
may be added to the water in a croup kettle, and so dissipated through 
the air of the room. Codeine and cannabis indica may be used to relieve 
excessive, painful cough; but large doses of these drugs should not be used, 
because they prevent the expectoration of the pus, and if the patient sleeps 
soundly while under their effects, rupture of the abscess may cause fatal 
asphyxia. 

CONGESTION OF THE LUNGS. 

Definition. — Strictly speaking, there is a congestion of the lungs when- 
ever severe exercise is taken, but this, of course, is not referred to here; 
nor is it the intention to consider that form which precedes, or rather con- 
stitutes, the early stage of croupous pneumonia, and which ends in the forma- 
tion of a croupous exudate. The form of congestion here referred to is that 
due to mechanical causes which interfere with the proper passage of blood 
through the pulmonary vessels (passive congestion), or that due to intense 
irritation caused by inhaling irritant vapors or fumes. 

Etiology and Pathology. — The most common cause of pulmonary conges- 
tion is progressive valvular inadequacy at the left auriculoventricular orifice, 
or, in other words, mitral disease, either obstructive or regurgitant. These 
lesions dam the blood back into the lungs, and the right ventricle undergoes 
hypertrophy in an endeavor to drive it onward. As a result the pulmonary 
capillaries are placed under abnormal strain, increased hemolysis occurs, 



426 DISEASES OF THE LUNGS 

and when the condition becomes chronic there is produced what is known 
as brown induration of the lungs. At autopsy they appear of a dull red- 
dish-brown hue, the incised surfaces becoming brighter red after exposure 
to the air. The supporting tissue of the lung is thickened and less elastic 
than normal, and the organ is heavy, as shown by the fact that when placed 
in water it does not float so high as normal lung-tissue. Microscopically 
the connective tissue and the alveolar epithelium, some of which is desqua- 
mated, contain granules of brownish pigment derived from the haemoglobin 
content of the disintegrated red blood cells. 

The bloodvessels are tortuous, and the capillaries which line the walls of 
the alveoli project in loops or tufts into the air spaces. Sometimes haemop- 
tysis of moderate degree arises from rupture of these vessels or those which 
are in the bronchial tubes. It can be readily understood why it is that a 
person with these lesions is a ready victim for pneumonia, hypostatic con- 
gestion, and infarction. 

Acute pulmonary congestion resulting from sudden failure of the left 
ventricle is often the cause of sudden death in the course of an attack of 
sunstroke or after the inhalation of irritant gases. 

Closely connected with this form of congestion from an etiological stand- 
point is hypostatic congestion of the lungs. In this state the lower portions 
of the lungs are commonly affected because the patient is usually in the 
dorsal decubitus and the blood accumulates in the most dependent part of 
the organs. Associated with this accumulation of blood in the vessels of 
the lung, an excess of serum collects in the intervesicular structures, pro- 
ducing oedema, or, passing into the vesicles, causes the affected part to be- 
come essentially airless. 

The causes of hypostatic congestion are not very different from those of 
ordinary congestion as just described, save that the failure of the right side 
of the heart is more marked and the condition is more frequently met with 
as the result of profound asthenia occurring in the course of some malady 
like severe typhoid fever or advanced renal disease. That the dorsal decubi- 
tus is not the chief cause is proved by the fact that many persons suffering 
from certain maladies which require the maintenance of this posture do 
not suffer from hypostatic congestion. That posture exercises some influence, 
however, is shown by the fact that if the patient remains on one side the 
stasis is often unilateral. 

Autopsy in cases of hypostatic congestion reveal the involved areas 
darkened in color, often black or purplish-black in hue. They may be 
airless, with frothy accumulations in the bronchial tubes, loss of crepitation 
on pressure, and a doughy condition when one finger is pressed upon the 
lung, resembling the sensation produced by oedema elsewhere. In some 
cases, not only a serous exudation takes place into the vesicles, but red 
and white blood cells are extruded, which may render the lung so red that 
it looks somewhat as if true croupous pneumonia were present. To this 
state has been applied the term "splenization," in distinction from the red 
solidification in true pneumonia called "hepatization" or " hypostatic pneu- 
monia." Still less frequently actual hemorrhage into the lung occurs as 
the result of giving way of the walls of small vessels. 



CONGESTION OF THE LUNGS 427 

The causes being identical on both sides of the chest, it is natural that 
hypostatic congestion should usually be found to be bilateral. It begins at 
the bases and slowly creeps upward, until it may involve the lower lobes of 
each side, and even the middle lobe on the right side and part of the upper 
on the left. 

Symptoms. — The symptoms of that form which is due to valvular disease 
at first are those of shortness of breath, with repeated attacks of bronchitis, 
which may become chronic. The mucus expectorated may contain tiny 
clots of blood arising from the dilated vessels just described. If the hem- 
orrhage is free an infarct of the lung may develop into an area of consolida- 
tion and haemoptysis may occur. Sometimes this accident follows an 
improvement in the condition of the heart, which is produced by rest and 
tonics, because the renewed strength of the right ventricle ruptures a weak 
and tortuous vessel. 

The symptoms of hypostatic congestion differ greatly with trje rapidity 
with which the condition develops, and the underlying cause. When the 
exudation rapidly takes place evidences of respiratory embarrassment 
develop and dyspnwa and cyanosis are often marked. If the condition is 
slow and gradual, as in most instances, when it complicates some state of 
adynamia, as in severe typhoid fever, the symptoms are so gradual in onset 
that not until the lungs are seriously involved is attention called to respiratory 
disorder. Cases of the acute type are seen chiefly as the result of renal 
disease and cardiac failure, whereas, as just stated, the gradual type comes 
on in the course of the infectious diseases. 

The physical signs of hypostatic congestion are not well marked in the 
early stages. Careful light percussion may reveal slight impairment of 
resonance, and auscultation may discover a few moist rales, which are chiefly 
bronchial, forming small rhonchi or sibilant sounds. These are the signs 
which it is important to recognize,, since it is at this time that the physician 
can do much, in many cases, to limit or even prevent the spread of the condi- 
tion which is beginning to develop. Later on the condition is so well marked 
that the merest tyro can recognize it by reason of the bronchial breathing, 
the moist rales, and the absence of vesicular sounds which have been put 
aside by the exudation. The only thing to be done at such a late hour is to 
endeavor to support the circulation, so that the lesions will not spread and 
so that the patient may be kept going till absorption or resolution occurs. 

The presence of hypostatic congestion is often not recognized, because 
the physician does not carefully examine the lungs. In many cases, too, it 
is agonal, particularly if death comes slowly. 

Diagnosis. — Hypostatic congestion must be separated from catarrhal and 
croupous pneumonia, and from pleural effusion, serous or purulent. An 
important point in the differentiation is the fact that in both forms of 
pneumonia the temperature is usually febrile, and if they complicate some pre- 
existing state the fever is usually exacerbated when the pulmonary condition 
develops, whereas distinct febrile movement is unusual in hypostatic con- 
gestion unless it is in turn associated with a true pneumonic process. 
The sputum, if any is raised, is frothy in cases of congestion, but is sticky 
and rusty in croupous pneumonia, and perhaps mucopurulent in the 



428 DISEASES OF THE LUNGS 

catarrhal form. The cough is loose and productive (juicy) and not hard 
and difficult as in pneumonia. Then, too, the onset of congestion is not 
characterized by a chill nor by pain in the chest. Pleural effusion may be 
separated from hypostatic congestion by a change in the level of dulness 
on percussion when the patient changes his posture, by the fact that the 
percussion note in congestion is rarely as flat as in effusion, by the fact 
that pleural effusion is rarely bilateral, and if at all profuse usually displaces 
the heart to the left if it be on the right side and downward if it be on the left. 

Prognosis. — This depends largely on the promptness with which hypo- 
stasis is discovered and treated, the cause of the condition, and the vitality 
of the patient. When due to renal disease and associated with a general 
tendency to oedema, the prognosis is bad, So, too, if it ensues in a prolonged 
exhausting fever the prognosis is bad because it indicates great feebleness. 
In old persons and in young children it is very often the cause of death 
during the course of other diseases. 

Treatment. — This consists in preventive measures, such as changing the 
posture of the patient every hour, in the use of cold sponging if fever is 
present, to readjust the circulation, and in the proper use of stimulants if 
the heart seems feeble. As soon as any signs of the malady appear, the 
patient should be made to lie on one side and then on the other and not 
upon the back. Two or three dry cups should be applied to the chest over 
the base of each lung posteriorly, or in their place a mustard plaster may be 
used. If the heart is feeble, strychnine, digitalis, and belladonna are useful. 
It may be wise in urgent cases to give strychnine and atropine hypodermic- 
ally and to use Hoffmann's anodyne in the dose of a drachm every hour 
for several doses. Sometimes if the patient is strong enough to stand active 
purgation colocynth or elaterium are valuable cathartics, the latter being 
given in the dose of ^ grain, but when the symptoms are urgent and the 
venous system is engorged free venesection should be practised. 

Manifestly it is the physician's duty in all these cases of exhausting disease 
to carefully listen to the chest at every visit during an illness, to note the 
first sign of this insidious state. 

TUMORS IN THE LUNGS. 

Tumors in the lungs are rarely met with. They may be benign or malig- 
nant, but are usually the latter, and occur as primary or secondary growths ; 
tumors secondary to growths elsewhere being much the more frequent. 
The benign tumors are chondroma, fibroma, osteoma, and dermoid cyst. 
The malignant tumors are sarcoma, carcinoma, and occasionally endothe- 
lioma. The sarcoma and carcinoma usually occur as nodular masses which 
as they grow push the lung-tissue aside, or more rarely they occur as infil- 
trating growths which extend along the bloodvessels or bronchial tubes. 
If the tumors are placed peripherally or are primary, it may be difficult to 
determine whether they are pleural or pulmonary. In cases of Hodgkin's 
disease and in leukaemia typical masses of lymphomatous tissue are quite 
frequently found infiltrating the lung, and they may cause consolidation 
throughout considerable areas. 



TUMORS IN THE LUNG'S 429 

When the malignant growths are secondary they are usually found in 
both lungs unless the tumor is the result of extensive infection, as in the case 
of tumor in the chest wall directly involving the lung tissue through the 
pleura. In such an instance the growth at first is single, whereas when 
it has spread by metastasis it is multiple. Secondary cancer of the lung 
is more frequent in women than in men because of the frequency with which 
women suffer from carcinoma of the breast. 

Symptoms. — The symptoms are not characteristic. They depend largely 
upon the situation of the growth and upon the degree of pressure which they 
exercise upon surrounding tissues. If they press upon nerve trunks they 
cause severe pain; if upon a large bronchus they produce cough and expec- 
toration; and if a considerable area of lung-tissue is involved they cause 
dyspnaa, particularly if the growth or growths press upon the bloodvessels 
and so cause pulmonary congestion or stasis, so that as the disease ad- 
vances pulmonary oedema aids in decreasing the area for the oxygena- 
tion of blood. Great and manifest engorgement of the superficial veins 
of the neck and head is sometimes present as the result of pressure on 
the superior vena cava, and if the vagus or the recurrent laryngeal nerves 
are pressed upon cardiac neuroses and laryngeal spasm or paralysis may 
ensue. 

Diagnosis. — The diagnosis of tumor of the lung when no primary growth 
exists elsewhere is extremely difficult. The presence of thoracic pain, 
in the absence of signs of aneurysm, and inability to discover cardiac 
disease, aortitis, or disease of vertebrae should arouse the suspicion of the 
presence of a growth, which may be confirmed by the presence of dulness 
on percussion in the area affected. When these symptoms develop in a 
patient who has a growth elsewhere, or has had a growth elsewhere which 
has been excised, as in carcinoma of the breast, they possess much more 
diagnostic value. Stokes considered that prune-juice sputum was a very 
typical sign of malignant growth in the lung. Emaciation may be a marked 
symptom, as it is so often in cases of malignant growth elsewhere in the 
body, but the maintenance of flesh by the patient does not negative malignant 
growth, as sometimes little weight is lost. 

It is hardly necessary to add that the malignant tumors are more fre- 
quently met with in middle life or in advanced age than in youth. 

No treatment is of any avail so far as cure is concerned. The most that 
can be done is to support the system by good food and relieve pain by 
morphine. 



430 DISEASES OF THE PLEURA 

DISEASES OF THE PLEURA. 

PLEURITIS. 

Definition. — The term pleuritis, or pleurisy, is applied to an inflammation, 
either acute or chronic, of the serous membrane which lines the thoracic 
cavity and in its reflections covers the lung; the so-called parietal and 
visceral layers of the pleura. This inflammation is always the result of 
an infection by some pathogenic micro-organism. It occurs in four forms, 
namely, as dry or fibrinous, serofibrinous, purulent, when it is called 
empyema, and that due to tuberculosis, or tuberculous pleurisy. Sometimes 
malignant disease affects this membrane, and this may be considered a fifth 
form of pleural inflammation (Figs. 57 and 58). 

Fig. 57 




Carcinomatosis of the costal pleura;. (Kast and Rumpler.) 

Etiology. — As just stated, pleurisy is practically always due to an infection 
by some micro-organism. In a large number of cases it arises as the result 
of an invasion of the lung by the pneumococcus, with or without an associ- 
ated pneumonia. In other instances it is due to the entrance of pyogenic 
organisms such as the staphylococcus and streptococcus, and in still other 
cases from invasion by tubercle bacilli. Infection of the pleura may also 
take place through the pericardium, the mediastinal tissues, the vertebrae, 



PLEURITIS 



431 



and the diaphragm. Sometimes, though rarely, it is from the chest wall 
itself, after injury to the thorax or by extension of infection from the mammary 
gland. Pulmonary abscess may, by the extension of the inflammatory process, 
produce pleuritis, or a bronchopneumonia may cause a secondary infection. 
In some cases, however, the inflammation of the pleura is a primary lesion 
without any pathological change in the lung except as a secondary condi- 
tion. 

The relative frequency with which acute pleurisy is produced by each 
specific micro-organism is unknown, since recovery takes place in mild 



Fig. 58 




Metastatic carcinoma of the visceral pleura. (Kast and Rumpler.) 



cases and no opportunity of determining the provoking cause presents 
itself. The pneumococcus is, however, the cause in the majority of 
cases. 

When empyema follows pleurisy the necessity of setting free the pus 
enables us to determine the character of the infection in the great majority 
of cases, and the statistics derived from this source give us some conception 
of the relative frequency with which pleurisy follows infection by different 
organisms. (See Empyema.) 



432 DISEASES OF THE PLEURA 

Frequency. — Pleurisy is most commonly met with between the ages of twenty 
and forty, but it is by no means confined to these decades of life. On the 
contrary, it is very frequent in young children — at least, as a complication 
of pneumonia in its various forms — and is also not rarely met with in persons 
of advanced years. In adults pleurisy occurs more than twice as often in 
males as in females, but in early childhood this predominance does not 
occur. As an illustration of these facts it is interesting to note that in 651 
cases in St. Bartholomew's Hospital, London, 465 were in males and only 
186 in females. The distribution of these cases as to age was as follows: 
five years and under, 25; ten years, 59; fifteen years, 50; twenty years, 54; 
thirty years, 179; forty years, 149; fifty years, 85; sixty years, 35; over 
sixty years, 15. 

Pleurisy occurs most frequently in the early spring and late autumn, 
when great changes in temperature take place. This does not mean that 
exposure to cold produces pleurisy directly, but rather that the exposure 
reduces vital resistance to such an extent that infection takes place. 

So, too, a number of acute and chronic diseases result in pleurisy, not 
because they have any direct effect on the pleural membrane, but because 
they lower vital resistance at the same time that they expose the pleura to 
infection by their specific germ. Thus, pleurisy may be indirectly pro- 
duced by the acute specific fevers and by Bright's disease, the first of 
which provides a predisposing cause and a specific germ, while the latter 
lowers vital resistance in general. So, too, it is possible for damage to the 
chest wall to result in acute pleuritis. 

It is to be constantly borne in mind that of all specific infections that by 
the tubercle bacillus is the most important, because of the prognosis, because 
it is often insidious, and because it is probably one of the most frequent 
causes of pleurisy. 

The pathology, morbid anatomy, symptomatology and treatment of the 
various forms of pleurisy are best considered under the specific description 
of each type. 

Dry Pleurisy. — Dry pleurisy, as its name indicates, is an inflammation of 
the pleural membrane with a minimum amount of serous exudate. It may 
be circumscribed or localized, as over a tuberculous cavity, or may be dif- 
fused over a large area, as in croupous pneumonia. The pathology and 
morbid anatomy of pleurisy of the dry type may be described as follows : As 
in all inflammations of serous membranes, there is an acute hyperemia 
followed by infiltration and exudation of blood cells, fibrin, and, it may be, 
serum. The pleural membrane is lustreless in appearance, and roughened 
or granular, and is somewhat thickened, partly because of infiltration, but 
chiefly by reason of the fibrinous exudate on its surface. This exudate is a 
primary factor in the formation of adhesions between the visceral and 
parietal layers of the pleura. Sometimes the exudate is remarkably profuse 
or perhaps a number of layers are formed, so that the pleura may exceed a 
quarter of an inch in thickness, and is somewhat reticulated or uneven on 
the surface. Such an exudate is rarely completely absorbed after the attack 
has passed, and it often organizes and produces impaired resonance on 
percussion and other morbid physical signs during the lifetime of the patient. 



PLEURITIS 433 

Symptoms. — The onset of acute dry pleurisy is characterized by a severe 
pain, or "stitch," in the side and by the development of some fever. The 
pain in the side is sharp and stabbing in character and the patient " catches his 
breath," to use a popular expression, when he endeavors to inspire. Speaking, 
coughing, or any movement which causes increase in the thoracic movement, 
greatly increases the pain, which can, however, be markedly relieved, as a rule, 
by strapping the side of the chest which is affected, and so diminishing its 
freedom of movement. The pain which is developed by pressure on the 
chest wall is sometimes of two types, namely, severe pain produced by deep 
pressure, and exquisite tenderness of the skin over that part of the pleura 
which is inflamed. In the great majority of cases the patient states that 
the greatest pain is between the mammary line and the posterior axillary 
line, but it may be complained of in many other parts ox the chest, particu- 
larly if the disease be due to tuberculosis. Young children who have not 
been trained in the localization of pain often state that the suffering is in 
the epigastrium, or in the left or right hypochondrium, and even in adults 
I have more than once seen physicians misled into a diagnosis of appendicitis 
because of the pain referred by the patient to this region, when in reality 
the cause was acute pleuritis. In all cases of pain below the diaphragm it is 
a good rule for the physician to examine the condition of the thoracic viscera 
before asserting that abdominal disease is present. As severe stabbing 
pain in the thorax is sometimes due to aneurysm, muscular rheumatism, 
or intercostal neuralgia, these possibilities must be excluded before we can 
decide that the cause is pleuritis. 

The most important physical sign which determines the diagnosis of this 
affection is the so-called "friction sound" produced by the rubbing of the 
visceral layer of the pleura upon the parietal layer, both layers being rough- 
ened and dried by the early stage of the inflammation. This friction sound 
is usually best heard just below and just back of the nipple on the side 
involved. (See Fig. 59.) In persons who have very thick chest walls and 
who breathe superficially, by habit or because of the pain, it is often necessary 
that they take a deep breath before a friction sound is produced. Sometimes 
the friction sound is so creaking and loud that it sounds like the noise made 
by a new leather saddle when it is first used; at other times it so soft that 
only the most careful auscultation will reveal it, and it may resemble the 
fine rales of croupous pneumonia. In other cases this creaking can be felt 
by the hand of the physician. If the pleurisy be situated near the heart 
the action of that organ may cause the pleural friction sound to occur as 
often as the heart beats, and so lead one to the diagnosis of pericarditis. 
This is called a pleuro pericardial friction sound, and may also depend upon 
a simultaneous development of pericarditis and pleuritis. 

A second important physical sign is the diminished respiratory movement 
on the side of the chest which is affected, as may be seen by the eye and 
recognized by the feeble respiratory sounds when auscultation is performed, 
the semi-fixation of the chest being an effort to decrease the thoracic move- 
ment, and so limit the degree of pain. My colleague, Coplin, has suggested 
that the fixation is in part due to changes in the intercostal muscles them- 
selves. (See article on Croupous Pneumonia.) This fixation may extend to 
28 



434 



DISEASES OF THE PLEURA 



one side of the diaphragm, and so result in decreased abdominal movement 
on that side. The rate of respiration may be increased in order to com- 
pensate for the shallow breathing, but it is never the hurried or urgent 
respiration met with in cases of real dyspnoea. 

There are two other signs of pleurisy which are of some diagnostic value, 
namely, the suppressed cough, which the patient attempts to stifle in order 
to prevent pain, and the attitude of fixation of the body so that inadvertent 
movement of the patient himself, or change in his position made by his 







Fig. 59 






I .'■" 


1 




w 


:l 


- 











Area in which a right-sided pleural friction sound is usually heard best. 



attendant may not produce pain. Sometimes if the skin is not hyperaesthetic 
the patient lies on the affected side to render it fixed, or he may lie on the 
well side to avoid pressure on the involved pleura. 

The fever in acute pleurisy is rarely high in adults, although it may be in 
young persons. Often it never rises above 102°, and the pulse is usually 
only increased by reason of the fever; so that it bears no direct relation- 
ship to the disease. 

Diagnosis. — Dry pleurisy is separated from muscular soreness due to 
strain by the facts just given and by the history of an injury; from muscular 
rheumatism by the fact that signs of this malady are to be found elsewhere; 
from intercostal neuralgia by the inconstancy of that affection, and by the 
fact that ordinary breathing does not increase the pain in the majority of 
cases, and, further, that all three of these conditions are not accompanied 



PLEURITIS 435 

by any febrile movement or evidence of general systemic disturbance. 
Acute pleurisy of the dry type lasts from a few days to two weeks. A 
longer attack than this should arouse the suspicion of the presence of a 
more persistent disease, such as tuberculosis. 

Prognosis. — Barring complications the prognosis is favorable. (See 
Empyema, and Pleurisy with Effusion.) 

Treatment. — The treatment of dry pleurisy consists in applying adhesive 
strips two inches wide, and overlapping one another one inch, from the 
middle line of the vertebra? to the middle line of the sternum, not following 
the line of the ribs, but passing from behind forward horizontally. They 
should be applied from below upward, and with a sufficient degree of pressure 
to produce almost complete fixation of that side of the chest. The pain, 
if it is extensive, may be further controlled by the administration of 3 grain 
doses of Dover's powder every two or three hours. If necessary, a hypo- 
dermic injection of morphine may be given. If the fever is high an ice-bag 
may be applied to the head, and tepid or cold spongings over the entire 
body may be employed. An ice-bag may also be applied to the side of the 
chest which is inflamed, for the relief of pain. 

In the earliest stages of an acute dry pleurisy, in a strong, healthy indi- 
vidual of a plethoric type with a bounding pulse, there can be no doubt that 
the administration of sufficiently large doses of the tincture of veratrum 
viride or the tincture of aconite is advantageous, as it may diminish the 
local hyperemia in the pleura and decrease the action of the heart so that 
it pumps less blood into the inflamed area, thereby causing determination 
of blood to the peripheral capillaries. This vascular relaxation, associated 
with sweating, tends to still further relieve the local congestion, and 
altogether exercises a beneficial influence upon the local lesion. These 
depressant drugs, however, are distinctly contraindicated unless the patient 
is strong and hearty, and after the first twenty-four hours of the illness 
they are probably useless. Indeed, after this time they may do harm. If 
they are used at all, they should be given freely. Thus, 3 minims of the 
tincture of veratrum viride may be given every half-hour until the patient 
is very slightly nauseated or until his skin becomes moist, when the drug 
should be stopped. A similar method of employing aconite may also be 
practised. 

The employment of a poultice, or cotton jacket, in the treatment of 
pleurisy is less and less resorted to at the present time. There is no reason 
to believe that its influence is advantageous, and it very greatly increases 
the discomfort of the patient because of the heat and consequent sweatings 
which are produced. Further than this, there is always danger of the patient 
taking cold by the poultice becoming chilled, or during the removal of 
the poultice or cotton jacket for cleansing purposes. 

It is important to remember that the presence of a moderate pleural effusion 
does not require the physician to institute measures for its immediate relief, 
because in a very considerable proportion of cases absorption will take 
place by natural processes, and so nature will produce a cure. 

Finally, all patients convalescing from an attack of dry pleurisy should 
be instructed to present themselves to the physician several times at intervals 



436 DISEASES OF THE PLEURA 

of a few days, in order that he may have the opportunity of determining 
whether the pathological condition has entirely disappeared. It happens, 
all too frequently, that such patients are discharged "cured" at the end 
of a few days, when they actually have an insidious tuberculosis, the primary 
pleurisy having been due to this cause. 

Pleurisy with Effusion. — While a large proportion of cases of acute 
pleurisy are dry, in the sense that no excess of serum is poured out by the 
inflamed serous membrane, it is not to be forgotten, on the other hand, 
that a considerable number of cases of pleural inflammation terminates in 
more or less profuse outpouring of fluid into the pleural sac. This forms 
what is sometimes called "pleurisy with effusion," or "pleuritic exudation." 
While the dry type often only involves a patch, or small part, of the pleural 
membrane, that form which is accompanied by effusion, unless limited by 
adhesions, usually affects the entire pleura of one side, and, indeed, it may 
be bilateral, although this is, fortunately, a rare occurrence. 

The exudate is composed of two parts: (1) a solid portion, consisting of 
fibrin and cells, which is attached to the surface of the pleura and which con- 
stitutes the basis by which adhesions binding the two layers of the pleura 
together may be formed, and (2) serum or fluid exudate, which may be so 
abundant that the pleural sac is completely filled. This fluid is always 
turbid or cloudy from the presence of degenerated and exfoliated endothe- 
lial cells, particles of fibrin and blood cells, particularly leukocytes. It is 
worthy of note that the pleura in cases of pleuritis, accompanied by 
serous effusion, is usually not so markedly infiltrated as in the dry type. 

These effusions are usually the result of infection by the pneumococcus, 
the staphylococcus pyogenes, and the tubercle bacillus. The latter infection 
is always to be suspected in subacute cases with much fluid and little plastic 
exudate. 

An examination of the literature on the bacteriology of this state 
shows that a large number of organisms have been found in pleural effusions 
and also that in many cases the effused fluid is sterile. (See Empyema.) 
For example, Lemoine made cultures from the fluid of 38 cases of serofibri- 
nous pleurisy, and found it sterile in 28 instances. 

Recovery, which takes place in the majority of cases, occurs by the 
absorption of the serum and the partial absorption and shrinkage of the 
fibrin, but the chief change in the plastic exudate is organization brought 
about by the formation of granulation tissue, which finally becomes dense 
and cicatricial in character. 

There is probably no form of pleural effusion so prone to confuse the 
clinician as loculated or ensacculated effusions. These may form between 
lobes, between the base of the lung and the diaphragm, or on the mediasti- 
nal aspect of the organ. Their localization is maintained by marginal 
adhesions that prevent the diffusion of fluid throughout the pleural cavity. 
Empyema, similarly limited, offers identical difficulties in diagnosis. 

The lung may be markedly distorted, displaced, or compressed by the 
adhesions, and even the heart may be forced from its normal position. 

Symptoms. — The symptoms of pleurisy with effusion are not very char- 
acteristic, except in so far as the physical signs are concerned, but these are 



PLEURITIS 437 

typical, and some of them pathognomonic. If the onset of the attack of 
pleurisy has been sharp the severe pain already described passes away as the 
effusion takes place and so separates the inflamed layers of the pleura, at the 
same time probably depleting them. The fever often diminishes or disap- 
pears when the stage of effusion is reached. Dyspnoea may or may not 
be present, according to the size of effusion, the spaciousness of the chest, and 
the ability of the healthy side to do enough work to compensate for the part 
which is impaired in function. Strong, hearty individuals often seem to be 
more dyspn&ic than feeble ones, probably because in the former case the 
effusion is more rapid and the restricting adhesions are more firm. Cough 
in this stage of effusion is usually not severe, and may be absent, except on 
exertion. It is often due to an associated bronchitis. 

The posture of the patient, if the effusion be large, is usually character- 
istic, in that he persists in lying on the affected side, in order to permit the 
healthy lung to have full play. Turning him on the affected side may 
cause urgent dyspnoea and a sudden change to the erect posture may do 
likewise, since the pressure of the fluid on the diaphragm interferes with its 
movements or with the action of the heart. 

Physical Signs. — The physical signs of pleural effusion are as follows : 
Inspection shows decrease in respiratory movement on the affected side, 
with increased activity on the healthy side; bulging of the entire chest on 
the diseased side, with fulness of the interspaces and some fulness it may 
be in the hypochondrium. Palpation reveals an absence of vocal fremitus 
on the affected side, and if the effusion be on the left side the apex beat of 
the heart is displaced downward and to the right. 

Percussion elicits flatness, or marked dulness, except at the apex above 
the fluid, where the percussion note is peculiarly high-pitched, and almost 
tympanitic — the so-called Skodaic resonance. Percussion of the liver, if 
the effusion be on the right side, may show that the lower margin of liver 
dulness is abnormally low. If the effusion is on the left side, percussion 
shows dulness in Traube's semilunar space. (See Fig. 60.) 

Auscultation discovers that there is an absence of breath sounds in the 
area where percussion gives flatness, except it may be for distant and 
transmitted bronchial breathing. Along the vertebral column and near the 
inner edge of the scapula on the affected side sego phony, or the " bleating 
voice" sound, may be heard if the patient speaks, while vocal resonance in 
the apex of the lung, where Skodaic resonance is present, is greatly 
increased, even to the degree of pectoriloquy. At this place above the 
effusion bronchial or tubular breathing may be very marked. Sometimes 
the breath sounds are even amphoric in character. 

Occasionally, as the result of the formation of adhesions, pleural effusion 
is circumscribed within narrow limits, and the presence of an inflammatory 
exudate produces an area of dulness which is much larger than that space 
occupied by the fluid. The introduction of an aspirating needle for diag- 
nostic purposes may, therefore, readily mislead the physician, since a dry 
tap will often occur unless the needle happens to enter that portion of the 
area of dulness which actually contains the fluid. The mere introduction of 
the needle into the centre of the area of dulness is not necessarily followed 



438 



DISEASES OF THE PLEURA 



by the withdrawal of fluid, since it not infrequently happens that a consider- 
able mass of inflammatory exudate lies to one side of, or above or below, the 
fluid. These loculated effusions are more common in cases of empyema than 
in ordinary cases of pleurisy with effusion. (See Empyema.) 

The rate at which effusion takes place varies very greatly. Rarely the 
chest may become filled in a few days; more commonly it takes a week or even 
three weeks. Rapid effusion is more dangerous than the delayed type, 
because the thoracic viscera in the former case do not have time to adjust 
themselves to the altered conditions. I have seen a case of rapidly forming 
pleural effusion in which sudden death followed the turning of the patient 
on his well side. 

Fig. 60 




_ 




WHBn 



Showing at x mark the so-called area called Trauhe's semilunar space, where, in health, percussion 
gives a tympanitic note, which becomes flat in left-sided pleural effusion. The solid block represents 
hepatic and cardiac dulness. 



The duration of pleural effusion varies very greatly. Small effusions are 
often absorbed with surprising speed within a few days, but large ones are 
often very slowly absorbed and may not be absorbed at all until some of the 
pressure is removed by aspirating the chest. 

Diagnosis. — It is a noteworthy fact that while the diagnosis of pleural 
effusion is very readily made in some cases, in other instances it is so difficult 
as to baffle the most experienced clinician. 

Pleurisy with effusion is to be separated from pneumonia, from tuberculous 
consolidation, from pulmonary oedema and hypostatic congestion, from 



PLEURITIS 439 

new-growths in the lung, pleura, and mediastinum, and from pleurisy 
with great fibrinous exudation and thickening. 

If on examining one side of the chest it is found to present impaired move- 
ment, impaired percussion resonance, and absence of breath sounds, it is 
fair to suppose that the cause is effusion, if in addition we find, in disease of 
the right side, displacement of the apex beat to the left, or, if it be left-sided, 
obliteration of Traube's semilunar space. This opinion is still further 
confirmed if the area of dulness on percussion varies with a change in the 
posture of the patient, and if Skodaic resonance is present above the area 
in which resonance is impaired. On the other hand, it is not to be forgotten 
that high-pitched resonance is often met with in that part of the lung which 
is over an area consolidated by pneumonia. In pneumonia distinct bronchial 
or tubular breathing is usually heard throughout the consolidated area, and 
this, of course, is not the case in effusion; but if the bronchial tubes become 
plugged by secretion in pneumonia, this important differential point is 
destroyed. Again, it sometimes happens that if the physician auscults the 
chest with the unaided ear he can readily hear bronchial breathing even if 
an effusion be present, although if he uses a stethoscope bronchial breath- 
ing seems absent. In pneumonia, however, bronchial breathing is usually 
associated with rales which are absent in effusion. 

Very useful in the differentiation of the two affections is the history of 
the patient, in whom the early symptoms of the two diseases are usually 
quite at variance, unless the case has been one of primary pleuropneumonia. 

In cases of tuberculous consolidation the appearance of the patient and the 
history of onset may be valuable differential points, and if loss of flesh or 
fever is present these facts are still further emphasized. 

When pulmonary oedema is present the presence of moist rales, the 
feeble heart action, and the discovery of some prolonged preceding illness, 
or of renal disease predisposing to pulmonary cedema, and bilateral dulness, 
are the points of value in making a diagnosis. 

In cases of acute pleurisy with great thickening of the pleural membrane 
there may be marked impairment of resonance on light percussion, and a 
friction sound may be heard, but deep percussion may elicit normal pul- 
monary resonance. 

Growths in the lung, or pulmonary abscess, usually are so peculiarly placed 
and surrounded by healthy tissue that careful examination of the chest and 
a study of the patient's history will be sufficient to make the differentiation. 

Pneumothorax is separated from pleural effusion by its high-pitched 
resonance on percussion and the other physical signs of that condition which 
are only partly modified if the pleura is chronically thickened. 

There still remain two important diagnostic points in these cases which 
have to be studied before diagnosis can be reached, viz. : Are the physical 
signs due to the possible presence of subphrenic abscess, which, pushing the 
diaphragm upward, encroaches upon the thoracic space, or are they due to 
abscess or hydatid cyst in the liver? These conditions become manifest if 
the patient is carefully examined for them. Further, their rarity is a point 
against their presence. 

Lastly, it is important to determine the size of the effusion in order that 



440 DISEASES OF THE PLEURA 

the danger to the patient may be appreciated. It is not possible to even 
approximate the actual quantity, because the capacity of the chest varies 
greatly in different cases, but the extent of the effusion can be decided by 
the line at which percussion dulness first changes to impaired resonance, 
and higher to high-pitched resonance. 

After a diagnosis of pleural effusion has been made, the question which 
arises is whether the effusion is serous or purulent, and if serous whether 
it is the result of inflammation or transudation. This is a most important 
question, since the treatment is quite different in each instance. 

This may be determined by performing paracentesis thoracis and to a 
great extent by an examination of the fluid after it is withdrawn by 
aspiration. Its specific gravity, if the cause be of an inflammatory nature, 
varies from 1.010 to 1.018, and it contains large amounts of fibrin and 
albumin. On the other hand, the fluid due to transudation in dropsy 
shows a specific gravity of only about 1.008 and contains little fibrin and 
albumin. (See Hydro thorax.) When the effusion is due to tuberculosis 
the specific gravity is very high (1.012 to 1.024). The symptoms and 
diagnosis of empyema will be found discussed below. 

Cytoscopy in Pleural Effusion. — In 1900 Widal and Ravaut called 
attention to the cytologicai examination of the fluid of pleural effusion, 
asserting that the nature of the pleurisy can be determined by the organized 
elements held in suspension in the exudate. According to their observations, 
the fluid of tuberculous pleurisy is characterized by the presence of lympho- 
cytes, that of the acute infective pleurisies by polymorphonuclear leukocytes, 
and that of the pleurisies dependent upon new-growths and the aseptic pleu- 
risies accompanying renal and cardiac disease, by shreds of endothelium. 
Further investigations have not confirmed these results, for Naunyn found 
that the effusions complicating Bright's disease often contain lymphocytes 
instead of endothelium shreds, and Tarchetti and Rossi found lymphocytes 
in only a portion of the tuberculous effusions which they examined. More- 
over, Patella's investigations convinced him that lymphocytes are not char- 
acteristic of primary tuberculous effusions. On the other hand, Barjone and 
Cade, and Gemelli, of Milan, have found lymphocytes in the fluid of all 
tuberculous pleurisies. From what has been said, it is evident that the sub- 
ject is yet in its experimental stage, but the discovery of a marked lympho- 
cytosis in the fluid is certainly of some value as indicating tuberculosis, 
particularly if it is associated with other signs. So too high a count (60 to 
90 per cent.) of polymorphonuclear cells is indicative of an infection by 
the pneumococcus. 

Prognosis. — The prognosis in cases of pleural effusion is favorable, except 
in two conditions. If the formation of the fluid is very rapid and very copious, 
pressing upon the heart and lungs and seriously impairing their action so 
that dyspnoea becomes urgent, the prognosis is, of course, grave, unless relief 
is given by thoracentesis. Again>if the effusion is primarily due to tuberculosis, 
or to nephritis, which, by decreasing vitality, has permitted infection to take 
place, the prognosis must be correspondingly grave as to ultimate recovery. 

Treatment. — The early stages of pleurisy with effusion are, of course, 
treated in a manner identical with that already described for a dry pleurisy. 



PLEURITIS 441 

It is only when the effusion has formed and is in such large quantity that it 
produces pressure upon a vital organ, or, again, when it remains un- 
absorbed for a considerable period of time, that the physician should 
undertake measures for its removal. 

The only measure of any value when the pressure is sufficiently great to be 
producing serious symptoms is " tapping" the chest by means of an aspi- 
rator. The skin over the affected side should be first thoroughly cleansed, 
as if for the performance of a minor surgical operation. A hollow needle 
having a moderately wide calibre, and attached to a rubber tube three feet 
long, which is filled with fluid, is then pushed into the pleural cavity in the 
sixth or seventh interspace in the midaxillary line. Care should be taken 
that the aspirating needle should be kept well down on the upper surface 
of the nether rib, in order to avoid injuring the intercostal artery, and the 
physician should grasp the needle with his thumb and forefinger not far 
from its point, so that after it pierces the skin it will not suddenly plunge 
into the chest for several inches, and so, perhaps, do damage to deep-lying 
tissues. No sooner does the needle enter the pleural cavity than the end of 
the rubber tube is lowered to a level with the floor and the contents of the 
pleura is in this way siphoned out of the chest. The advantage claimed for 
this method of treatment is that the degree of suction is at no time great, 
and, furthermore, it is constant. Again, there is no danger of the fluid being 
withdrawn with too great rapidity. 

A very much more frequently resorted to measure of performing paracen- 
tesis thoracis is to attach a large needle, or trocar and cannula, to a piece of 
rubber tubing, which, in turn, is attached to a tube running through the 
cork of a bottle in which a vacuum has been produced by a small hand- 
pump. The entrance to the bottle is guarded by a small stopcock. After 
the needle has been placed in the chest, the trocar is withdrawn, the stop- 
cock is turned, and the fluid is drawn by the vacuum from the chest into 
the bottle. It is rarely if ever proper to completely empty the chest by 
this means at one sitting, particularly if the effusion has been a large one. 
Too rapid withdrawal of the pressure in the thorax may cause serious 
disturbance of the action of the heart, or too rapid an expansion of that 
portion of the lung on the affected side which has been compressed by the 
fluid, with the result that damage is done to the pulmonary tissue, or that a 
peculiar form of gelatinous exudation into the lungs takes place, which is 
only relieved by constant and exhausting cough, and sometimes results 
fatally. 

Should constant cough develop during paracentesis, it is best to discon- 
tinue the operation at once. 

It is also important to remember that not infrequently the withdrawal of 
a small quantity of the effusion, by the relief of pressure and the establish- 
ment of normal lymphatic and blood circulation in the chest wall, may 
result in the natural absorption of the remaining fluid with a very consider- 
able degree of rapidity, so that even if the chest is not emptied by the 
aspiration it may become so in a few days by a natural process. This holds 
true with particular force in those cases of large pleural effusion which do 
not require interference because of pressure symptoms, but which do not 



442 DISEASES OF THE PLEURA 

undergo absorption by natural means until after absorption has been 
stimulated by the performance of paracentesis. 

It is necessary that the physician should exercise care in inspecting his 
needle before he employs it. Experienced clinicians have frequently been 
infected by a dry tap when they were skilful enough to diagnose an effusion, 
but careless enough not to notice that their needle was plugged. 

A pleural effusion should not be permitted to remain too long in the chest, 
since its presence tends to increase the organization of the inflammatory 
process on the surface of the lung, or results in the formation of such 
firm adhesions that decortication of the lung by the surgeon is necessary if 
recovery is to ensue. 

The employment of purges, diuretics, or diaphoretics in cases of pleurisy 
with effusion, with the object of causing an absorption of the fluid, is, for 
very good reasons, futile in almost every instance. It has already been 
pointed out that in this disease the pleura is almost invariably covered by a 
dense fibrinous exudate, which is plastic in character and mechanically 
interferes with the absorption of the exudate. Even if the physician is able, 
by the administration of powerful hydragogue cathartics, to cause a concen- 
tration in the blood, this concentration does not result in the absorption 
of' the pleural effusion, because of the obstruction just spoken of, and also 
because absorption takes place from the pleura chiefly by the lymphatic 
vessels, and not by the bloodvessels. The only result of administering pow- 
erful diaphoretics and cathartics to patients suffering with effusion following 
pleurisy is to exhaust their vitality without materially influencing the local 
condition. 

The application of blisters to the chest, with the hope that they will 
stimulate absorption, is probably quite as futile as the employment of 
purgatives, although they may indirectly result in the absorption of fluid 
by stimulating the removal of the film of plastic exudate which covers the 
pleural membrane. 

The condition in pleural transudations following, or accompanying, car- 
diac or renal dropsy is quite a different one from that due to inflammation. 
In the latter condition there is not any fibrinous exudate, and the effusion 
takes place by a process of transudation from the vessels, the fluid being 
quite different in its character from that found after the acute inflammatory 
process just discussed. Purgatives may therefore do good. 

Aside from the operative measures, which are necessary in about one- 
half the cases of pleurisy with effusion, the physician should administer 
mild tonics, with the object of aiding digestion, and he should support 
the system by the administration of proper quantities of nutritious food. 
If after tapping the fluid it recurs, it should be withdrawn a second time. 
Such a recurrence rarely takes place in the effusion following pleurisy, 
although it is not infrequently met with in cases of ordinary transudation 
into the pleural cavity in other pathological states. 



PURULENT PLEURAL EFFUSION, OR EMPYEMA 



443 



PURULENT PLEURAL EFFUSION, OR EMPYEMA. 

Definition and Etiology. — By empyema we mean a condition in which pus 
has accumulated in the pleural space or spaces. It was taught at one time 
that such an effusion might primarily be serous and by infection become 
purulent, but at present this view is not generally held. Empyema occurs 
as a sequel to infection from the lung in the great majority of cases, but it 
may arise from primary infection of the pleura. The condition is far more 
common in children than in adults (Fig. 61). In children it is generally 
the result of the presence of the pneumococcus, which commonly causes a 













































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61 


















































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cases occurring in five hospitals in the United States and England. 



444 



DISEASES OF THE PLEURA 



bronchopneumonia or a croupous pneumonia first and an empyema after- 
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Chart showing morbidity percentage of empyema due to the pneumococcus at different ages, based 
on 286 cases collected by Netter. Large percentage in childhood. 



Empyema is sometimes due to infection by the Bacillus tuberculosis, and 
it is a fact worthy of note that the pus in such cases is usually sterile, only 
revealing the presence of tubercle bacilli, when by chance some of the exudate 
which lines the pleura is obtained through the aspirator. In other words, 
sterile pus from an empyema raises a suspicion of tuberculous infection. 
Bacteriological examination of pus from 311 cases of empyema, occurring in 
hospitals in the United States, Canada, England, France, Germany, Austria, 
and Italy, showed that the pneumococcus was the infecting organism in 92 



PURULENT PLEURAL EFFUSION, OR EMPYEMA 445 

cases, the streptococcus in 58; the tubercle bacillus in 30. In the remaining 
cases the pus was sterile, or more than one micro-organism was found. If 
children are excluded from these statistics, the streptococcus becomes the 
most common infectious agent. 

When no pulmonary lesion can be discovered in a case of empyema, it 
must be recalled that a very small and insignificant lesion in the lung, and, 
therefore, one which is easily overlooked, may be the focus for a very severe 
pleural infection, and, therefore, the inability of the physician to find a 
primary pulmonary lesion does not prove that it has not existed. 

The character of the pus found in cases of empyema varies considerably 
in different cases, the variation depending in part upon the micro-organism 
which has produced the condition, and upon the duration of the malady at 
the time the effusion is examined. Usually it is creamy and homogeneous; 
in other cases it is thin and separates on standing into a thick and thin layer. 
When the effusion is an old one, the pus may be quite thick and curdled in 
its appearance, containing clot-like masses or shreds of fibrin, which plug 
the aspirating needle and make aspiration impossible. While the color is 
commonly a creamy yellow, it is sometimes slightly pinkish in appearance, 
and may be greenish in hue, and in still other cases, when a considerable 
amount of blood has been extravasated into the effusion, it is a dirty, pale- 
cocoa color. In some instances, as in cases due to infection by the pneu- 
mococcus, the pus is almost odorless, while in others, particularly if the 
empyema has ruptured into a bronchus, it is fetid. 

Purulent effusion in the pleural space is usually profuse. Indeed, it has 
been taught that as a class these collections are larger than are serous effu- 
sions, which is not, however, always true by any means. On the other hand, 
they are very much more likely than are serous effusions to be walled off and 
encysted by reason of adhesions, thereby forming a small pocket of pus. 

Symptoms. — If after an attack of pneumonia the temperature does not fall, 
or if, after it has been normal or near normal, it begins to rise again, and 
the patient has chills or chilly sensations, empyema should be sought for. 

The symptoms of empyema in general are those of impaired health. The 
patient is, as a rule, pale and ill-looking, suffers from loss of weight, and 
sweats, which are particularly prone to come on when he sleeps. 

A moderate fever may be present, and suppressed or even well-developed 
chills may recur. It is important, however, to remember that in some cases 
none of these constitutional symptoms are manifest, the fever in particular, 
being so mild that they fail to attract attention, so that the condition of 
empyema is suspected only when some shortness of breath calls attention to 
the thorax. 

The pus in cases of empyema sometimes becomes so completely walled off 
from the surrounding tissues that it remains for weeks without producing 
any signs of its presence, but in other cases, and these are the more numerous 
it causes such severe pressure symptoms or so much evidence of sepsis that 
relief is demanded by the patient. In other cases — and these are often those 
in which the empyema has not been recognized — the pus burrows its way out, 
rupturing into a bronchus or perforating the chest wall. Very much more 
rarely it empties into the pericardium, or even into the oesophagus. In other 



446 DISEASES OF THE PLEURA 

instances it has perforated the diaphragm, although this process is, curiously, 
much more rare than the rupture of a subdiaphragmatic abscess into the 
pleural cavity. 

Statistics as to the relative frequency with which rupture into a bronchus 
takes place are not in accord. Thus, of 195 cases of empyema occurring in 
St. Thomas' Hospital, London, and in the Leeds General Infirmary, 11 
ruptured into the lung, a percentage of 5.64; while an analysis of a large 
number of cases of empyema collected by Netter gave a percentage of 26.2 
rupturing into the lung. These latter figures certainly must be far too high. 

The physical signs of empyema have already been discussed when describ- 
ing those of serous effusion, for in both states they are practically the same. 
Sometimes the presence of pus may be shown by an adema of the superficial 
tissues, which is often met with over deep-seated suppurations. Empyema 
is also apt to produce more bulging of the intercostal spaces than is serous 
effusion, perhaps because there is more wasting, and so the bulging is more 
readily observed. In some instances of empyema, however, the contrac- 
tion of the thickened pleura draws the edges of the ribs so closely to one 
another that bulging of the interspaces is obliterated. 

When pulsation is transmitted to the purulent effusion, so that the impulse 
is manifest through the interspaces, it is called " empyema necessitatis ." 

Complications. — The chief complications of empyema have already been 
named, viz., sepsis and perforation. The signs of sepsis are similar in this 
state to those produced by accumulations of pus elsewhere, and require no 
further discussion. The symptoms of perforation into a bronchus consist 
of an attack of violent coughing, during which the patient expels, in large, or 
sometimes in small amount, a quantity of almost pure pus. After the pus 
first appears, it is commonly brought up in mouthfuls several times a day, 
and more rarely in such large quantities as to threaten the patient with 
suffocation. This drainage of pus through the lung, curiously enough, 
rarely causes serious permanent damage to the lung, which may ultimately 
entirely recover if the physician will but provide an opening in the chest wall 
for proper drainage. 

When the pus escapes externally by burrowing, it most frequently does so 
about the sixth intercostal space in the axillary area, but it sometimes bur- 
rows a great distance and escapes by way of numerous openings. In other 
instances it burrows far down the trunk and discharges as low down as the 
pelvis. Indeed, Barton has reported a pulsating empyema in the left lumbar 
region. These openings may persist for many years, and if the suppurative 
process persist, amyloid disease of the liver and kidneys may ensue. 

Diagnosis. — The differentiation of empyema from serous effusion is to be 
made by the presence of the septic symptoms just named, and by the use of 
an aspirating needle to determine the character of the fluid. The localized 
types of empyema are those which offer real difficulty in diagnosis, since the 
pus may be between two lobes of the lung, or at the base of the lung next 
the diaphragm, or be extended over a considerable area while very shallow, 
or, again, the inflammatory process in the adjacent lung tissue causes the 
presence of the physical signs of consolidation of the lung or of large effusion, 
when in reality the purulent collection is a small one. In these cases the 



PURULENT PLEURAL EFFUSION, OR EMPYEMA 447 

introduction of the aspirating needle may fail to reveal the presence of pus, 
because the instrument does not happen to exactly strike the purulent focus. 

When the pus is localized by adhesions in the neighborhood of the heart, 
this organ may be displaced by the pressure and transmit its impulse to the 
effusion, so giving rise to the belief that a purulent pericarditis is present; 
the absence of this more serious state being revealed only when the pus is 
set free. 

A still more difficult condition to discover is interlobar pleurisy with 
effusion. In such cases if the accumulation is pus, it may rupture into the 
bronchi and give rise to the belief that the patient has true pulmonary 
abscess. 

Prognosis. — The prognosis in empyema in children, over three years of 
age, if the condition is due to the pneumococcus, and if the pus is allowed to 
escape before it has done much damage, is surprisingly good, both as to rapid 
and complete recovery. Not only do many of these cases soon cease to form 
any more pus, but the compressed lung expands with remarkable rapidity, 
and may, in the course of a few months, fill the pleural cavity so well that 
nearly all traces of the disease may disappear. When the disease affects 
infants the outlook is bad, because of their susceptibility to wasting processes 
and their low vital resistance. 

In streptococcus infection the prognosis is not so favorable, nor is it good 
in tuberculous empyema, for in the first type the formation of pus is persistent 
and the deformity of the chest is very apt to be great, while in the second 
type a primary infection elsewhere is usually present. 

It has been stated by some authors that an empyema may undergo absorp- 
tion. While a decrease in the size of the effusion may result from the absorp- 
tion of some of its fluid constituents true disappearance of pus from the 
thorax does not take place unless it is let out or escapes spontaneously. It 
may, however, become inspissated and encysted. 

Treatment. — There is but one thing to be done in cases of empyema, 
and that is to let out the pus, treating the case as one of ordinary abscess. 
If the quantity of the fluid is sufficiently large to compress and displace 
adjacent organs, particularly the heart, it is better to first relieve some of this 
pressure by aspiration, as in a case of serous effusion, removing enough of 
the pus to permit the heart and vessels to slowly regain their normal position. 
As the pus in these cases is often under great pressure, so that it squirts 
several feet when an incision is made, I am confident that this preliminary 
modification of the pressure is wise in most cases. On the following day 
or, if need be, immediately after aspiration, an incision should be made 
between the sixth and seventh, or seventh and eighth, ribs in the middle 
axillary line, and this opening should be maintained by the insertion of a 
doubled, or extra-large, drainage tube or by a gauze drain. If the ribs have 
been drawn so closely together by the contraction of the parietal pleura 
that free drainage cannot be obtained, then the upper surface of the lower 
rib should be cut away until drainage is free, or, if need be, several 
inches of the rib or of several ribs should be resected. This is usually 
necessary in streptococcus infection. As a rule, the milder measures suffice 
in children, but if the formation of pus persists resection should always be 



448 DISEASES OF THE PLEURA 

performed. For the details as to the exact technique of these operative 
procedures reference should be made to a surgical work. 



CHRONIC PLEURISY. 

Definition. — Chronic inflammation of the pleura may be nothing more 
than a sequence of some of the acute conditions already discussed. If a 
fluid accumulation, serofibrinous or purulent, be allowed to remain within 
the chest cavity, important alterations take place in the serous membrane. 
With the subsidence of infection reparative efforts lead to the production of 
fibrous tissue, which greatly thickens both parietal and visceral layers and 
ensheaths the collapsed lung, eventually forming such a dense investing 
membrane that re-expansion becomes impossible. In other cases the fluid 
is absorbed and the pleural surfaces coated by inflammatory products come 
in contact, coalesce, and become fused by permanent organization of the 
exudate. In the latter group of cases the pleural cavity may be obliterated, 
or partial adhesions only may form. In some cases unattended by frankly 
expressed acute inflammation, hyperplastic thickening of large or small 
areas, usually with adhesions, occurs. In such cases the newly formed 
inflammatory tissue may attain a thickness of 1 cm. or more and not in- 
frequently contains calcareous plaques. 

The third form is called "primitive dry pleurisy" in the sense that it 
begins without effusion and often without pain, and is not associated with 
fever. The patient may himself feel the pleural friction. Finally, limited 
adhesions occur between the layers of the pleura, but they do not cause 
marked interference with the lung nor deformity of the chest. 

The fourth type is the so-called "primitive dry pleurisy" described by 
Sir Andrew Clarke, in which the layers of the pleura become adherent and 
thickened as in the forms just described. From the visceral layers of the 
pleura bands of connective tissue penetrate and traverse the lung almost 
as if they were true trabecular. The effect of these bands as they contract 
is to produce bronchiectasis and some distortion of the lung in its lower 
lobe, where the process is nearly always situated. The condition is really 
a pleurogenous interstitial pneumonia. These cases are not identical in 
character with those due to old empyema. 

Occasionally in chronic pleurisy large calcareous or even bony plates are 
developed in the newly formed inflammatory tissues. 



HYDROTHORAX. 

This condition is to be clearly separated from ordinary pleural effusion 
due to inflammatory changes. Pleural effusion due to inflammation is 
usually unilateral, but hydrothorax is generally bilateral. The fluid in the 
pleural cavities is present as a result of transudation in cases of renal disease, 
cardiac disease, profound ansemia, or any cause which tends to impede cir- 
culation or to increase the readiness with which the serum can escape from 



PNEUMOTHORAX, HYDROPNEUMOTHORAX, PYOPNEUMOTHORAX 449 

the bloodvessels. Thus it may develop in cases of thrombosis of the vena 
azygos during the course of typhoid fever. While it is true, as already 
stated, that hydrothorax is usually bilateral, it sometimes happens that it is 
unilateral, if perchance the obstruction to the flow of blood or lymph is pro- 
duced by some lesion which affects only one side of the chest. This occurs 
much more frequently on the right side than on the left, in those cases in 
which the cause is cardiac disease. Many years ago Jaccoud pointed out 
that this is due to pressure upon the major azygos vein by the dilatation 
of the inferior vena cava and the right auricle, and more recently Steele 
and Stengel have called attention to this class of cases. 

When it is present in the course of cirrhosis of the liver it is probably 
due to the presence of associated pulmonary tuberculosis. Osier asserts 
that such an effusion may occasionally occur in what he designates as 
"perfectly healthy men." 

The fluid in hydrothorax is usually of low specific gravity (see Pleurisy 
with Effusion), and clear or but slightly opalescent, yellowish or straw- 
colored. It is not rich in cells, and those cells that are present consist 
largely of relatively voluminous flat endothelial cells. Fibrin is usually 
absent. If an injury or obstruction of the thoracic duct is present, the fluid 
may be chylous in character. 

Again, if such a patient is given iodide of potassium and the fluid is 
withdrawn by aspiration iodine will be found in it, whereas if the fluid is 
due to inflammation iodine is absent. The fluid is placed in a test-tube, 
a few drops of fuming nitric acid are added, and then it is shaken with some 
chloroform, when if iodine is present a red color will appear, which sinks to 
the bottom of the tube with the chloroform. 

Hydrothorax can often be relieved by the free use of a saline purgative, 
such as half an ounce of magnesium sulphate given every morning before 
breakfast and by cardiac tonics if they are needed. If it causes symptoms 
by pressure it must be removed by aspiration. (See Pleurisy with Effusion.) 

Bloody effusion into the pleura is met with in cases of cancer of the pleura 
and of Bright's disease. It is more indicative of the presence of the former 
malady. I have more than once seen a simultaneous pleural and abdominal 
bloody effusion due to a general carcinomatosis. 

When pleural effusion is tapped a second time, or when the needle has 
been introduced more than once in the search for fluid, it not infrequently 
happens that the liquid obtained is blood-stained, owing to wounding of a 
bloodvessel by the instrument. Of course, this possibility must be remem- 
bered when a bloody effusion is found. Sometimes a true hemothorax 
arises from this cause, or it is due to a leakage from an eroded bloodvessel. 



PNEUMOTHORAX, HYDROPNEUMOTHORAX, PYOPNEUMOTHORAX. 

Definition. — Pneumothorax — that is, the presence of air in the pleural 

spaces — is rarely present as the result of disease unless it is associated with 

fluid (hydropneumothorax) or pus (pyopneumothorax). As the result of 

injuries to the chest and to the lungs it not rarely appears as true hydro- 

29 



450 DISEASES OF THE PLEURA 

pneumothorax, as after the fracture of a rib, or as the result of a stab 
wound. 

History. — As long ago as the time of Hippocrates a succussion sound on 
shaking a patient suffering from empyema or pleural effusion was recognized, 
but it was not until the time of Laennec, about 2200 years later, that the 
value of this sign was appreciated as indicating the presence of both fluid 
and air in the chest. 

Etiology. — The most common cause of pneumothorax is pulmonary tuber- 
culosis, and it arises as a result of the perforation of the pleura by the rupture 
of a cavity through the visceral layer; in order that air may enter the pleura 
the tuberculous cavity must directly or indirectly communicate with a 
patulous bronchus, thereby affording a communication between the lung 
and the thoracic cavity. West believes that fully 90 per cent, of the 
cases are due to this cause. In many cases this accident is prevented 
by an acute or subacute pleurisy occurring at the area diseased, so that the 
pleura is thickened or the two layers glued together, This is particularly 
prone to be the case when a cavity has formed; and were it not for this 
protective process the condition of pneumothorax would be commonly met 
with. In still other cases, however, these very adhesions result in pneumo- 
thorax, for during some severe exertion they are torn, and so the air finds 
an opening through which to escape. 

As a rule, the perforation occurs in the lower part of the upper lobe, or 
in the upper part of the middle lobe. Pneumothorax develops on the left 
side nearly twice as often as on the right. West, however, believes that the 
two sides are nearly equally affected. At times the opening through which 
the air escapes is so small that it cannot be found. Sometimes there is 
more than one perforation. 

Very much more rare as causes of pneumothorax are bronchiectasis, 
pulmonary abscess, and pulmonary gangrene. So rare are they that when 
cases of this kind occur they should be reported. This holds true as well 
of cases which develop from rupture of a vesicle in cases of emphysema of 
the lungs. Pneumothorax has arisen in the course of whooping-cough, 
diphtheria, and typhoid fever. 

Pneumothorax occurs three times as often in men as in women. 

Symptoms. — The onset of pneumothorax is often very sudden and severe, 
but at times it develops so insidiously that no signs of its presence are noted 
by the patient until he attempts to make some exertion, when dyspnoea 
ensues. In cases of sudden onset there is not only urgent dyspnoea, but 
sometimes syncope to the point of unconsciousness. These severe symptoms 
are much more prone to develop in a patient who has slight pulmonary 
disease than in one who has well-advanced lesions, because in the latter 
case, the lung being already partly useless, the other lung is ready to com- 
pensate for the inactivity of the diseased part. When the accident occurs 
on the comparatively healthy side death may speedily ensue. In some 
instances the pain may be so severe that angina pectoris is thought to be 
present. 

Physical Signs. — The physical signs in these cases of pneumothorax 
consist in bulging of the interspaces on the affected side, and at times the 



PNEUMOTHORAX, HYDROPNEUMOTHORAX, PYOPNEUMOTHORAX 451 

development of subcutaneous emphysema. There is also in many cases a 
distinct increase in the size of the chest on that side. If the air escapes on 
the right side the liver is markedly depressed and the heart is displaced to 
the left. In left-sided cases the heart may be pushed to the right of the 
median line. 

Percussion reveals hyperresonance unless there has been an old pleurisy 
with secondary pleural thickening. If the lung is adherent to the chest wall 
and collapsed by pressure, or consolidated by tuberculosis, a dull note may 
be present. In a case of this character recently under my care, in a patient 
whose general health seemed to negative the possibility of tuberculosis, this 
state was confirmed at autopsy, much relief being given before death by 
frequently permitting the air to escape from the chest, over part of the chest 
wall through a hollow needle. 

Auscultation reveals an absence of vesicular murmur over the area of 
hyperresonance, and, perhaps, loud amphoric breathing over the lung, 
particularly if it contain a cavity which freely communicates with the 
pleural space. 

When hydropneumothorax is present the lower part of the chest is flat 
on percussion as in ordinary pleural effusion, above this is an area of hyper- 
resonance, and above this again is the Skodaic resonance due to the 
compressed lung. On shaking the patient a succussion sound is heard, 
and when the patient is at rest auscultation reveals "metallic tinkling," 
which is supposed to be due to the dropping of fluid into the liquid at the 
base of the chest. Succussion and metallic tinkling are the most important 
signs of hydropneumothorax. Another valuable sign is the so-called "coin 
sound" produced by striking a large coin, held against the chest wall, with 
another coin. The physician listens to the back of the chest as the percussion 
is done, by an assistant, on its anterior surface, and closes his unoccupied 
ear with his finger-tip. If the coin be struck so that the sound has to be 
transmitted through the chest at the level of the fluid the sound is very 
indistinct. At the level of the air it is transmitted with startling clearness, 
and at the level of the lung its transmission is again impaired. 

Diagnosis. — In considering the possible presence of pneumothorax in the 
type which is insidious the following conditions must be included : A large 
cavity may give somewhat similar physical signs, but the limited area over 
which they are manifested or demonstrable separates the two states. Emphy- 
sema of the lungs is excluded by the universal presence of breath sounds 
and the fact that the condition is bilateral. Rupture of the diaphragm with 
diaphragmatic hernia should be considered if some injury has been suffered, 
and pyopneumothorax subphrenicus must be excluded by study of the pul- 
monary signs above the area involved and of the condition of the epihepatic 
and epigastric areas. 

Prognosis. — The prognosis of pneumothorax depends largely upon the 
cause of the condition and the associated states of effusion and empyema. 
Much depends upon the suddenness of onset. I have seen death occur in 
twelve hours in cases with sudden onset, and cases are on record of death 
in twenty minutes. On the other hand, if the dyspnoea is not severe the 
pulmonary condition may be actually benefited by the temporary rest 



452 DISEASES OF THE PLEURA 

enforced by the collapse of the lung. West has placed the mortality at 
70 per cent., and of these fatal cases 75 per cent, died within two weeks 
and 90 per cent, within a month. In those cases which do not die soon 
after the onset of this condition death may result either from empyema and 
exhaustion, or from the progress of the underlying disease. If the heart is 
feeble, if the other lung is far advanced in disease, and if the strength of 
the patient is badly impaired the prognosis is, of course, bad. Recovery 
takes place in about 10 per cent, of the cases of simple pneumothorax 
without fluid. 

Treatment. — The treatment of pneumothorax consists in the relief of 
pain, if it be very severe, by a small dose of morphine — say, J of a grain 
given hypodermically. If the dyspnoea is marked a large hollow needle, or 
aspirating cannula, should be introduced into the chest, but not attached to 
the aspirator. The pressure in the chest will cause more air to escape than 
will flow in, and as the lung is already collapsed any damage caused by its 
entrance is done. To prevent the air from entering, the finger may be tem- 
porarily used as a valve on each inspiring movement until a wash-bottle can 
be so arranged that the air will escape through the water it contains and then 
cannot return. If the air constantly re-accumulates the case should be treated 
by a drainage tube inserted as in the treatment of empyema. (See Empyema.) 

If oedema of the other lung is threatened, dry cups should be applied over 
its base. 

When serous effusion is present, or when empyema is a complication, the 
conditions should be treated as described when discussing these conditions. 

A most exhaustive study of this subject has been made by West in London, 
and more recently by Emerson in Baltimore during 1903. 

DISEASES OF THE MEDIASTINUM. 

Under this heading are considered diseases of the mediastinum other than 
those of the heart and aorta. In my Fothergillian Prize Essay I collected 
520 cases of mediastinal disease, and the facts there presented form the basis 
for the following views. The statistics on their face show that there were 
134 cases recorded as carcinoma, 98 as sarcoma, 21 as lymphoma or lymph- 
adenoma, and 115 as abscess. In other words, a large proportion of cases 
of disease in this area are due to malignant growths, for the remaining 
lesions were non-malignant or inflammatory. The statistics apparently 
indicate that cancer is by far the most frequent form of individual growth. 
While we have no right to go "behind the returns," in the sense that cases 
reported as cancer may be regarded as sarcoma, it is nevertheless probable 
that sarcoma is really the most frequent growth in the mediastinum, because 
tissues favorable to its growth are found there in great abundance and 
tissues susceptible to carcinomatous growth are scanty. Again, it is well 
known that up to the middle of the last century, and later, little distinction 
was made between cancer and sarcoma, and so many cases of sarcoma were 
probably reported as cancer. Finally, lymphoma and lymphadenoma are so 
nearly allied to sarcoma that it is fair to add them to the so-called sarcoma- 
tous cases, making the total 119 reported as sarcoma. 






DISEASES OF THE MEDIASTINUM 453 

The non-malignant tumors of the mediastinum are fibroma, teratoma, 
dermoid cyst, and hydatid cyst. 

Notwithstanding the fact that the middle and posterior mediastinal spaces 
are more richly provided with lymphoid tissues than the anterior mediastinum, 
the statistics prove that malignant growth is more common in the latter space 
than in the other spaces. Thus, of the cases reported as sarcoma and cancer, 
in which the space affected was stated, 81 were in the anterior space as 
against 28 in the posterior space, and only 5 in the middle space alone, 
although in many other instances the entire mediastinum was invaded. 

For this reason we should expect to find that sarcoma in a very large pro- 
portion of cases occurred as a secondary growth in the mediastinum; but an 
examination of the literature of the subject, both as regards general opinion 
and reports of cases, shows such a conclusion to be erroneous. Indeed, 
the mediastinum seems to rarely suffer from any form of this disease save 
the primary, and even in those cases in which the lesions were scattered all 
through the body from head to foot, this space seems to have escaped 
secondary contamination. Should the growth appear in the mediastinum, 
secondarily, it generally affects the posterior or middle spaces, owing to 
the large number of lymphatic glands and like tissues which are found in 
these cases. 

It is a curious fact that mediastinal growths are twice as common in men 
as in women, although women so much more frequently have malignant 
growths in nearby tissues, and in them, as already stated, malignant growth 
of the lung is said to be more common. 

The average age affected by mediastinal tumors is about thirty-seven 
years. 

Symptoms. — The symptomatology of mediastinal tumor is by no means 
clear and well defined, since so many other conditions may produce signs 
of the same character, and it has been stated very positively by certain 
writers that such a growth cannot be diagnosticated during life. 

Although this assertion seems rather sweeping, there is, nevertheless, 
some truth in it, and in many cases, where we have no history to guide 
us and no evidence of a growth elsewhere, the diagnosis may be well-nigh 
impossible. 

Large tumors are found, in the anterior mediastinum, which have 
not been diagnosticated or suspected until a postmortem has been 
made, not from any lack of ability on the part of the physician, but 
because the symptoms of mediastinal disease have either been entirely 
absent or masked by others of more importance elsewhere. Thus, in 
a case reported by Bruen, an old woman, aged seventy years, entered the 
Philadelphia Hospital with decided symptoms of renal disorder, which in 
a few days caused her death. Although an examination was made of 
the chest, as a matter of routine duty, no special physical signs were 
discovered, and the disease, which was sarcoma in the anterior mediastinum, 
was not discovered until the body was placed on the postmortem table. 
The only symptoms of such a condition of affairs before death consisted 
in slight dyspnoea and cough, both of which were supposed to arise from 
the renal lesions; and this is the more remarkable, since the growth weighed 



454 



DISEASES OF THE PLEURA 



Fig. 63 



fourteen ounces, was six inches long by five inches broad and four inches 
in diameter, or, in other words, was about the size of a normal adult heart. 
No signs of sarcoma existed elsewhere in the body from which one might 
suspect any malignant disease. 

The first symptoms complained of by the patient vary quite as much as 
do the later ones, and depend, as do their successors, upon the parts most 
involved. By far the largest number of sufferers notice some interference 
with respiration, particularly on exertion, which soon increases, so that 
there may be constant dyspnoea, and even attacks of partial suffocation. 

The dyspnoea and other disturbances of respiration are, in many instances, 
due to several rather than any single cause, since, in addition to the mechanical 
pressure by the growth on the air-passages, we 
may also have such interference with the circula- 
tion of the blood, particularly in the thoracic veins, 
that pleural, pericardial, or mediastinal effusions 
of serum may occur. 

Effusions into the abdomen may occur, owing 
to involvement of the ascending vena cava, but 
such a condition is rather rare, probably owing 
to the fact that the ascending cava more frequently 
escapes than does the descending. Dropsy of the 
lower extremities, without abdominal effusion, some- 
times comes on. 

In still another class of cases the pulmonary 
vein may be obstructed, and oedema of the lung 
may develop. Hypostatic congestions are by no 
means rare, the patient often being forced, by car- 
diac weakness, pleural effusion, or pressure on the 
trachea, to lie in one position. In some cases loud 
venous murmurs can be heard in the jugular and 
other large superficial veins, and care has to be 
exercised as to the diagnosis of the true cause of 
the distress. The ribs and sternum may undergo 
gradual erosion and destruction from pressure, and 
the growth appear on the surface of the body. 

In a certain number of cases the nerves of the 

thorax seem to be more affected than the rest of 

its contents, and involvement of the vagi or the recurrent laryngeal nerves 

may bring on a long train of obscure and dangerous symptoms, both 

as regards the circulation, respiration, digestion, speech, and swallowing. 

Tumors of the mediastinum invading the lungs have frequently been 
mistaken for chronic and even acute pneumonia, growing, as they do, along 
the larger bronchial tubes and bloodvessels. 

Without doubt, in a certain number of cases, either hypostatic pneumonia, 
or pneumonia due to pressure on the bronchial vessels, develops as the tumor 
invades the lung, and in such cases it is absolutely impossible to make a 
diagnosis unless there are symptoms of pressure in the mediastinum. 
Walsh has stated that if the lesion be due to a tumor, the affected side will 




Kronlein's case of retro- 
tracheal tumor of the medi- 
astinum. 



DISEASES OF THE MEDIASTINUM 455 

increase in bulk rather than diminish, and that dyspnoea out of proportion 
to the degree of consolidation points to a mediastinal disorder rather than 
one confined to the lungs. 

In a very large proportion of cases of mediastinal disease the condition 
is one of abscess. There were 115 cases in my collection of 520 of medias- 
tinal disease. The proportion of acute and cold abscess in 79 cases in which 
the differentiation was made was 48 to 31. 

The most constant and severe symptom is, in nearly all cases, the deep- 
seated pain, which increases in severity from first to last, seldom remitting 
until suppuration has taken place and the pus has found some outlet. If 
the case be one of cold abscess, these painful symptoms may be masked by 
other more pressing ones, such as dyspnoea and cedema from pressure; 
although it should not be forgotten that such symptoms may appear with 
equal severity in both varieties of the disease. In the acute variety all the 
symptoms of ordinary inflammation appear, such as rigors and periodical 
or constant fever. 

As recovery took place in about 40 per cent, of the cases of mediastinal 
abscess according to the statistics of preantiseptic days, it ought to occur 
much more frequently now. 

Mediastinal growths are usually of such a nature as to be beyond either 
medicinal or surgical treatment, but abscess, dermoid cysts, and teratomata 
are sometimes operable. 



DISEASES OF THE CIRCULATORY SYSTEM. 



DISEASES OF THE PEEICAEDIUM. 

PERICARDITIS. 

Acute Pericarditis. Definition. — Acute pericarditis, sometimes called 
acute fibrinous or acute serofibrinous pericarditis, is, as its name implies, 
an acute inflammation of the pericardium, the serous membrane which 
envelopes the heart. 

Etiology. — Acute pericarditis is practically always due to the presence of 
some infecting micro-organism, although certain conditions existing simul- 
taneously may predispose to the infection by lowering vital resistance. In 
the great majority of cases it is due to acute articular rheumatism, in com- 
paratively few it develops as a complication of croupous pneumonia, the 
pneumococcus being its cause, and it also develops as a complication of 
scarlet fever, in which disease the streptococcus associated with this malady 
is probably the provoking factor. Acute pericarditis is also frequently 
associated with renal disease, and is often, under these circumstances, a 
form of terminal infection. So, too, it may develop in the course of various 
infectious diseases, such as smallpox, erysipelas, typhoid fever, and even in 
measles. Septic infections, such as general septicaemia and ulcerative endo- 
carditis, may cause it. In diabetes it occurs as a terminal infection. Of 
course, tuberculosis and syphilis, diseases which affect every tissue, may 
also affect this one. 

Acute pericarditis also develops by direct extension from inflammation in 
neighboring parts, in distinction from infection which takes place through 
the blood. Thus, inflammation of the mediastinal tissues may produce it, 
as in diseases of the bronchial glands, of the sternum, or of the vertebrae. 
So, too, pneumonia and pleurisy affecting nearby portions of the lung may 
cause inflammation of the pericardium. In infections involving the myo- 
cardium the overlying serosa — that is, the visceral layer of the pericardium — 
rarely escapes. So, too, pericarditis may be the first indication of impending 
rupture of that part of the aorta covered by pericardium. 

Pericarditis may also be due to injury to the chest wall or to the mem- 
brane itself. 

It is evident, therefore, that acute pericarditis is nearly always a condi- 
tion secondary to some other affection, and that it is very rarely primary. 
When it is primary it is usually due to tuberculosis. (See articles on 
Croupous Pneumonia, Acute Rheumatic Fever, and Typhoid Fever.) 

(457) 



458 



DISEASES OF THE PERICARDIUM 



Frequency. — The frequency of pericarditis as a primary disease is very 
limited, but as a secondary affection it is great. Very many cases present 
no sign of it during life, yet the condition is found at autopsy. It occurs 
almost as frequently in children as in adults, although at one time this class 
of patients was supposed to be not so commonly attacked as older persons. 
Sturges found it present in 94 out of 100 cases of fatal heart disease in chil- 
dren. Of these cases 54 were of rheumatic origin. Indeed, it is probable 
that the disease is less prevalent after than before puberty. It occurs far 
more frequently in males than in females, and this is particularly true after 

Fig. 64 




Heart and pericardium, acute serofibrinous (pneumococcal) pericarditis. Most of the anterior 
parietal layer of the pericardium has been cut away, showing the villous (shaggy) irregular projec- 
tions of the fibrin. To the left, where the parietal pericardium is reflected over the right auricle and 
great vessels, cohesion of the layers may be seen; later, had the patient recovered, such fusion of the 
layers would have constituted the basis from which organized fibrous adhesions would have formed. 



puberty, when the greater exposure and activity of males become domi- 
nant factors in causing rheumatism and other infections. At this time the 
proportion is from 4 to 1 to 6 to 1. 

Pericarditis, as we would expect, develops more commonly in severe cases 
of acute rheumatism than in mild cases, but, on the other hand, it is to be 
borne in mind that even in those cases with very mild joint symptoms severe 
pericardial involvement may occur. Prior attacks of rheumatism seem to 
increase the frequency of pericarditis in subsequent attacks. The condi- 
tion usually comes on during the first week of the disease. This is, how- 



PERICARDITIS 459 

ever, by no means always the case, and it may appear as late as the sixtieth 
day of the illness or during a relapse. 

Pericarditis due to renal disease, the Pericardite Brightique of the French, 
is distinctly a state of advanced years, occurring most commonly after forty- 
five or fifty years of age. It is more commonly met with in patients suffering 
from contracted kidney than in those that present the parenchymatous 
form of renal disease. 

Pathology. — As in inflammation of the pleura, so in inflammation of the 
pericardium, it is well to recognize three forms of acute pericarditis, viz., 
the acute dry or fibrinous, the acute exudative (serofibrinous), and the puru- 
lent type. In the first stage of all these forms of pericarditis the lining sur- 
face of the pericardium is lustreless, opaque, and somewhat roughened 
by a delicate fibrinous exudate. It is also hypersemic and may be dotted 
with petechia?. It is the rubbing together of the two layers of the pericardium 
at this stage that causes the characteristic friction sound of the disease. 
As the inflammation progresses the membrane becomes completely covered 
by the exudation of fibrin, which may assume a villous formation. Adhesions 
between the layers of the pericardium also take place. 

In the serofibrinous form a considerable quantity of serum is poured out 
into the sac, and particles of fibrin and leukocytes are found in it. The 
quantity may be so large as greatly to distend the sac, displace the heart, 
and interfere with its function, particularly by pressure upon the auricles and 
cavse. In many cases as much as three pints have been found in the sac. 
West quotes cases in which the pericardial sac contained no less than five 
pints (due to scurvy), yet recovery occurred after aspiration. 

In the purulent form (pyopericardium) the serum and fibrin are mixed 
with pus cells and erythrocytes. Pyopericardium may arise as a primary 
purulent pericarditis or be converted from the serous form by infection 
with the Streptococcus, Pneumococcus , or Staphylococcus pyogenes aureus. 
Sometimes the tubercle bacillus acts as a pyogenic organism in this space. 

There is some difference of opinion as to the frequency of pyopericardium. 
Two opinions which represent the two sides of this question are as follows : 
Samuel West speaks of it as "one of the rarest of clinical rarities," but 
Battin says "it is a disease seldom suspected, still more rarely diagnosed, 
and hardly ever treated, and yet it is one that is present in 3 per cent, of the 
deaths in the records of the Children's Hospital.' , 

That the latter view is correct is shown by the fact that Breitung in 324 
cases of pericarditis found that 108 were serofibrinous, 30 hemorrhagic, 
and 20 purulent, or 6.1 per cent. In 769 autopsies collected by Still 24 
instances of pyopericardium were found, and 11 were due to infection by 
the pneumococcus. Scott found it in no less than 16 cases out of 40 (40 
per cent.), and in 38 cases of croupous pneumonia the same reporter found 
pyopericardium in 17, or 44.7 per cent. 

Symptoms of Acute Fibrinous Pericarditis. — The symptoms of acute fibrinous 
pericarditis are often not pronounced. Pain would supposedly be a well- 
marked symptom, but it is not present in all cases, although when it is present 
it may be severe. Fortunately pain from this cause is rare in children. 
When it occurs it is usually felt from the right edge of the sternum to the 



460 



DISEASES OF THE PERICARDIUM 



left nipple and is fairly constant, although it has sharp exacerbations. In 
other cases the pain is chiefly situated in the epigastrium, or a sense of 
precordial distress develops, and the breathing may be oppressed. The 
action of the heart is rapid, often reaching 100 or 120 and even 160 beats per 
minute in severe cases. The temperature is usually increased, but seldom 
rises above 102° or 103°. In some cases it is not abnormal. Nervous 
symptoms are sometimes notable and great restlessness or even active de- 
lirium may ensue, resembling that of delirium tremens. Vomiting is a 
common symptom. 



Fig. 65 




Area in which pericardial friction sound is best heard. 



Physical Signs. — The physical signs of acute fibrinous pericarditis 
are as follows: Palpation over the base of the heart at the third inter- 
space may reveal friction fremitus in well-marked cases, and auscultation 
will show a distinct friction sound in the same area when the disease is 
established. This sound is creaking and dry and has been called the 
"saddle-leather sound," in that it resembles the creaking of an ordi- 
nary English leather saddle when it is first used. It differs from the fric- 
tion sound of pleurisy in that it is to and fro and does not occur with the 
respirations. At times it has a gallop rhythm with a triple sound as of a 
horse galloping. If the stethoscope be pressed against the chest the sound 
can usually be intensified. These sounds vary with the severity of the in- 
flammation of the pericardium and the action of the heart, being more 
sharply defined when the action is violent than when it is depressed. 



PERICARDITIS 461 

Indeed, variation in the action of the heart may cause a loud friction 
sound at one visit and a lack of it at the next. As a rule the pericardial 
friction sound is limited to the area of the cardiac base about the third 
or fourth interspaces, but it may be heard at the apex or along the sternum. 

Diagnosis of Acute Fibrinous Pericarditis. — Acute dry pericarditis can 
scarcely be confused with any other state, but several conditions resemble 
it somewhat. Thus in cases of early phthisis there is occasionally heard, 
near the apex of the left lung, a cardiopulmonary murmur or puffing sound 
during inspiration, occurring with each beat of the heart, and persisting if 
the patient holds his breath on a full inspiration, but disappearing on expira- 
tion. Another similar condition is the so-called " pleuropericardial friction 
sound," which is apparently due to the beating of the heart against the 
margin of the lung. Both of these sounds are, however, more in the nature 
of murmurs than friction sounds. 

Symptoms of Serofibrinous Pericarditis. — With the development of effusion, 
in cases which go on to that state, symptoms of cardiac embarrassment begin 
to show themselves. The evidences of cardiac disturbance are not always, 
however, in direct proportion to the amount of fluid, for in some instances 
large accumulations of fluid cause so little inconvenience as to be over- 
looked, while in others in which the fluid is moderate in quantity they are 
severe. It is important that these variations in the severity of the symptoms 
be remembered, because it is humiliating in the extreme to find after some 
time that an unsuspected pericardial effusion is present. Probably the most 
constant symptoms are dyspn&a, a dusky skin, an anxious fades, and a rapid 
pulse, which varies in volume and speed with the respirations. The voice 
is somewhat husky, and active delirium may be present as in the dry form. 

Diagnosis of Pericardial Effusion. — When the pericardium is well filled 
with fluid the sac presents a peculiar pear-shaped swelling which consists 
of two spheres superimposed, the smaller one above the larger one. It 
extends across the middle zone of the chest from a little to the left of the 
right nipple to a little to the left of the left nipple, and from the central 
tendon of the diaphragm nearly to the top of the sternum. The pressure 
of this fluid upon the heart and its great vessels may very markedly inter- 
fere with their proper movement, but it does not greatly change its position. 

Physical Signs. — The physical signs of pericardial effusion are as follows : 
On inspection the apex beat is absent and in many cases it cannot be found on 
palpation unless the patient is turned on his face. The chest over the heart 
may be slightly bulging, and palpation may reveal the fact that the first rib can 
be felt projecting more prominently from beneath the clavicle than in health. 
So, too, inspection may reveal some prominence of the epigastrium, and 
there may be unusual tenderness on palpation of this area. 

The heart sounds, on auscultation, are distant and feeble and the area of 
cardiac dulness is greatly enlarged. Thus it extends to the right of the 
sternum to a level below that which forms the base of the cardiac triangle, 
and to the left of the nipple. There is also enlargement of the area of cardiac 
dulness at the base toward the left. The presence of dulness in the fifth 
interspace, to the right of the sternum (Rotch's sign), of dulness as high 
as the second cartilage or second interspace (Sansom's sign), combined 



462 DISEASES OF THE PERICARDIUM 

with dulness over the sternum between these points, are pretty sure signs 
of pericardial effusion, particularly if at the left infrascapular angle there is 
dulness on percussion (E wart's sign). The area of dulness is that of a flat- 
tened cone, or, as Ewart has well said "it is that of a bag of fluid spreading 
out at the base." This view has been combated by Dr. Frederick Shattuck, 
but the distended sac does undoubtedly take this shape, although ina- 
bility to demonstrate its outline does not exclude effusion by any means. 

In doubtful cases, resort to the x-ray may aid greatly in deciding the 
question of the presence of effusion. 

The most important states to be differentiated from pericardial effusion 
are cardiac dilatation and hypertrophy, and aneurysm of the aorta with 
some leakage into the pericardial sac. The first is the condition most apt 
to mislead the physician. I have seen this occur several times and I have 
seen the heart punctured on two occasions in an endeavor to aspirate the 
pericardial sac in the belief that effusion was present when in reality the 
condition was one of great cardiac dilatation with pericardial adhesion. 
The presence of feeble and distant heart sounds, the absence of a definite 
apex beat, and the manifest cardiac embarrassment all aided in producing 
an erroneous view in these cases. In such a case the history of old valvular 
difficulty and the diffuse character of the apex beat should help us to a 
clear view of the condition. In cardiac hypertrophy the distinct apex beat, 
the strong action of the heart, and its clear sounds separate the two con- 
ditions. An aneurysm of the root of the aorta with some pericardial effu- 
sion may be most misleading. In a case of this kind, seen by me, aspira- 
tion of the pericardial sac caused rupture of the aorta and instant death. 

Very large pericardial effusions have been taken for left-sided pleural 
effusions, and an encapsulated pleural effusion has been taken for an effusion 
into the pericardium. 

Prognosis of Acute Pericarditis with and without Effusion. — This is good in 
cases in which the heart is not seriously crippled by the effusion or by 
associated endocardial changes. The outlook is favorable in proportion to 
the smallness of the effusion and the benignity of the disease causing it. 
In pneumonia and renal disease the prognosis is worse than it is in rheuma- 
tism, in which disease it is good. 

In the great majority of cases pericardial effusion undergoes absorption. 
This happens in this sac far more frequently than in the pleural sacs, perhaps 
because of the constant action of the heart. When the effusion persists it 
must be removed. (See Treatment.) Life is sometimes prolonged for many 
weeks even after pyopericardium develops. Coutts has recently reported 
the case of a child of four years that lived seventeen weeks and died only 
after operation. Nevertheless, pyopericardium is a very fatal condition. 

Treatment. — In the early stages of acute pericarditis, if the heart is over- 
acting and irritated, tincture of aconite may be given with advantage to 
quiet its action and to diminish friction. An ice-bag may be placed over 
the praecordium in cases of pneumonia with this complication, and in rheu- 
matism several flying blisters may be used. Later if the heart becomes 
feeble the best stimulants are the aromatic spirit of ammonia, Hoffmann's 
anodyne, and alcohol. Digitalis except in small doses is rarely of any value, 



PERICARDITIS 463 

and may be prevented from acting properly by reason of the fever or 
because there is not room in the pericardial sac for full diastole to take 
place under its influence. 

If the quantity of effusion be very great it must be removed by aspira- 
tion or incision. The latter operation is always essential if pus is present, 
and even if serum is present incision is safer because it is by no means easy 
to diagnosticate the presence of fluid beyond a doubt and more difficult 
still to be sure of the part of the sac farthest away from the heart. Aspira- 
tion may be therefore in the nature of a plunge in the dark. Incision care- 
fully made is safer. The best spot for operative interference depends upon 
the individual conditions and the position of the apex beat. The usual 
areas of election are in the fourth interspace at the left edge of the sternum 
and at the fifth right interspace at the edge of the sternum. 

When incision is practised for pyopericardium the mortality is high, but 
nevertheless it must be performed if recovery is to occur. Out of 51 cases 
collected by Porter 20 recovered and 31 died. 

The use of purgatives, diuretics, and diaphoretics to cause the removal 
of the fluid is almost useless. If any drug is of value for this purpose it is 
iodide of sodium in doses of 20 grains three times a day. 

Chronic Pericarditis (Adhesive Form). Definition and Pathology.— By 
chronic adhesive pericarditis is meant a condition in which one or all of the 
following pathological conditions arise as a result of an inflammatory process, 
which involves the pericardium and often the tissues that surround it : 

(1) There may develop a state in which partial or localized adhesions take 
place between the visceral and parietal layers of the pericardium. Several 
such adhesions may be present in the pericardium at the same time. These 
adhesions may be immediate or consist in long strings of fibrous tissue 
stretching across the pericardial sac. They are commonly found near the 
base, but also occur at the apex. 

(2) In the second class of cases the two layers of the pericardium are 
closely adherent, and the walls of the sac in some cases are much thickened. 
Here again the adhesion may not be universal, but in patches, although 
at times the entire sac is obliterated so that the heart is surrounded by a 
thick and tough capsule composed of the two layers, which cannot be separated. 

(3) In still a third class the inner surfaces of the pericardium are not so 
much involved as the outer surface, and as a consequence we find adhe- 
sions to the chest wall or to the pleura. It is perhaps hardly fair to class 
this type with those already named, because the pericarditis in these instances 
is usually the result of a spread of inflammation from neighboring parts, 
as from the pleura or mediastinal tissues. 

(4) Another type, and the most serious of all, is that in which the internal 
and external layers are glued together, and the external layer is adherent to 
neighboring tissues so that the heart, its membranes, and adjacent parts 
are bound up in an inflammatory mass or mat. If the mediastinal tissues 
are not affected the condition is called "pericarditis externa et interna," 
but if the mediastinal tissues are included it is given the name of " indurative 
mediastinopericarditis." In some cases the tissues for nearly the whole 
length of the left edge of the sternum may be involved. 



464 



DISEASES OF THE PERICARDIUM 



(5) Finally, a form of chronic pericarditis occurs which affects the 
visceral layer of the pericardium almost solely, and encloses the heart in 
a thickened inner layer. 

Related to the latter condition is the so-called "multiple serositis" 
or the " pericarditic pseudocirrhosis of the liver' , of Pick, to which the 
name "iced liver " has been given by Curschmann. .In such cases the 

Fig. 66 




Heart, left ventricle. Adherent pericardium, with lipomatosis of the adhesions and slightly fatty 

infiltration of the myocardium. 

pericardium suffers from a chronic hyperplastic or fibroid inflammatory 
process, which likewise affects the serous membranes elsewhere, whence the 
name " multiple serositis." In other words, in this diseased state all serous 
membranes of the thoracic and upper abdominal zones are involved in a 
hyperplastic process which is prone to affect the pericardium in particular. 
In some instances the pericardial sac contains fluid, but in others it is 



PERICARDITIS 465 

closed by the adhesions between its walls and even go on to calcification. 
When the condition is well developed the pericardium and pleurae are 
adherent to one another and to all adjacent tissues, and the peritoneum is 
also thickened and adherent to nearby organs. The liver is adherent to 
the diaphragm and even to the stomach, colon, omentum, and belly wall. 
It is the profuse hyperplasia of the peritoneum which causes the organs it 
covers to look as does a cake which has been " iced." 

The two symptoms of this condition which are most constant and char- 
acteristic are large ascites and a gradually increasing failure of cardiac power. 
The cause of the excessive ascities is the perihepatitis and the compression 
of the abdominal vessels by the newly formed connective tissue. Beyond 
these two symptoms the manifestations of the process are practically 
identical with those of adherent pericardium, as will be described below. 
The malady is a very slow and chronic process lasting, it may be, for 
years. 

The result of these adhesions is enlargement or hypertrophy and dilatation 
of the heart. This change, however, does not occur in all cases and it is 
chiefly present in cases in which valvular lesions coexist. The pressure 
produced by the thickened membranes results in some obstruction to the 
flow of blood in the great veins at the cardiac base, and this causes jugular 
distention. 

Symptoms of Adhesive Pericarditis. — The symptoms of the milder forms 
just described are so moderate that no thought of their existence is had till 
autopsy reveals them. It is in the well-developed types that the condition 
may cause symptoms which are definite, although they may be very indefi- 
nite. Indeed, in some cases it may be impossible to correctly diagnosticate 
even the most severe forms. The subjective symptoms are pain in the prce- 
cordium, or a sense of constriction. This pain may be dull and constant or 
paroxysmal, arousing the suspicion of true angina pectoris. Palpitation is 
another common symptom and in some instances the action of the heart is 
irregular and hobbling. Shortness of breath on exertion is also present and 
at times the right ventricle becomes engorged and secondary engorgement of 
the liver and lungs ensue. Finally, what is taken for ordinary cardiac 
dropsy due to valvular disease develops. In other cases pleural effusion 
develops from this cause. 

Diagnosis of Adhesive Pericarditis. — The physical signs to be searched for 
in making a diagnosis are as follows: 

Inspection may reveal depression of the precordial area and a drawing 
together of the ribs so that the intercostal spaces are narrowed. In place 
of this condition in this part of the chest, there may be distinct bulging. 
Again, the apex beat is often much displaced and as the pericardium is 
adherent to the chest wall changes in posture do not alter its position. The 
usual displacement of the apex is upward and outward. In other instances 
the apex beat cannot be seen or felt in its usual place, but a transmitted 
impulse can be found in the epigastrium. Perhaps the most important diag- 
nostic symptom is retraction of the chest wall at systole. This retraction 
may be at the apex or along the left edge of the sternum in the third, 
fourth, and fifth interspaces. Roberts states that if the right ventricle is 
30 



466 DISEASES OF THE PERICARDIUM 

greatly enlarged the impulse can be seen to the right of the sternum. 
Broadbent has called attention to the fact that in many of the well-marked 
cases of adherent pericardium marked systolic retraction of the lower ribs 
on the posterolateral aspect of the chest is visible, if the patient is in a good 
light and the physician regards his back and side from a distance. This 
retraction is in the nature of a tug at systole. It is emphasized by a deep 
inspiration. Again, if the physician will place his head directly against the 
chest in this area he may have transmitted to it a shock at the time of systole. 
In some cases the adhesions between the pericardium and the diaphragm 
may prevent the normal epigastric respiratory movements. 

Percussion may reveal in some cases an increase in the area of cardiac 
dulness, but it is not constant. Auscultation may show reduplication of 
the pulmonary second sound, and a rough and widely distributed friction 
sound, and a somewhat prolonged presystolic murmur at the apex which is 
not necessarily due to mitral stenosis. 

The pulse often presents irregularities, particularly at the time of the 
inspiratory movements, the so-called pulsus paradoxus. Sudden collapse 
of the cervical veins on diastole may also be present. 

It must be distinctly understood that these signs are often absent or are 
difficult to discover. There is perhaps no more difficult diagnosis than 
that of some cases of adherent pericardium. The history of a severe or 
repeated attacks of acute rheumatic fever is an important point in judging 
of the likelihood of its presence, particularly if there is also a history of 
pericarditis. Progressive cardiac weakness without valvular lesions in a 
young person should raise the suspicion of the presence of this state, 
particularly if an insidious ascites and dropsy of the lower extremities 
develop. 

Prognosis of Adhesive Pericarditis. — The prognosis is of course very grave 
if the symptoms are severe and if the occupation is strenuous. With 
adequate rest life may in some cases be prolonged for years if the inflam- 
matory state is stationary. 

Treatment of Adhesive Pericarditis. — The treatment cannot be curative 
for obvious reasons. It can only be palliative, by rest, good food, and the 
relief of dropsy by purges and diuretics. Digitalis usually cannot act use- 
fully because the heart is too firmly bound down to permit of increased 
diastole. 

HYDROPERIOARDIUM. 

This is a state of fluid in the pericardium due to transudation from vessels 
which are pressed upon by growths, or it results from hsemic or vascular 
changes due to renal disease. It is not an inflammatory effusion. 

Symptoms. — Symptoms and physical signs are absent except when the 
fluid becomes copious enough to cause cardiac embarrassment, when the 
condition of the patient is found to be like that produced by an ordinary 
serous pericardial effusion due to true pericarditis. 

Prognosis. — The prognosis depends upon the cardiac state and the under- 
lying cause. It is usually grave, because of the underlying malady. 



PNEUMOPERICARDIUM 467 

Treatment. — The treatment consists in free purgation, if the patient is able 
to stand it and the use of diuretics. Otherwise it is that of general dropsy. 
(See Chronic Parenchymatous Nephritis.) 



HiEMOPERICARDIUM. 

Blood in the pericardial sac arises from stab and other wounds, and it is 
also present in cases of purpura and of profound diseases of the blood. In 
other cases it arises from aneurysm of the aorta early in its upward course, 
and finally it may be due to rupture of the heart or aneurysm of one of the 
coronary arteries. Even in these cases death may be postponed a number 
of days. If a large amount of blood escapes into the pericardium the heart 
is stopped by the pressure on its surface and on the great veins at its 
base, so death is not due to actual loss of blood. This result is what one 
would expect, and I proved its truth some years ago in an experimental 
research. 

When the condition is due to disease it usually is hopeless. When due 
to injury the pericardium should be opened, the blood removed, and if a 
wound in the heart exists it should be closed. There are many cases of 
this sort on record in which operation has been performed and in which 
life has been saved. 

PNEUMOPERICARDIUM. 

Air or gas in the pericardium appears as the result of injury, whereby air 
enters the sac, or again as the result of a cavity in the lung perforating, 
through adhesions, into this space. It also may develop in cases of cancer 
or other ulcerative lesions of the oesophagus, with adhesions between this 
tube and the pericardium, followed by perforation of the growth. Again, 
it occurs rarely, as the result of perforation, in pneumopyothorax. Cases 
are on record in which a gastric ulcer has caused adhesions to the diaphragm 
followed by perforation, and so pneumopericardium has developed. In still 
other instances the gas which is present is due to the presence of the Bacillus 
aerogenes capsulatus or other gas-producing. organisms. 

The mere presence of air, or gas, in this cavity is such an abnormal state 
that some serous effusion nearly always takes place within a few hours; 
so that all cases of pneumopericardium are really to be considered as 
hydropneumopericardium primarily, and as they speedily become purulent 
by infection they are usually instances of pyopneumopericardium. 

Symptoms. — The symptoms resemble those of pericarditis with effusion, 
except that a considerable part of the area of cardiac dulness may give a 
high-pitched resonant note on percussion. This area of resonance varies 
greatly with the posture of the patient, being larger when he is recumbent 
than when he is erect. Another symptom which is quite characteristic, if it 
can be discovered, is a peculiar crackling sound due to the action of the heart 
in stirring up the fluid and the air. Sometimes these sounds are gurgling 
or churning in character. They have been compared to the splashing of 



DISEASES OF THE HEART 

water on a mill-wheel. There is but one condition which can produce 
symptoms like these, and that is a large cavity in the lung near the heart 
in which the fluid contents are disturbed by the movements of the heart. 

Prognosis. — The prognosis is, of course, very grave, but recovery has 
occurred. 

Treatment. — The treatment depends largely upon the cause. If the case is 
one of perforated oesophageal cancer it is of course hopeless ; in an instance 
of traumatism with perforation surgical interference may give good results. 



PYOPERICARDIUM. 

(See Pericarditis with Effusion.) 



DISEASES OF THE HEAET. 

HYPERTROPHY AND DILATATION OF THE HEART. 

Definition. — Hypertrophy of the heart is a condition in which there is 
a growth above normal of its muscular fibres resulting in an increase in the 
size and particularly in the muscular power and weight of the viscus. 

In dilatation one or more of the cardiac cavities is more capacious than 
normal; the wall may be normal, increased or decreased in thickness, 
with a cardiac power less than its muscular development would indicate. 

These conditions, which at first glance seem diametrically opposed to 
one another, are in reality nearly always present simultaneously in varying 
degree. For this reason I consider them side by side. 

When the wall of the ventricle is increased in thickness without any 
alteration in the size of its cavity the condition is called simple hyper- 
trophy. When the cavity is larger than normal it is called eccentric hyper- 
trophy, or hypertrophy with dilatation, and when the cavity is decreased 
in size it is known as concentric hypertrophy. 

When dilatation is combined with hypertrophy it is called active dilatation. 
When there is no hypertrophy, but thinning of the walls alone, it is called 
passive dilatation. 

Hypertrophy of the Heart. — The existence of concentric hypertrophy 
has been denied. It certainly is very rare. Simple hypertrophy is also rare, 
but eccentric hypertrophy is one of the most common of secondary patho- 
logical changes 

A large number of causes produce cardiac hypertrophy with dilata- 
tion. Sometimes they act singly, but not rarely several of them are 
associated. The most common cause is valvular disease, which by its 
resulting regurgitation or obstruction increases the labor of the heart. The 
second cause of importance is a state of the bloodvessels which renders the 



HYPERTROPHY AND DILATATION OF THE HEART 469 

propulsion of the blood more difficult than in health. This obstruction to 
the free flow of blood may be general, as in cases of arteriocapillary fibrosis; 
or localized, as when there is roughening or narrowing of the aorta, or when 
a tumor presses upon the aorta; or, again, in cases of aneurysm. Other 
localized causes of hypertrophy are emphysema of the lungs or chronic 
phthisis and adherent pericardium. 

The increase in the size of the heart in cases of hypertrophy is sometimes 
very great. Thus, this organ, which in the healthy man weighs about 
nine ounces, or 270 grams, and in the healthy woman about eight ounces 
(240 grams), may weigh as much as 53 ounces (1590 grams). Usually, 
however, the increase does not go beyond fifteen ounces (450 grams). 

A heart which has undergone hypertrophy is broadened or widened 
at its apex, but the actual increase in the size of this organ at this point 
depends largely upon the part of the heart which is chiefly affected. 
Thus, in cases in which the right ventricle is chiefly involved, this part 
of the heart is often far larger than that part formed by the left ventricle, 
which seems small by contrast. When a hypertrophied heart is incised, its 
walls are found to be much thickened and the columnar carnese and papillary 
muscles larger than normal. The enlargement is due to both an increase 
in the number and size of the muscle fibres. 

Symptoms and Physical Signs of Cardiac Hypertrophy. — The chief symptom 
of ordinary eccentric hypertrophy, when it is adequate to compensate for 
the valvular lesion, or to overcome resistance, may be said to be the 
maintenance of a comfortable life and a normal circulation. Many persons 
develop this state without any knowledge of there being present any valvular 
disease, and remain in perfect health for years. 

If the physician chances to examine such a case he may find a cardiac 
murmur and then, on closer study, discover the following physical signs, 
provided the process is well developed. On inspection the prsecordium is 
bulging, but the impulse transmitted to the chest wall is regular and 
deliberate in distinction from the cardiac hurry and irregularity present 
when compensation is ruptured. The apex beat is more diffuse than 
is normal and is often in the sixth or seventh interspace instead of in the 
fifth, and it is farther toward the axilla than in health. On palpation the 
apex beat is found to be forcible and it may be heaving, but if the patient 
be a full-chested individual these local signs may not be present. If em- 
physema of the lungs causes these enlarged organs to overlap the heart 
they may hide much of the hypertrophy. Percussion may reveal increase 
of the area of cardiac dulness to the left, to the right, and downward. 
Auscultation, instead of revealing an exaggeration of the first sound, reveals 
that it is more distant, perhaps because the thickness of the heart walls 
muffles the sound, but the aortic sound is accentuated unless the aortic 
valves are diseased. 

If the patient takes violent exercise he may complain of palpitation and 
the thumping of his heart. 

When hypertrophy begins to fail the patient complains of shortness of 
breath on exertion, of palpitation and oppression, and if he persists in 
keeping on his feet the symptoms of cardiac failure (see Valvular Disease) 



470 DISEASES OF THE HEART 

develop. The first physical signs of the failure will be some reduplication 
of the first sound and diminution in its clearness. This reduplication is 
best heard just inside the apex beat when it first develops, but later it can 
be heard over a large area. The period between the first and second sound 
is prolonged as if the ventricle was able, only with the greatest endeavor, to 
slowly expel its blood. This means diminution of the period in which the 
heart muscle can obtain nourishment through its coronary vessels. 

The causes for this failure are various. In some instances the degenerative 
changes in the myocardium and in the bloodvessels which are incident to 
old age are the determining factors. In others some acute illness — as typhoid 
fever, influenza, pneumonia, or renal disease — may be the cause; or, again, 
severe exercise may produce so much exhaustion of the heart muscle and 
acute dilatation that the cardiac power is impaired for all time. 

Diagnosis. — Cardiac hypertrophy must be separated from several im- 
portant conditions which are by no means rare. From dilatation hyper- 
trophy is differentiated by the facts that the impulse in the former is feeble, 
in the latter it is strong, and by the feeble heart sounds in the former as 
compared to the stronger ones in hypertrophy. So, too, palpation of the 
apex in dilatation reveals a diffuse and feeble impulse and in hypertrophy a 
forcible beat. 

From pericardial effusion it is differentiated by the fact that, though the 
area of cardiac dulness is increased in both states, the cardiac impulse and 
cardiac sounds are muffled in effusion and exaggerated in hypertrophy. 
From displacement of the heart it can be differentiated by the fact that 
though the apex beat is displaced the general area of cardiac dulness is not 
increased in cases of displacement. 

Again, in certain cases in which the chest wall is thin and the lung is 
retracted so that it fails to cover the heart as in health, the heart may be 
so close to the chest wall that its area of dulness will be abnormally large 
and its apex beat unduly forcible and diffuse. In such a case the careful 
study of the state of the lung and pleura will make the condition clear. 

Of the functional disorders that produce overaction of the heart and 
so cause apparent but not real hypertrophy, "tobacco heart," the irritable 
heart of exophthalmic goitre, and that of neurotic individuals must be 
remembered. 

Prognosis. — As cardiac hypertrophy in its common form is compensatory 
in character, and as it very rarely becomes excessive, in the sense that it is 
beyond the needs of the patient, the prognosis in a case in which it is present 
deals not with the question of how much greater will hypertrophy become, 
but rather how much longer will hypertrophy enable the heart to supply the 
bloodvessels with blood in satisfactory quantities. Unlike most alterations 
from the normal as the result of disease this change is distinctly advantageous 
to the patient. 

The question as to how long the hypertrophy will be maintained can 
only be answered after its provoking cause or causes have been determined. 
If the hypertrophy following valvular disease of the heart is adequate, 
if the patient is a young and otherwise healthy adult, -and if the valvular 
lesion is not progressive, the prognosis as to the maintenance of the con- 



HYPERTROPHY AND DILATATION OF THE HEART 471 

dition is usually good, but will depend upon the good habits of the 
patient, particularly as to alcohol, hard work and exposure, and upon the 
particular valve which is diseased. (See Prognosis of Valvular Lesions.) If 
the hypertrophy is the result of arteriocapillary fibrosis with its associated 
renal changes, the duration of life except under the most favorable conditions 
is brief, because the arterial obstruction is constantly increasing and the 
heart is constantly exposed to increasing strain, increasing toxaemia, and is 
poorly nourished by its own coronary arteries. 

Treatment. — There is no treatment for compensatory hypertrophy except 
to maintain it by care as to manner of life, and the use of digitalis and rest 
if its integrity or maintenance is threatened. I have seen a few cases 
of aortic regurgitation with great hypertrophy in which rest in bed and 
moderate doses of tincture of aconite have given better results than rest 
and digitalis, but in these cases the patient had been accustomed to severe 
toil, and when he was put at rest seemed to have excessive cardiac power, 
as shown by throbbing and oppression. On the other hand, when hyper- 
trophy seems excessive, it is not rarely in reality lacking, and the violence 
of the heart movements may be abortive efforts at circulation. Often the 
use of nitroglycerin at such times will be advantageous if the arterial 
pressure is high. 

Dilatation of the Heart. — Passive dilatation (without hypertrophy) may 
be caused by valvular lesions, as the result of which the cavities of the 
heart become distended, but hypertrophy does not develop. Of these the 
chief cause is sudden and prolonged strain, and the feebleness often due to 
myocardial disease. Obstruction to the flow of blood in the pulmonary 
vessels may cause dilatation of the right side of the heart, as in cases of 
pneumonia, in cases of pleurisy with effusion, and in cases of acute pul- 
monary oedema complicating uraemia. 

A common cause in men over fifty years is sudden effort, as in lifting a 
heavy weight or climbing rapidly a steep flight of steps. In the young and 
vigorous sudden strain may be followed by rapid return of the dilated heart 
to its normal size, but in those further on in years, or who have valvular 
or myocardial disease, an acute strain often results in permanent dilata- 
tion. It is very common for old men to try to prove that they are "as 
young as they used to be," and to attempt athletic feats which are followed 
by acute dilatation and perhaps immediate death or death in a few days or 
weeks. In other instances the heart suffers from a gradual dilatation from 
prolonged strain, as in soldiers on the march. Not rarely dilatation de- 
velops during the course of one of the acute infectious diseases or during 
convalescence. 

When the strain is very gradual, instead of meeting the increased demand 
by increased effort, the heart slowly dilates and is perhaps never able to 
empty its cavities of blood. 

The intrinsic causes of dilatation are myocarditis, fatty degeneration, 
fatty infiltration, and serous infiltration from pericarditis. In some cases, 
however, no adequate intrinsic or extrinsic cause can be found. 

Symptoms of Cardiac Dilatation. — The symptoms and physical signs of 
passive dilatation are usually such that a diagnosis is readily made. When 



472 DISEASES OF THE HEART 

it is sudden in onset an acute or partial syncope with labored respiration 
and thoracic oppression may be present. 

When the onset is more gradual the main symptoms are impaired circula- 
tion, a tendency to syncope on suddenly standing or sitting up, congestion 
of the kidneys causing albuminuria, and the poor capillary circulation which 
causes the skin of the hands to remain pallid long after pressure. Many 
persons so afflicted cannot lie down without urgent dyspnoea and cardiac dis- 
tress. The pulse is small and irregular, and the arterial tension low. In 
other cases the pulse wave may be voluminous, but feeble. 

An inspection of the praecordium shows that the apex beat, if visible at 
all, is diffuse and displaced outward and downward. On placing the finger- 
tip on the spot where the apex beat seems most marked, the examiner is 
surprised to find no impulse or one which is very slight. There is often 
visible, but rarely palpable, pulsation near the ensiform cartilage or in the 
epigastrium. Care must be taken that overlying lung does not lead to an 
erroneous belief as to the presence of cardiac feebleness. If the whole hand 
is placed over the disturbed surface of the prsecordium it is remarkable how 
little impulse is discernible. Percussion shows an increase in the area of 
cardiac dulness to the left ; to the right, and downward. Often it is also 
increased upward. 

On auscultation the first sound of the heart may be short and small, 
valvular and flapping, though fairly loud, and if the heart is strong enough 
there may be a systolic murmur at the apex, due to mitral regurgitation 
arising from stretching of the mitral orifice. As in ruptured compensatory 
hypertrophy the sounds of the heart may be equalized and the space between 
them may be altered so that the sounds are like those of the fetal heart 
or like the ticking of a watch. In other cases the first and second sounds 
may occur close together and the diastolic pause be prolonged. Very often 
great arhythmia is present. If in addition to these signs there is a history 
of acute strain near or remote, or symptoms of cardiac feebleness, and 
particularly if the onset has been sudden, without the presence of an acute 
infection to cause valvular disease, the diagnosis of dilatation may be made. 

Prognosis. — The prognosis depends upon the degree of the dilatation, the 
state of the vessels and of the heart muscle and of the kidneys, and last, 
but not least, the lungs. When the latter are filled with rales the state is 
alarming, and if the vessels and kidneys are diseased the outlook is hopeless 
for much betterment. If the state of the vessels and the general condition 
of the patient indicate fatty myocardial degeneration the prognosis is also 
bad. If these states are absent, and rest can be maintained, distinct improve- 
ment can be hoped for, but a complete cure in the sense of old-time vigor is 
rarely reached. 

Treatment. — The treatment is, first of all, rest in bed, or in an easy chair 
if bed is impossible because of orthopncea. The second object to be gained 
is the removal of the cause of the dilatation, if that be possible, as the reduc- 
tion of high arterial tension by the use of nitroglycerin. Third, the employ- 
ment of digitalis and strychnine for effect, recalling the fact that once this 
drug has produced its action smaller doses will maintain its influence, and 
also bearing in mind the additional fact that when it is in full effect sudden 






DISEASE OF THE MYOCARDIUM 473 

changes of posture are dangerous, and that it may cause so much ventricular 
stimulation as to overdistend the auricles, which are poorly protected by 
the relaxed mitral ring. 

When the lungs and kidneys are engorged, the application of several dry 
cups over them is useful, and if jugular distention and hepatic congestion is 
marked, the patient may be freely bled if he is plethoric. So, too, hydra- 
gogue cathartics, such as jalap and compound extract of colocynth, may 
be used to unload the bowels and liver, but care must be taken that the 
patient is not exhausted by purging. Blue mass in the dose of 8 grains 
once a week is useful, and the pill of calomel, squill, and digitalis men- 
tioned under Endocarditis may be used. If ascites is a pressing symp- 
tom tapping is indicated, while for general anasarca the formula given 
under Endocarditis, or apocynum cannabinum may be used, or the digi- 
talis given more liberally. 

The diet should be light and nutritious, and often it is well to give pan- 
creatized foods or starches with taka-diastase. Great care must be taken 
that the stomach is not distended by food or drink, and if gas accumulates 
in the stomach it should be expelled by the use of Hoffmann's anodyne in 
drachm doses, and by the employment of a turpentine stupe. When dyspnoea 
is urgent morphine and strychnine are useful drugs. 

High altitudes should be carefully avoided and only gentle exercise on 
level ground be allowed. 



DISEASE OF THE MYOCARDIUM. 

Disease of the myocardium may be divided into two classes, viz., degenera- 
tive and inflammatory. 

Degenerative Changes. Etiology and Pathology. — The degenerative con- 
ditions are as follows: In the granular form, sometimes called "parenchy- 
matous degeneration," there develops in the protoplasm of the cardiac 
muscle fibres albuminous granules which differ in size and in number, 
and may be present in such an excess as to obscure the nuclei and stria?. 
The affected muscle is cloudy, softened, and paler than in health, its strength 
decreased, and the circulation is proportionately depressed. In a later stage 
some degree of fatty degeneration may also be present. 

This type of degeneration is observed in the course of acute infectious 
diseases, as diphtheria, typhoid and typhus fever, the pyaemias, and even 
as a result of severe burns, and in debilitating conditions associated with 
severe cardiac work or the presence of toxic bodies in the blood. 

In fatty degeneration of the heart the affected fibres contain fat-globules, 
which, in marked cases, replace the structural elements, both the nuclei and 
protoplasm. In some instances this degenerative process is restricted to a 
single focus, or it may be scattered about or diffuse; in others it is universal. 
When the heart is examined at autopsy it is seen to be mottled and the 
papillary muscles in particular will reveal the fatty areas, the so-called 
"Tiger Herz" of the Germans. 

Diffuse fatty degeneration is caused by prolonged nutritional disorders. 



474 DISEASES OF THE HEART 

Pernicious anaemia and leukaemia may also cause it, as may poisoning by 
arsenic, phosphorus, and antimony. Less commonly it is a sequence of 
various acute infectious diseases like diphtheria and scarlet fever or typhoid 
fever, and by degenerative or atheromatous changes in the coronary arteries. 
The local or circumscribed forms follow embolism or other types of rapidly 
developed coronary occlusions. 

It is important that fatty degeneration be clearly separated from fatty 
infiltration, in which state the muscle fibres are not altered, but have been 
separated by the projection of fatty masses between them. This may cause 
some wasting or atrophy of the muscle fibres. This state is most commonly 
met with in very fat persons and in those who are addicted to excessive 
beer-drinking. Occasionally forms of amyloid and hyaline degeneration of 
the heart fibres occur. 

Brown induration or atrophy of the heart is often seen in cases of 
chronic valvular disease and in old persons. The muscle is more dense 
than normal and reddish-brown in hue, and about its nuclei brown pig- 
ment is deposited. Calcareous degeneration, in which the muscle fibres 
become infiltrated with lime salts, is rare. 

Under the name of fragmentation and segmentation there is seen a state 
of the heart muscle in which its fibres are broken across in fragments, or 
its cells are separated at the point of junction (segmented). These changes 
may occur in acute infectious diseases or in cases of central nervous dis- 
ease. In some cases they are probably agonal, and it may be that similar 
appearances are of postmortem origin, but the frequency with which 
granular change is seen at autopsy strongly indicates that it may be 
present and unrecognized in life, not only in fatal cases, but in those 
who recover. 

Symptoms of Myocardial Degeneration. — The symptoms of degeneration 
of the heart of the albuminous type cannot be considered as pathognomonic. 
Indeed, there may be no evidence of cardiac failure until a sudden and 
perhaps fatal attack of syncope, after a slight exertion, reveals the alarming 
state of the heart muscle. In other instances the feeble cardiac sounds on 
auscultation indicate the real condition of the heart. 

When fatty degeneration is present the same absence of symptoms may 
exist until the final fatal syncope, or the patient may suffer from repeated 
attacks of syncope, or of vertigo with anginoid seizures. (See Stokes-Adams 
Disease, page 475.) The frequency and severity of these attacks are, 
however, by no means in direct proportion to the extent of the lesion in 
the heart muscle. In one instance a fatal syncope occurs, yet the heart 
scarcely seems altered in its fibres. In another case the life of the patient 
persists and fairly good health is maintained for years, yet at autopsy the 
heart muscle is so fatty and soft that the fingers can be pushed through it 
as if it were wet paper. 

In some instances the symptoms complained of by the patient seem to 
be epigastric and due to disordered digestion. How often do we hear of a 
man of advanced years dying of acute indigestion, which is really cardiac 
failure with gastric symptoms, or cardiac failure caused by an overdistended 
stomach. 



DISEASE OF THE MYOCARDIUM 475 

The heart sounds when the patient is in his average state of health are 
distant and feeble, and his slow pulse is small and of low tension. Not 
rarely his radial and temporal arteries are very calcareous, but in other 
cases they are soft and devoid of resistance on pressure. 

There still remains to be considered several notable facts in connection 
with this disease. Notwithstanding the great feebleness of the heart in 
some cases and the exceedingly weak circulation of blood, dropsy in any 
form is a very rare condition. Indeed, if dropsy occurs it is certainly due 
to some complicating state. A second fact is that in some cases in place 
of anginoid attacks an epileptiform or apoplectiform seizure occurs. The 
epileptiform seizure is not that of grand mal, but petit mal, with this differ- 
ence, that while, as in petit mal, there are no convulsions, there is a period 
of profound unconsciousness which is rather a syncope than a coma, such as 
is seen in true epilepsy. 

The apoplectiform seizures may very closely resemble true cerebral 
hemorrhage, even to the stertorous breathing, the hemiplegia, the uncon- 
sciousness, and Cheyne-Stokes respirations. That the case is not one of 
apoplexy is usually proved by finding that the high-tension pulse of cerebral 
hemorrhage is absent and replaced by the low tension and slow pulse of 
fatty degeneration. 

Prognosis of Myocardial Degeneration. — The prognosis in all cases of 
cardiac degenerative change is, of course, very grave. When it is present 
in children after acute infectious diseases recovery may ensue under a 
course of arsenic, phosphorus, and nux vomica, with absolute rest, and 
fresh air and sunshine, but even in this class of cases sudden death often 
intervenes. In the fatty heart of advanced age, whether the years be great 
or the patient prematurely old, the outlook is bad; but as no one can tell 
the extent of the lesions in the heart, a statement as to a brief duration 
of life is very prone to bring the physician's opinion into discredit if 
he attempts to name the time of dissolution. The wise physician rarely 
expresses a positive opinion as to the probable time of death in any case, 
much less in fatty heart. 

Stokes-Adams Disease. — Cases of extreme slow pulse with vertigo, or 
syncope, or apoplectiform or epileptiform seizure, have been given the 
name of the "Stokes- Adams syndrome." 

Associated with the slowness of the pulse there is marked pulsation in 
the veins of the neck, and to use Stokes' own words, written in the Dublin 
Quarterly Journal of Medical Science in 1846, the number of reflex pulsa- 
tions is difficult to be established, but they are more than double the 
number of the manifest ventricular contractions. Experimental and clinical 
studies by Erlanger {Journal of Experimental Medicine, vol. vii., No. 6, 
November 25, 1905, pp. 676-724, and vol. viii., No. 1, January 25, 1906, 
pp. 8-58), with clinical and autopsy findings by Stengel and others, indicate 
that the symptom-complex in most if not all cases of this condition is due 
to what is now denominated "heart-block." In this state the auricles 
beat two, three, or four times as rapidly as do the ventricles. Erlanger 
has repeatedly produced at will any particular rhythm or even entire in- 
dependence of the auricular and ventricular contractions in the dog by 



476 DISEASES OF THE HEART 

varying mechanical compression of the auriculo-ventricular muscle bundle 
of His. This muscle bundle, which is 17 to 20 mm. long, 2.5 mm. wide, 
and 1.5 mm. thick, extends from a point in the auricular septum below 
the foramen ovale downward through the auriculo-ventricular junction and 
terminates in the ventricular septum a short distance below the beginning 
of the aorta. The impulse which causes ventricular contraction appears 
to be transmitted from the auricles to the ventricles through this bundle 
and consequently lesions affecting it lead to slowing of the ventricle. When 
the latter chambers cease beating for some seconds syncope ensues. Most 
cases of Stokes- Adams disease appear to be primarily arteriosclerotic or 
syphilitic in nature though myocardial lesions of other origin may be the 
cause. Autopsy in some reported cases has shown no evident lesion and 
these have been pronounced neurotic in character. Erlanger states, how- 
ever, that as yet there has been described no typical case of Stokes-Adams 
disease which might not have been caused by heart-block. A point to be 
noted in autopsies upon cases of this disease is whether lesions of the 
mesial leaflet of the tricuspid valve can interfere with the integrity of the 
muscle bundle of His. 

Myocarditis. Definition. — This term is an unfortunate one in that it is 
often loosely applied to the degenerative changes just described as well 
as to those about to be mentioned. It is also unfortunate because it seems 
to indicate that there is a primary inflammatory state of the cardiac muscle 
fibres, whereas the changes in the fibres are secondary to inflammatory 
affections of the interstitial tissues of the heart and of its bloodvessels, which 
thereby cause atrophic and degenerative changes in the muscle. 

There are several forms of so-called myocarditis, of which the most com- 
mon is a slow, low-grade inflammatory change called chronic interstitial 
myocarditis, manifested by a wasting of the muscle fibres and the inter- 
calation of fibrous or fibroelastic tissues. There is also an acute process, 
acute interstitial myocarditis, of which there are suppurative and non- 
suppurative varieties, the former being a manifestation of pyogenic 
infection of the heart wall. 

In the great majority of cases the chronic form is the result of patho- 
logical changes in the coronary arteries. These vessels suffer from an 
obliterative arteritis in their finer branches, undergo atheromatous change, 
or become plugged by an embolus or thrombus. The lesions which result 
from these changes differ widely in character, but all greatly impair the 
usefulness of the heart. In all conditions lessening the vascular lumen and 
so decreasing the nutrition of the heart, there develops an overgrowth of 
interstitial tissue with atrophy of the muscle fibres. It is probable that 
the process is at no time a true inflammation, but rather one in which 
diminished blood supply causes atrophy of the muscle, followed by a substi- 
tutive fibrosis. 

When a branch of a coronary artery is plugged the affected area may 
manifest the changes seen in an infarct, or when enough nourishment is 
available to prevent actual necrosis the deficient nutrition gives rise to 
fatty degeneration. In either case the affected area may become softened, 
and give way, causing rupture, or fibrous tissue gradually takes the place of 






DISEASE OF THE MYOCARDIUM 477 

the degenerated fibres. Later the scar tissue yields to pressure and a cardiac 
aneurysm ensues. 

Hy'pertrophied hearts may show a slight increase in the fibrous tissue, 
and in failing compensation and progressing dilatation this increase in 
interstitial tissue may be conspicuous. 

In some instances chronic myocarditis is not the result of vascular 
change, but of inflammatory processes in the pericardium and endocardium; 
and in syphilis there is often seen a marked increase in the interstitial 
tissues of the heart, which is not surprising in view of the serious changes 
produced by this disease in the small bloodvessels everywhere. Chronic 
myocarditis is more common in males than in females. 

Symptoms of Myocarditis. — The immediate effects upon the patient produced 
by the lesions just named vary to an extraordinary degree. Plugging of 
one of the large branches of a coronary artery usually results in sudden 
death. 

In some instances, however, the patient survives a severe attack of cardiac 
disturbance, but under these circumstances the plugging is usually in a 
small vessel, and a gradual substitution circulation is established, not by 
anastomosis, for these vessels are end arteries, but by the so-called ves- 
sels of Thebesius, which in some cases are able to supply the heart with an 
adequate quantity of blood. 

When the closure of the vessel is gradual it not rarely happens that 
necrosis of the area deprived of blood is prevented by a blood supply 
through the vessels of Thebesius, so that the death of the patient is post- 
poned until a very extraordinary degree of atheroma and narrowing in 
both coronary arteries is developed. The coronary arteries of a well- 
known member of the medical profession in Philadelphia, who died a few 
years since, were so diseased that only a thread-like passageway existed in 
these vessels, yet he led an active life to the end. Such patients may have 
no marked cardiac symptoms, but, as a rule, repeated attacks of angina 
pectoris of increasing intensity give warning of the sudden death to come. 
The other symptoms are the same as those described under fatty degen- 
eration of the heart. 

The physical signs of myocardial degeneration are feebleness of the 
apex beat, equalization of the first and second sounds of the heart, and 
evidences of feeble circulation in the lungs and in the peripheral systemic 
vessels. 

The prognosis depends entirely upon the situation and the degree of the 
cardiovascular change. So far as recovery is concerned, that is impossible. 
The probable duration of life is also difficult to determine. Many cases 
with all the symptoms of severe myocarditis live a long period, while others 
die with unexpected suddenness. 

Treatment. — We cannot expect very much from treatment in patients 
suffering from chronic myocarditis. It must be evident from what has 
been said, under the discussion of the pathological conditions which 
cause these states, that the harm is done before the physician has an 
opportunity to place the patient under treatment. The only hcpe is 
that by regulating the manner of life, by increasing the action of the 



478 DISEASES OF THE HEART 

kidneys, if they are sluggish, by attending to the digestive apparatus, 
and by preventing undue cardiac strain through excessive muscular or 
mental exercise, we may be able materially to prolong the patient's life. 
In instances in which the bloodvessels are distinctly atheromatous or 
fibroid, the use of the iodide of strontium or sodium, in doses varying from 
10 to 40 grains three times a day, is usually advantageous. This treat- 
ment may be continued for several weeks, and then the patient may 
receive a course of Fowler's solution as a general tonic, with perhaps a 
small quantity of nux vomica or strychnine added to it. 

If arterial tension is high, he should be given nitroglycerin in doses vary- 
ing from y-g-Q- to j-q of a grain three or four times a day, in order that the 
resistance which is offered by tense vessels to the action of the heart may be 
lessened. Under these circumstances, too, small doses of digitalis sometimes 
act advantageously, particularly if nitroglycerin is given at the same time. 
To give digitalis to a failing heart and yet to permit the arterial tension 
to remain high is of little ultimate advantage to the patient, since it 
increases the labor of the heart without material advantage. It is much 
more important to diminish the labor by the use of nitroglycerin than to 
stimulate this viscus to increased endeavor by large doses of foxglove. 
Five minim doses of tincture of cactus grandiflora often do much good under 
these circumstances. It must be remembered that if the heart has under- 
gone distinct degenerative changes there is little muscular fibre upon which 
the digitalis may exert its stimulating influence, and there may be danger 
by increasing intracardiac pressure of causing rupture of some area of white 
necrosis, thereby causing cardiac aneurysm. 

It is hardly necessary to add that these patients should be warned against 
excessive muscular exercise or any severe cardiac strain, and they should 
be advised to lie down and rest several times a day, in order that the 
heart may at each period of rest recover as much strength as possible. 

Digestive disturbances, which by accumulation of gas may disturb the 
action of the heart, must be prevented by the institution of an easily digested 
and simple diet, small quantities of food being taken often so as to avoid 
overloading the stomach. If there is a tendency to an accumulation of 
gas in the bowel salol may be given as an intestinal antiseptic, or in its 
place the capsule of taka-diastase, pancreatin, nux vomica, and capsicum, 
which is recommended in the article on Angina Pectoris, may be adminis- 
tered. Some of these patients seem to be greatly benefited by the use of 
gentle massage every day or every other day, with the object of aiding in 
the circulation of the juices of the body. Great care should be taken that 
the massage is not so vigorous that the patient is fatigued by it. Strychnine 
in the dose of -^ of a grain three or four times a day is often exceedingly 
beneficial to these patients, particularly if there is any tendency to shortness 
of breath on lying down. 

In many instances when the heart is feeble as the result of fibroid changes 
in its muscle, or when the patient is convalescing from some disease like 
influenza, which seriously impairs the functional activity of this organ, 
excellent results are sometimes obtained by the institution of what is known 
as the Nauheim baths, which were originally brought before the profession 



CARDIAC ANEURYSM 479 

by Schott, of Nauheim in Germany. These baths are composed of water 
which is charged by nature with large quantities of carbonic acid gas. 
The water is also naturally warm. The patient is immersed in a bathtub, 
and immediately there is attached to the surface of his skin myriads of 
tiny bubbles of carbonic acid gas, which as they break produce a slight 
tingling sensation and exercise a stimulant influence upon the peripheral 
capillaries, as the result of which these capillaries are dilated and dermal 
hyperemia is induced. In this manner the circulation is equalized, internal 
congestions are overcome, and the heart finds it easier to pump blood through 
the dilated superficial capillaries than under ordinary conditions. Not 
infrequently when the patient first enters the bath a primary contraction 
of the peripheral capillaries ensues, and this results in a momentary increase 
in the work of the heart, so that the patient for a time feels somewhat 
oppressed. Usually he remains in the tub for ten or fifteen minutes, but 
this period is governed by the physician who superintends the use of the 
baths. On his removal from the bath the patient is carefully dried by an 
attendant and has absolute rest for one or two hours. After the baths have 
been used for some time additional salt is added to the bath, and water 
containing larger quantities of gas is employed. In addition to these baths 
the patients are subjected to gentle resistance movements and massage so 
as to improve the circulation of blood and lymph in the muscles. Great 
care must be taken that these movements are not sufficient to tire the 
heart. When valvular disease is very marked, these baths are contra- 
indicated. 

The Nauheim baths are also contraindicated in cases of advanced arterio- 
sclerosis, and in chronic Bright's disease if it is well developed, although if 
the renal difficulty is largely due to congestion this plan of treatment is 
advantageous. Aneurysm also contraindicates them, and bronchial asthma 
and chronic bronchitis contraindicate them, or at least require great caution 
in their use. Cases of pulmonary tuberculosis with cardiac disease also 
should not be subjected to this method, nor should patients who are suffer- 
ing from far-advanced degeneration of the heart muscle receive it. These 
baths should never be taken except under the care of a local physician. 

Attempts have been made to introduce artificial Nauheim baths in this 
country, but it has been found impossible to satisfactorily charge the water 
with carbonic acid, and the difficulties connected with the preparation 
of the bath have been such that its employment, except at Nauheim, has 
largely passed out of use. 

It is important to note that the resistance exercises, which are carried out 
in connection with this plan of treatment, are probably equally beneficial, 
if not more beneficial, than the baths themselves. They consist in having 
the patient extend and flex his joints against the resistance offered by the 
attendant. 

CARDIAC ANEURYSM. 

Aneurysm of the heart may occur in one of three forms, viz., aneurysm of 
the heart walls, aneurysm of the valves, and aneurysm of the coronary arte- 
ries. Aneurysm of the cardiac walls consists in a localized dilatation or 



480 



DISEASES OF THE HEART 



Fig. 67 



pouching of the wall, and is to be separated from dilatation of the heart, to 
which the term aneurysm is sometimes applied by French writers. The 
aneurysm usually affects the ventricular wall. Hall has recently collected 112 
cases, in which the site of the aneurysm was as follows : left ventricle, 92 
cases; right ventricle, 1 case; left auricle, 2 cases; ventricular septum — 
(a) muscular part, 8 cases; (6) membranous part, 7 cases; auricular septum, 
2 cases. 

The left ventricle is therefore affected more commonly than all of the 
other chambers combined. The aneurysm is usually near the apex of the 
ventricle or in the anterior wall, just above the apex; 67 of Hall's cases were 
so situated. 

The condition, as one would naturally expect, is found more frequently in 
males. In the relative frequency in the two sexes, Thurnam's, Legg's, and 
Hall's and my own statistics show a remarkable resemblance. Of Thur- 
nam's 40 cases, 30 were males, 10 females; of Legg's 88 cases, 64 were males, 
24 females; and of 80 cases collected by me, 59 males, 21 females. In a 
total of 208 cases, 74 per cent, were males, and 26 per cent, females. 

Aneurysm of the heart is a sequel of the secondary myocardial changes 
already described. Thus the fibrous tissue which replaces the tissues which 

have undergone necrotic change may gradu- 
ally yield before the blood pressure in the 
ventricle and form a sac, which is a true 
aneurysmal dilatation. This sac may com- 
municate with the ventricle by a small open- 
ing. In other cases the ventricular wall at 
this point yields, so that the opening may 
be the full width of the sac. As in aneu- 
rysm of the bloodvessels, the wall of the sac 
is composed of several layers made up of 
the visceral layer of the pericardium, and 
perhaps of the parietal layer as well, if it 
has become adherent. Under this is the 
fibrous tissue, and beneath this again form- 
ing the inner layer is the endocardium. 
Rarely several sacs are present. 

Three conditions may develop in such 
sacs. They may give way under pressure, 
causing sudden death, they may become 
filled with a clot, or their walls may be 
calcified. Sometimes an aneurysm of this 
sort forms in the septum and ruptures into 
the right ventricle. 

In some cases the aneurysm maybe due 
to fatty degeneration, without primary vas- 
cular disease. A softened spot in the heart 
muscle may bulge under strain, and rupture 
may occur before any real sac is formed. 
This is commonly called rupture of the 




Front view of heart, showing aneu- 
rysm of left apex of ventricle, which has 
perforated into the pericardium. The 
swelling of the aneurysm is visible ex- 
ternally, and the heart wall at the apex 
is no thicker than brown paper. No 
pericardial adhesion. The interventric- 
ular branch of the left coronary artery 
is dissected out, and is very atheroma- 
tous, and at the upper end of the groove 
is completely blocked by a thrombus, 
which extends downward for two and 
one-half inches. (From a specimen in 
Dr. Littlejohn's Museum.) 



ENDOCARDITIS 481 

heart, and usually involves the anterior wall of the left ventricle near the 
septum ; but it may affect any part of the walls of the cardiac cavities. 

Death by rupture of the sac does not occur as frequently as would be 
imagined, and in this respect cardiac aneurysm resembles aortic aneurysm. 
Out of 60 cases collected by Legg, only 6 died by rupture. 

Aneurysms of the cardiac septa are so rare as to be curiosities. Hall states 
that only 2 cases have been reported in twenty years. 

An aneurysm of a valve is sometimes formed as a result of endocarditis. 
This condition usually affects the aortic and mitral leaflets with about equal 
frequency. One leaflet is contracted or destroyed and another leaflet then 
yields or sags, partly because of deficient support, forming a pocket or sac 
which projects into the left ventricle. Sometimes this sac ruptures, and so 
the valve becomes perforated. In other instances the entire valve becomes 
sacculated. 

Although atheroma of the coronary arteries is a very frequent lesion, aneu- 
rysm of these vessels is exceedingly rare. Hall could find only 25 recorded 
cases, of which 17 were in males. 

Symptoms. — The symptoms of cardiac aneurysm are not definite at any 
time, and, unless the sac is large, there may be none. Hall tells us that out 
of 76 cases an antemortem diagnosis was made only once. When the sac is 
large it may cause a marked increase in the area of cardiac dulness near the 
apex, and produce distinct pressure symptoms. A skiagraph may give valuable 
information of the lesion. 



WOUNDS OF THE HEART. 

Wounds of the heart are by no means uncommon, as the result of shooting 
or stabbing. Cases of recovery after both of these forms of trauma are 
recorded in considerable number. The stab wounds probably recover in 
greater number than those which suffer from bullet wounds. Death is 
usually due not to the direct injury of the heart, but to the fact that the peri- 
cardial sac soon becomes filled with blood, and the heart is unable to expand. 
In other words, even severe injury to the heart is not fatal unless the hemor- 
rhage be free, or the organ is damaged in some vital spot, as in Kronecker's 
"co-ordinating centre." I proved these facts in a research carried out on 
dogs many years ago, and a number of surgeons have now reported cases in 
which a stab wound of the heart has been exposed and sutured, and recovery 
has ensued. Further than this, I have seen the heart punctured and blood 
aspirated from its cavities without injury to the patient. 

Gibbon and Stewart, of the Jefferson College Hospital staff, have recently 
reported interesting cases in which cardiac wounds were stitched with 
success. 

ENDOCARDITIS. 

Definition. — Endocarditis in an inflammation of the lining membrane of 
the heart, the endocardium. In the great majority of instances it chiefly 
affects the endocardium where it covers the valves (valvular endocarditis), 
31 



482 DISEASES OF THE HEART 

and rarely it involves that part which covers the walls of the cavities (mural 
endocarditis). A distinction should also be drawn between the acute and 
chronic form of the disease and between the acute simple, or benign, 
form, and the so-called acute malignant, or ulcerative type. It is proper 
to state, however, that many persons deny the correctness of this division, 
and regard the two conditions as different stages or degrees of the same pro- 
cess. Finally, it is to be recalled that there are two types of chronic endo- 
carditis, namely, that which is the result of the acute variety and that which 
arises in association with chronic arteriocapillary fibrosis and atheroma, 
which is a slow, retractile form of the disease. 

Acute Endocarditis. — Synonyms: Verrucous Endocarditis, Simple Endo- 
carditis, Benign Endocarditis, Papillary Endocarditis. 

Etiology- — The bacterial origin of endocarditis is generally admitted, but 
all efforts to identify any particular organism as the specific cause have 
proved fruitless. Many organisms have been identified in the vegetations. 
Of these should be mentioned those found in acute rheumatism, pneumo- 
cocci, streptococci, and staphylococci, and, less frequently, the colon 
bacillus, typhoid bacillus, influenza bacillus, tubercle bacillus, and a number 
of other bacteria. 

In the article on acute Articular Rheumatism attention has already been 
called to the frequency with which this condition complicates that malady. So 
constant is this lesion during the course of acute articular rheumatism that it 
may be regarded as the condition next in constancy to the inflammation about 
the joints. It is probable that in all cases of acute rheumatism a slight endo- 
carditis is present, but it may be so slight that no physical signs of its exist- 
ence can be elicited. 

In children suffering from acute rheumatism the involvement of the 
endocardium is far more frequent than it is in adults. Thus, it is gener- 
ally considered that from 60 to 80 per cent, of children who have acute 
rheumatism develop endocarditis; whereas, the percentage usually accepted 
for adults is about 21 per cent. Eighty per cent, is probably too high, 
and 21 per cent, is certainly too low an estimate. It is especially important 
to bear in mind that mild articular symptoms are not rarely accom- 
panied by severe cardiac lesions, although, as a rule, the severity of the 
articular symptoms and the severity of the heart lesions go hand in hand. 
The first attack of rheumatic fever is more frequently the cause of cardiac 
lesions than subsequent attacks, and the signs of endocardial inflammation 
usually develop during the first ten days of the illness, although in rare cases 
a murmur may be heard before any arthritic signs develop. 

When acute rheumatism causes endocarditis, it commonly affects the 
mitral valve. The aortic leaflets are comparatively rarely affected, and the 
valves on the right side of the heart only in very rare instances. 

Next to acute rheumatism as a cause of acute endocarditis must be noted 
its association with chorea, in which disease, in its well-developed and typical 
forms, lesions of the lining membrane of the heart are very often present. 
The occurrence of endocardial disease in chorea is in direct proportion to the 
severity of the disease, but it is difficult to decide how frequently true endo- 
carditis is actually present, because many choreic patients present on auscul- 



ENDOCARDITIS 



483 



tation functional murmurs in the heart which disappear so rapidly that it is 
inconceivable that they could have been organic in origin. Again, so few 
cases of chorea come to autopsy during or immediately after the attack that 
it is impossible to study the exact state of the endocardium. If the various 
statistics of frequency of heart murmurs are added together, we find that 
these sounds occur in about 31 per cent, of cases of chorea. 

In a very considerable proportion of cases endocardial infection takes 
place during acute tonsillitis. Another cause of endocarditis is gonor- 
rhoea, which causes the ulcerative type of the disease more commonly than 



Fig. 68 




a cm. 

Heart, acute endocarditis. The lesion on the aortic leaflets is verrucose and at points ulcerating. On 
the lateral ventricular aspect of the mitral valves are a number of vegetations, although the contact 
line and auricular surfaces of this valve were not involved. The vegetations on the ventricular surface 
probably resulted from inoculation by projecting vegetations situated on the aortic leaflet. It is to be 
remembered that endocarditis affects the mitral valves more commonly than the aortic valves. 



the benign form. Scarlet fever may also be a causative factor, but whether 
this is due to direct infection of the endocardium by the micro-organism 
which causes scarlet fever or by its toxins, or results from the mixed infection 
so frequent in this disease, is not known. Rarely endocarditis is apparently 
due to tuberculosis, for this bacillus has been found in the valve lesions. 
Traumatic forms and endocarditis due to syphilis have been described. 
Occasionally acute endocarditis develops as a result of an exacerbation of 
the chronic form of the disease, 



484 DISEASES OF THE HEART 

Endocarditis has been reported as present in the foetus as a result of the 
infection of the blood through the placenta. In this period of existence the 
pulmonary valves are the parts affected. 

Pathology and Morbid Anatomy. — The degree of inflammation in the endo- 
cardium covering the cardiac valves varies greatly in different cases. Its 
frequency on the left side, particularly in the mitral valves, is due principally 
to the greater stress to which these leaflets are subjected and also to the 
higher oxygen content of the arterial blood. The lesions develop in the 
auricular aspect of the mitral leaflets and the ventricular side of the aortic 
valves ; this distribution depends upon the friction and impact of the blood, 
and the same factors determine the distribution of the vegetations along the 
lines of greatest pressure, where the leaflets impinge one upon another when 
closed. 

The earliest lesions are rarely seen, because death seldom occurs at this 
time. The affected area is clouded and the valves slightly swollen, due to 
cellular infiltration and oedema. In this softened condition the impact of 
one valve upon another roughens the surface along the line of contact, and 
there is deposited at this point blood platelets, leukocytes, and fibrin, the 
quantity of each varying at different stages and in different cases. This 
deposit on the leaflet, tendon, or muscle is at first microscopic, but by accre- 
tion may attain relatively massive proportions, and constitutes what is called 
a vegetation; essentially it is a thrombus. Often a row of these wart-like 
bodies is festooned along the line of contact or project into the blood stream. 
Their disturbance of the blood current by obstruction and by rendering 
accurate coaptation of the opposed leaflets impossible, and thereby permit- 
ting regurgitation, causes a murmur, an appreciation of which is necessary 
for accurate diagnosis during life. 

Once formed, these vegetations are subject to important changes. They 
may be detached and swept off into the circulation, or they may soften and 
possibly be absorbed. Adhesions between leaflets may occur, but commonly 
the vegetations organize and permanently alter the contour, flexibility, and 
elasticity of the valves, thereby interfering with their proper functions. 
Finally calcifying deposits may further add rigidity to the already damaged 
leaflets. In favorable cases the valve surface becomes smooth, but little 
thickening results, and function is more or less fully restored. 

i^cute endocarditis ends in one of three ways: 1. The acute inflammation 
may subside and leave little or no alteration behind it. 2. The vegetations 
may persist and form large masses of an almost nodular character upon valves. 
3. The valves become eroded or adherent, or cicatricial contractions may 
lead to distortions and consequent immediate insufficiency or obstruc- 
tion. 

Symptoms. — In distinction from physical signs, there are no symptoms of 
ordinary acute endocarditis of the benign form. It is true that the pulse 
may be a little quicker than before the endocardium was affected and the 
fever a little higher, but neither of these symptoms are constant or character- 
istic. Some palpitation may be present, but so frequently are all symptoms 
absent that all too frequently the physician who is not careful fails to dis- 
cover endocardial disease until the patient begins to move about and com- 



ENDOCARDITIS 485 

plains of cardiac weakness or dyspnoea, and then the damage is done and is 
almost irreparable. Even the presence, on physical examination, of a mur- 
mur over the mitral or aortic area does not prove the presence of endocarditis, 
because it not infrequently happens that a murmur due to anaemia or to 
relaxation of the orifice is present. The presence of the murmur, while not 
pathognomonic of acute endocarditis, is, however, sufficient ground for the 
physician to treat his patient as a case with this lesion. 

Complications. — These consist most commonly of pericarditis and embolism 
of one of the cerebral or pulmonary arteries. Rarely acute cardiac dilatation 
ensues, and sometimes in infectious cases pneumonia and pleuritis develop. 

Diagnosis. — Care must be taken, as just stated, that anaemic murmurs, 
murmurs due to relaxation of the orifices, and pericardial friction sounds are 
not mistaken for those due to endocardial disease. (See Valvular Disease.) 

Prognosis. — Death is very rarely due to acute simple endocarditis in the 
sense that death comes during the acute stage of the disease. All too fre- 
quently it follows as a consequence of the changes produced in the valves and 
heart muscle months or years after the acute stage has passed. A bad 
prognosis can always be given if the physician does not strenuously insist 
upon the patient resting in bed for several weeks after all articular and 
valvular signs have ceased. Ill-health and death may not come soon in these 
cases, but it often comes years afterward, as time and chronic disease weakens 
the valves and heart muscle. Children who develop acute endocarditis and 
are permitted to move about too soon almost always succumb before or at 
puberty to these secondary changes. 

Treatment. — To prevent endocarditis in the course of all infectious dis- 
eases, and particularly in acute rheumatism, the physician must insist on 
absolute rest in bed all through the illness and for some time after the attack 
has passed. The diet should be light and easily digested, and at no time 
should the digestive apparatus be overburdened, for active and prolonged 
digestion tires the heart. If acute rheumatism is present, the salicylates 
should be used freely at once, not that they protect the valves directly, but they 
shorten the illness and so diminish the chance of involvement of the endo- 
cardium. Over the praecordium, as a preventive of endocarditis and peri- 
carditis, should be placed six or eight flying blisters, and alkaline diuretics, 
like citrate of potassium, should be freely used. An ice-bag may be placed 
over the heart if it is very irritable, and tincture of aconite may be given for 
the same purpose. After the endocardial symptoms have developed, rest 
of the most absolute character is the only useful plan of treatment. During 
convalescence rest is again the sine qua non. For the anaemia often present 
iron and arsenic are useful, as is also cod-liver oil. Subsequent cardiac 
feebleness is to be treated by small doses of digitalis, as 3 to 5 drops of the 
tincture with 10 drops of tincture of nux vomica three times a day. 

Ulcerative Endocarditis. Definition. — Ulcerative endocarditis, of which 
the synonyms have already been given, is a state in which the endo- 
cardium is ulcerated, vegetations are present, and there is an actual loss of 
substance in the valvular tissues, so that a valve or even a septum may be 
perforated. A French physician, Bouillaud, first recognized this cardiac 
state with its associated signs of pyaemia, but Kirkes, of England, first 



486 DISEASES OF THE HEART 

emphasized the fact that the heart was the seat of the difficulty, and that the 
symptoms arose from its condition. Since his time a host of pathologists, 
including Virchow, Wilks, Murchison, Charcot, Vulpian, and Birch-Hirsch- 
feld in Europe, and Osier in this country, have studied this malady. It 
is important to remember that ulcerative endocarditis occurs in an acute 
and chronic form. 

Etiology. — The disease is always due to microbic infection of the endo- 
cardium. It may be due to a secondary infection, during the course of one 
of the acute infectious diseases like typhoid fever, scarlet fever, pneumonia, 
or tonsillitis, or it more rarely arises as a primary lesion. The organisms are 
usually the Staphylococcus pyogenes aureus, the Streptococcus pyogenes, and 
the Pneumococcus, the Bacillus typhosus, the Gonococcus, the Bacillus coli 
communis. Acute endocarditis due to the meningococcus of Weichselbaum 
is very rare. A number of cases have been reported in which the meningo- 
coccus has been found in the circulating blood : one by Gwyn in 1889, 
another by Salomon in 1902, and a third by Warfield and Walker in 1903. 
The last of these is the only one in which the meningococcus was demon- 
strated to be the cause of the endocarditis. Any damage, new or old, to the 
surface of a valve predisposes that part to infection. 

Pathology and Morbid Anatomy. — Anatomically, the ulcerative form may 
be but a later stage of the acute simple type, and many cases occur in which 
no sharp line of demarcation can be drawn. Not infrequently it is engrafted 
upon an old or chronic valvular lesion, and patients having such lesions 
should be watched closely during an attack of any infectious disease 
associated with the constant or frequent occurrence of bacteremia. The 
infective process in the ulcerative type leads to necrosis of the already formed 
or forming vegetations, and even of the affected leaflet or adjacent myocar- 
dium. The fragments thrown into the circulation cause infarction and 
metastatic lesions in many tissues, especially in the spleen, kidneys, and 
brain. Marrow lesions, joint complications, and other manifestations of 
septicopyemia are often conspicuous. Whether the secondary processes be 
suppurative or not depends upon the character of the infecting organism. 
When involving the valves of the right heart (as it does more commonly than 
the acute simple form), pulmonary complications may be conspicuous, 
which, taken with the fact that it may be a sequence or complication of 
pneumonia, further tends to obscure the seat of the primary lesion. Occa- 
sionally the almost symptomless progress of the malady is due to the low 
toxicity of the infecting organism, while intensely toxicogenic bacteria 
reverse the picture and cause evidences of severe infection and toxseniia 
to be manifest. 

Symptoms. — The objective symptoms of ulcerative endocarditis may be 
no more marked than those of the simple form. Fever may not occur. If 
the disease develops during the course of one of the acute infectious diseases 
or as a result of septicaemia, its existence may not be suspected. If it develops 
primarily the physician who does not carefully study the heart may believe 
that the fever in its acute period of rise and fall is the manifestation of one 
of the acute infectious diseases or he may suspect sepsis, typhoid fever, or 
malaria. Because of these symptoms, the disease may be divided into the 



ENDOCARDITIS 487 

septic form, the typhoid form, and the malarial form. A cerebral form also 
exists. 

In the septic form the patient presents the ordinary signs of septi- 
cemia. Chill after chill develops, and between the chills high fever and 
sweats are present. The patient looks profoundly septic, the tongue is dry, 
the eyes sunken, and petechia? may be present in the skin. The marked 
amemia is very noteworthy, and its severity is diagnostic. Leukocytosis is 
present. Multiple metastatic abscesses may be found. The heart may or 
may not produce a murmur, but its action is hurried and feeble. 

The typhoid type is closely allied to that just described. The dry tongue, 
the subsultus, the tympanites, the diarrhoea, the mental stupor, the swollen 
spleen, and the remitting fever may all present so typical a picture of a case 
of typhoid fever that only the constant recollection that such symptoms may 
be due to ulcerative endocarditis will save the physician from an error in 
diagnosis. Even epistaxis may develop. 

In the malarial type the constant recurrence of moderate chills, moderate 
fever, ansemia, and some sweating may be very misleading. 

In the cerebral form there is severe headache, unconsciousness, and 
convulsions due to an associated meningitis. In some instances the 
simultaneous development of septic arthritis makes the case resemble acute 
rheumatism. Burrows has reported a case in which vomiting and purging 
were so severe that he believed the patient to be suffering from homicidal 
poisoning. 

Cases are recorded in which the splenic enlargement was so great that the 
patient was thought to be suffering from splenomedullary leukaemia. In 
other cases the diagnosis of acute tuberculosis has been made. 

Albuminuria and hematuria are common symptoms, but renal infarction 
may take place without either albumin or blood being found in the 
urine. 

Endocardial murmurs are not always present. They are shifting in time 
and in character and may be found one day and be lost the next. Further, 
it sometimes happens that the murmurs change in character from day to 
day, owing to the progressive character of the lesions. When murmurs exist 
they are more frequently due to old lesions than to the new ones produced 
by the acute infection. 

Complications. — The complications of ulcerative endocarditis are many 
and serious. It not infrequently happens that a septic embolus not only plugs 
an important vessel, and so causes an infarct in such organs as the kidney, the 
lung, and the spleen, but it acts as a focus of septic development. Such 
embolic closure frequently occurs in the branches of the left middle cerebral 
artery, and causes temporary or permanent aphasia or hemiplegia. Peripheral 
vessels, such as the popliteal or brachial or lingual arteries, may also be 
affected. Occasionally violent abdominal pain, followed by bloody stools 
and signs of collapse, indicates that embolism of the mesenteric vessels has 
taken place. Sometimes uraemia, due to the septic nephritis which is present, 
ends the patient's life. 

Diagnosis. — The points of value in diagnosis are the suddenness of onset 
in some cases, the up-and-down temperature waves, which form steep curves 



488 DISEASES OF THE HEART 

on the charts, the repeated rigors, the presence of distinct leukocytosis, the 
presence of pyogenic organisms in the blood, the absence of the malarial 
organism and of the Widal reaction, and, finally, the presence of great feeble- 
ness and irregularity of the heart's action. In some cases, however, the 
diagnosis from physical signs may be practically impossible. The Widal 
test may throw much light on the case if persistently positive. 

Prognosis. — It is hardly necessary to state that the prognosis is most grave. 
Recovery rarely occurs, and death may take place in the first two weeks or 
earlier. Sometimes life is preserved for weeks. The duration depends 
largely upon the character of the infection, the condition of the heart and of 
its valves, and the occurrence of complications. Some cases extend over a 
period of several months, and most of them last for several weeks. That 
healing may take place and recovery occur in cases of true ulcerative endo- 
carditis is proved by a large number of cases now on record, in which the 
condition has been proved by subsequent autopsies to have existed, the 
patient dying of another malady. 

Treatment. — The treatment of ulcerative endocarditis is not very satisfac- 
tory. Antistreptococcic serum may be of benefit in a few cases, provided 
that the streptococcus is the cause of the disease, and provided that the variety 
of streptococcus used in the preparation of the serum is the same as that 
present in the heart. Aside from this specific treatment, the only thing to do 
is to support the system by the wise use of tonics, such as tincture of the 
chloride of iron and the tonic bitters. Full doses of quinine may be used. 
The most important function of the physician is to maintain nutrition by the 
use of good food and to order no drugs which, by disordering digestion, will 
interfere with the digestive and assimilative functions. 

Chronic Endocarditis. — As already stated, chronic endocarditis is fre- 
quently a sequence of one of the acute forms just described, and, therefore, 
as a rule, it affects the left side of the heart and the mitral leaflets oftener 
than the aortic valves. In some instances, however, it depends upon 
alcoholism, gout, and syphilis, in which case associated changes in the heart 
muscle and bloodvessels are also found. A slowly progressing valvulitis 
or sclerosis of the valves, which comes on insidiously, is frequently asso- 
ciated with arteriosclerosis (arteriosclerotic endocarditis), with chronic 
renal disease, chronic metallic poisoning, especially that due to lead, 
and other conditions associated with high arterial tension, with or 
without the presence in the blood of some specific irritant to which 
the changes may be ascribed. As the acute inflammatory process 
merges into the chronic form, one of two changes appear in the 
endocardium. There is an overproduction of connective tissue in the 
endocardium, with thickening, stiffening, and lessened elasticity, which 
chiefly affects the valvular leaflets. Following this condition, as a result 
of further degenerative changes, we find contractions or localized yieldings 
of the valves which produce an unevenness of their surfaces, so that their 
edges can no longer be accurately approximated; nor do they permit the 
free flow of blood through the orifice which they guard, since they are unable 
to yield during the period at which a free flow of blood should normally take 
place. Even when the valves are thickened and distorted they may still be 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 489 

adequately covered by endothelium, but in some instances the endothelium 
may be absent, thereby exposing calcareous and roughened surfaces upon 
which fibrin is sometimes deposited. The chief factors in producing cardiac 
failure in chronic endocarditis are irregular contractions which distort the 
valves, causing their edges to become everted, inverted, or curled up. In 
addition the chordae tendinese which control the valves guarding the auriculo- 
ventricular orifices become shortened and thickened so that they interfere 
with the free movement of the valves. (See Diseases of the Myocardium.) 
In that form of the disease in which mural endocarditis is present, patches 
of sclerosis or cicatrices may be seen over the walls of the ventricles. (See 
Chronic Valvular Disease.) 

CHRONIC VALVULAR DISEASE AS A RESULT OF CHRONIC 
ENDOCARDITIS. 

Chronic valvular disease of the heart is very constantly met with in 
medical practice, and its frequency is, as a rule, in direct proportion to the 
age of the patient examined. This is due to the sclerotic changes which are 
prone to take place in the valves as age advances, and to the fact that in 
those who have passed the period of middle life the heart in all its parts is 
unable to withstand the strains, which may come to it, as well as in earlier 
periods. The chief causes of valvular lesions may be placed in three divisions, 
namely: (1) those due to infectious diseases, particularly rheumatism, which 
may leave behind damage which only becomes apparent w T hen age or some 
unusual strain weakens the heart muscle; (2) fibroid or sclerotic changes 
ensuing as a result of age, gout, syphilis, and alcoholism; (3) definite 
myocardial degeneration and dilatation which does not cause direct but 
indirect valvular failure in function, as described elsewhere. (See Relative 
Insufficiency.) 

Experience in the larger London hospitals, some fifteen years ago, led me 
to believe that cardiac valvular disease was much more common in England 
than in America. It is interesting to note, however, that this view is 
incorrect, for out of 59,762 medical cases which are recorded in hospitals 
in London, there were 3059 cases of valvular heart disease, or a percentage 
of 5.1; and out of 91,985 medical cases in hospitals in different cities in the 
United States, there were 4108 cases of valvular disease, or a percentage 
of 4.4. The actual difference in frequency in England and America is, 
therefore, not very marked, not only as regards endocarditis, but acute rheu- 
matism as well. (See Acute Rheumatism.) 

Valves Affected. — Series of statistics differ somewhat as to the relative 
frequency with which different valves are affected. One difficulty is that 
there has never been a sufficiently large collection of statistics to give 
results free from error. Another difficulty lies in the differentiation of true 
and false aortic stenosis; for it is evident that certain, statistics which 
give a large percentage of this lesion include cases in which there is not 
true simple stenosis (which is quite rare without regurgitation) and cases in 
which atheroma and aortic roughening cause a systolic aortic murmur. 

All clinicians and pathologists are in accord in stating that mitral re- 



490 DISEASES OF THE HEART 

gurgitation is the most common lesion by long odds. Jiirgensen has 
analyzed 2470 cases of valvular cardiac disease, with the following results 
as to the relative frequency with which valvular disease occurs: mitral 
disease, 1616; aortic disease, 457; pulmonary valvular disease, 56; tricuspid 
disease, 10; associated aortic and mitral disease, 224; associated mitral and 
tricuspid disease, 45; lesions at the mitral, aortic, and tricuspid valves, 24; 
and at the aortic and tricuspid valves, 2. Unfortunately he does not state 
what the lesions are — i. e., regurgitant or stenotic. It is an open question, 
too, how many of the cases of so-called mitral disease and tricuspid disease 
were secondary murmurs due to dilatation of those orifices and not to true 
valvular defects. 

Some years ago, T. G. Ashton, my then chief of clinic at the Jefferson 
Hospital, made an analysis of 1024 cases of valvular disease met with in 
life insurance examinations. His results showed that of these 557 were cases 
of mitral regurgitation, 136 were aortic stenosis, 47 were aortic regurgitation, 
32 were mitral stenosis, and 11 tricuspid regurgitation. I believe that these 
statistics, while accurate in themselves, are to some extent misleading, and 
that the proportion of cases of aortic stenosis is too high. (See article on 
Aortic Stenosis.) The following figures obtained by the analysis of 908 
cases of valvular heart disease treated in Westminster Hospital, London, 
show that the most common single lesions are mitral regurgitation, mitral 
stenosis, aortic regurgitation, and aortic stenosis, 1 in order of arrangement, 
and that of double lesions at one orifice the relative frequency is double 
aortic, double mitral, double pulmonary, and double aortic with double 
mitral. Mitral regurgitation quite frequently occurs as the result of aortic 
regurgitation, through dilatation of the mitral orifice. 

Mitral disease affects more women than men; aortic disease more men 
than women. 

Aortic regurgitation is the most fatal lesion. Mitral stenosis ranks second 
in fatality, aortic stenosis third, and mitral regurgitation fourth. The mor- 
tality of double aortic lesions is greater than that of double mitral. 

The statistics of A. Lockhart Gillespie, based on a study of 1914 cases 
treated in the Edinburgh Royal Infirmary, are especially interesting in that 
they show the mortality of valvular lesions in the two sexes according to 
age. Gillespie found that the maximum mortality in males with aortic 
incompetence or stenosis occurs between the age of fifty and sixty-nine, 
but in those with double lesions the years from twenty to twenty-nine are 
those with the highest mortality. The female maximum mortality in aortic 
incompetence and aortic stenosis falls between the years of forty-nine and 
fifty. Mitral stenosis proves most fatal at from thirty to thirty-nine years 
in males, and from forty to forty-nine in females. The death rate in females 
between twenty and twenty-nine, forty and forty-nine, and fifty and sixty- 
nine is higher than in males at similar periods. The death rate in mitral 
incompetence in both sexes rises progressively with the age. In cases of 
double mitral lesion, the male maximum mortality falls between thirty and 
forty-nine, and in the female between fifty and sixty-nine. 

1 This probably refers to true stenosis and not to cases in which only the aortic systolic murmur was 
present. (See Aortic Stenosis.) 



Fig. 69 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 491 

Before proceeding to a consideration of the various valvular lesions it is 
essential that the mechanism of the valves in health and disease be clearly 
understood (Fig. 69). The cardiac valves are arranged in such a way that 
they prevent a reflux of blood into that cavity which the blood has just left 
in the progress of the normal circulation. As a rule, these valves are capable 
of fitting together so tightly that they completely and effectively close the 
orifice which they guard, but even without the presence of any condition 
of disease they may at times give 
way, and permit some reflux. The 
moderate reflux occurring during great 
muscular strain may be regarded as 
a physiological attempt to relieve the 
blood pressure in the cardiac cavities, 
and if it is not maintained for too 
great a length of time it does no harm. 

It must also be recalled that there 
are at least two ways in which the 
cardiac valves may become incompe- 
tent to prevent reflux of blood. In 
the first, and by far the most common 
type, the valves are diseased, as already 
described in the article on endocar- 
ditis, so that they cannot become 
closely approximated, or they are 
glued together in such a way that the 
same result is achieved, and so they 
also obstruct the flow of blood. In 
the second type the rings, which form 
the bases of the valves and the mar- 
gins of the orifices, yield, and as they 
relax the orifice becomes too large to 
be closed by the valves, which may still 
be practically normal in themselves. 
This condition exists for a brief space 
of time in acute cardiac strain, as just 
stated. It persists for a long time or 
becomes permanent in instances where 
the heart is feeble and the strain is very severe or prolonged, and it is fre- 
quently found in cases of dilatation and feebleness of the heart muscle. 

Those forms of valvular incompetence which occur in athletes or others 
after severe exertion can therefore be put aside as beyond the scope of 
these particular pages, although they will again be discussed under the 
head of functional disorders of the heart. 

In those cases in which the valve becomes incompetent to close an orifice, 
and so permits regurgitation to take place, the failure of the valve is so 
gradual, as a rule, that there develops simultaneously an increase in the 
size and strength of the heart muscle, so that it may by increased power 
and activity compensate for the leakage which occurs. As a result it very 




Diagram modified from Page to show the relation 
of the various valves. A study of this diagram 
will render clear the time of the various cardiac 
murmurs. Thus in mitral regurgitation the blood 
passes back from the left ventricle to the left auri- 
cle during systole, and is dammed up in the pul- 
monary veins, the openings of which are seen in 
the auricular wall, producing pressure on the 
pulmonary valves, the sounds of which are thereby 
accentuated. 



492 



DISEASES OF THE HEART 



frequently happens that this compensatory hypertrophy is fully equal to the 
increased demands made on the heart muscle, and not until the occurrence 
of a severe illness, or until advancing years impairs the power of its fibres, 
are any manifestations of valvular lesions to be found in the patient, save 
the physical signs of hypertrophy and the murmur caused by the regurgitating 
blood. Sometimes even the murmur may disappear for a time. 

In cases in which a valve is ruptured or severely damaged by disease so 
that it fails in its function before the heart can undergo compensatory 
hypertrophy, we often see signs of great circulatory embarrassment from 
the very first part of the illness. 

In all cases of valvular disease in their early stages much depends 
upon the inherent strength of the heart muscle and its ability to increase in 
power, and therefore it is evident that it is of vital importance for the 
patient to rest at this period in order that the strength of the heart may be 
conserved, and in order that it may not be subjected to a severe strain with 
associated dilatation at the most critical period of its existence. This is 
the more important because diseases which secondarily infect the valves 
usually impair, to some extent at least, the myocardium as well. 

In health, when the valves are intact, the heart always possesses a con- 
siderable degree of reserve energy and power, using only a small part of 
its store of energy in a day's work. As a consequence a healthy man can 
run a considerable distance, or leave his desk and go hunting, without 
engendering anything more than fatigue of his voluntary muscles and some 
healthy cardiac tire. This reserve energy is kept for just such purposes. 
On the other hand, if a man who is a sufferer from valvular or myocardial 
disease, even if he is seemingly in perfect health, attempts to follow the 
first one, he soon begins to suffer from cardiac embarrassment, and if he 
persists may become very gravely ill from acute cardiac failure, and rupture 
his compensation by excessive exercise to such an extent that he may be 
bedridden for the rest of his days. In the latter instance nearly all his 
reserve energy is being used daily in the maintenance of a normal circula- 
tion and, having little reserve, he cannot undertake feats that demand great 
calls upon his reserve. This is illustrated in the following squares: 



Reserve 

Energy 




Reserve 
Energy 




All Energy 
In 

Constant 

Use. 


In 

Constant 

Use. 


In 

Constant 

Use. 


health, large reserv 


e. In 


disease, small reser 


\re. J 


^ar advanced disease 
no reserve 



In the last square it is seen that all the reserve is in constant use, and, 
therefore, if any extra exertion is made, the heart promptly fails and death 
may occur. Even in those cases in which sufficient hypertrophy develops 
to adequately compensate for the leak in the valve, the heart is never as 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 493 

capable for work as in health because the reserve is never restored com- 
pletely and the degree of leakage may increase at any moment of strain. 

A consideration of these facts makes one therapeutic fact stand pre- 
eminent above all others, namely, that rest is the chief measure to be insti- 
tuted whenever compensation is failing, as by rest alone can we expect to 
restore reserve energy. 

These remarks have so far dealt with regurgitant conditions. In stenosis 
of the cardiac orifices the same facts hold true, for in such cases the question 

Fig. 70 




A large vegetation on the mitral leaflet. (Kast and Rumpler.) It can be readily seen that this 
would cause both a mitral obstructive and a mitral regurgitant murmur. 

is whether the heart muscle possesses enough strength to drive the blood 
through the obstructed area. 

Given a case of valvular disease the prospects of survival depend almost 
entirely upon the ability of the heart to undergo compensatory hypertrophy, 
and therefore the prognosis depends largely upon the state of the muscle, 
the absence of arteriocapillary fibrosis, which, if present, strains the heart 
and wearies it, the ability of the patient to pursue an easy occupation and 
his willingness to avoid habits of life which strain the heart. 

With these preliminary remarks we may pass on to a discussion of the 



494 DISEASES OF THE HEART 

individual valvular lesions, taking up first of all the most common of them, 
namely : 

Mitral Regurgitation. — Mitral regurgitation, often called "mitral incom- 
petency" or "mitral insufficiency," depends in the great majority of cases 
upon thickening, shortening, or distortion of the mitral leaflets, those bicuspid 
valves which in health guard the left auriculoventricular orifice, in such a 
way that the blood when pressed upon by the contracting walls of the 
ventricle cannot regurgitate into the left auricle. 

Associated with this valvular defect there are usually vegetations on the 
edges of the valves which prevent proper approximation of their edges. 
The chordse tendinese, which extend from the ventricular wall to the leaflets 
for the purpose of giving them support, are shortened so that they will not 
permit the full movement of the valves. In some instances the valves, their 
fibrous bases, the chordse tendinese, and even the endocardium are so com- 
pletely calcareous that the ordinary physiological functions of the part are 
impossible. It is evident that it is almost impossible for such advanced 
changes to be present without at the same time causing some obstruction 
to the flow of blood from the auricle to the ventricle, and therefore we find 
that in nearly all cases of well-developed mitral regurgitation some mitral 
stenosis also exists. 

Pathology. — The morbid anatomy has already been discussed under the 
heading of Endocarditis. The morbid physiology or pathology of mitral 
regurgitation is as follows: 

During systole the blood from the left ventricle in cases of mitral regurgi- 
tation flows in two directions. A larger part escapes into the aorta, as in 
health, and a smaller part of it regurgitates through the imperfectly guarded 
mitral, or left auriculoventricular orifice, into the left auricle. The results 
of this regurgitation are multiple. In the first place the auricle receives 
more blood during diastole than is normal, for it receives not only the blood 
which comes to it from the pulmonary veins, but it also receives the blood 
which regurgitates from the left ventricle. This excess of blood requires 
the auricle to dilate beyond its ordinary capacity, and if the excess of 
blood is great this dilatation of necessity means distention. If the regurgitation 
progresses gradually there is developed a certain amount of hypertrophy 
in the auricular walls which enables the auricle when it contracts to empty 
itself completely and to prevent continuous over distention, but the muscular 
fibres in the auricle are never well developed as compared to those of 
the ventricle, and therefore compensatory hypertrophy can never be so 
complete. 

The second result of this lesion is dilatation and hypertrophy of the left 
ventricle, which is due to several causes, namely, the fact that when the 
left auricle empties itself it delivers to the ventricle an excess of blood over the 
normal quantity, for the reasons just given. To hold this excess of blood 
the ventricle must dilate, and, to expel it on contraction, the ventricle must 
undergo hypertrophy. The general system still requires as much blood 
as before, and in order to provide it with that quantity the ventricle must 
increase its activity in order that the amount lost by regurgitation may be 
compensated for by increased cardiac action. 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 495 

The third result is found in dilatation and hypertrophy of the right 
ventricle, the labors of which are increased by the fact that the engorgement 
of the left auricle renders it difficult for the pulmonary veins to empty 
themselves into it. As a consequence they, and their tributary branches, 
become engorged, raising the resistance in the pulmonary vessels, and so 
the right ventricle finds it less easy to pump blood through the lungs. 
If the pulmonary engorgement is very marked, and dilatation develops 
in the right ventricle more rapidly than does compensatory hypertrophy, 
there is produced an insufficiency of the tricuspid valves guarding the right 
auriculoventricular orifice. 

Fourth, the right auricle now feels the same stress as was felt primarily 
by the left auricle, and it undergoes dilatation and hypertrophy, but this 
hypertrophy is rarely, if ever, adequate to the task set before it, and as it 
fails to properly empty itself, evidences of engorgement of the systemic 
veins becomes manifest in that they become swollen, the liver and kidneys 
are congested, and oedema develops in the lower extremities. 

Fifth, certain definite changes take place in the lungs. As a result of 
their being constantly engorged with blood, they suffer from brown induration 
and atheromatous changes appear in the pulmonary arteries and veins as 
years go by. Finally, when the systemic veins are engorged we find in 
addition serious congestion at the bases of the lungs as a result of impotence 
of the right ventricle and obstruction to the flow of blood from the pulmonary 
veins. 

Lastly, we find, at autopsy, in these cases red atrophy of the liver and 
engorged, cyanotic kidneys. 

In those cases in which there is no primary disease of the mitral leaflets, 
but in which they fail because of acute dilatation of the ventricle so that 
the auriculoventricular orifice is widened and the valves cannot close it, 
there is developed the same train of symptoms save that they are more 
rapid in onset and more severe. This condition develops after great cardiac 
strain, in which the aortic valves are ruptured or the left ventricle and its 
auriculoventricular orifice greatly dilated. The resulting engorgement of 
the lungs may be so severe that their bloodvessels may rupture and profuse 
haemoptysis ensue. These patients nearly always succumb shortly, or remain 
chronic invalids, because the stress develops so suddenly that compensatory 
hypertrophy cannot take place. We have, therefore, an apparent paradox, 
namely, that actual disease of the mitral valves is rarely so serious in its 
consequences as is incompetency of these valves due to other causes. 

Still another cause of mitral incompetence, aside from actual primary 
valvular disease, is Bright's disease, which increases arterial tension and 
thereby throws an increased strain on the left ventricle and the mitral valves 
when the blood is to be thrown out into the aorta. Usually in these cases 
the renal condition indirectly impairs the power of the ventricle, rendering 
its nutrition faulty through impoverishment of the blood and toxaemia, 
and valvular failure then arises as a result of gradual widening of the 
auriculoventricular orifice. 

Symptoms. — It must be evident from what has just been said that many 
cases of mitral regurgitation may present no symptoms for years after the 



496 



DISEASES OF THE HEART 



lesion is established, for as it develops so does a compensatory hypertrophy 
develop. It is only upon extra exertion, which the heart is not prepared to 
meet, that symptoms of cardiac embarrassment ensue, and if the exertion 
is not very severe and not repeated, the dyspnoea and palpitation from 
which the patient suffers may be considered by him as due to indigestion. 
If no illness impairs the heart muscle and no laborious pursuit causes it too 
great stress, the patient advances in comfort to old age, when symptoms 
develop as a result of the fact that his arterial tension gradually increases, 
thereby giving his heart more work to do at each beat, and at the same time 







Showing at x the apex beat, where the murmurs of mitral regurgitation and obstruction can be best 
heard. The arrow pointing to the axilla indicates the direction in which the regurgitant murmur 
is transmitted, and the arrow pointing to the sternum the direction of transmission of the obstructive 
murmur. 

his heart muscle undergoes the changes incident to advancing years. Under 
these conditions compensation " ruptures," to use the ordinary term applied 
to this unfortunate state, and subjective and objective signs appear. 

The subjective symptoms (that is, those felt by the patient) vary consider- 
ably in the early and mild degrees of failing compensation. In some instances 
shortness of breath on exertion brings the patient to the physician, in other 
instances digestive disturbances due to hepatic congestion and secondary 
gastric catarrh are complained of, and in others the patient may com- 
plain of a cough, which is due to a mild pulmonary congestion and bron- 
chitis having its origin in the cardiac failure. In still another class they 
may suffer excessively from cold in moderately cold weather, and perhaps 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 497 

become easily fatigued while walking in cold air because the cold contracts 
the peripheral capillaries and so increases the labor of the heart. When 
the failure of the heart is well marked, then dyspnoea, inability to lie down 
because of oppression, and pain in the epigastrium are perhaps the symptoms 
of which the patient will most complain. 

The objective symptoms (that is, those seen by the physician) are even 
more characteristic. The capillary circulation is sufficiently impaired to 
produce some stasis and consequent cyanosis of the lips and finger-tips or 
even of the face. The fingers, particularly in young persons in whom the 
disease has lasted for some time, are club-shaped — that is, they do not taper, 
but have thickened tips ; there is more or less wdema of the feet and ankles, 
and perhaps blood-spitting as a result of intense pulmonary engorgement 
or infarction. 

Physical Signs. — The physical signs in such a case are usually well 
developed. Inspection of the prsecordium reveals a diffuse and perhaps 
forcible apex beat. Palpation shows a distinct thrill in children, and in 
this class of patients this thrill can frequently be seen as well. The apex 
beat may be distinctly felt well outside and below the nipple line. If the 
compensating hypertrophy is well developed the apex beat may be forcible, 
but if compensatory hypertrophy is lacking it is feeble and diffuse. On 
percussing the prsecordium the normal area of cardiac dulness will be 
found to be enlarged. This enlargement is usually transverse or lateral, 
so that it may extend to the right edge of the sternum owing to enlarge- 
ment of the right ventricle, and as far as the left of the nipple from 
dilatation and hypertrophy of the left ventricle. 

Auscultation provides us with the signs that determine the exact nature 
of the lesions, for the signs so far described are not distinctive of mitral 
regurgitation. When the ear of the physician is applied over the apex of 
the heart there is heard a soft, and often quite loud, murmur, which occurs 
synchronously with the apex beat, or with systole, or contraction of the 
ventricle. This murmur is transmitted to the left axilla, and it may be 
to the angle of the left scapula. If it is very loud it may be heard in any 
part of the chest. If the regurgitation is great enough to cause engorge- 
ment of the lung the pulmonary second sound, due to a quick shutting 
of the pulmonary valves guarding the orifice of the pulmonary artery, may 
be louder than normal. This is best heard at the third left costal cartilage. 
When the regurgitation is severe enough to have resulted in tricuspid 
regurgitation from engorgement of the right side of the heart, there may be 
heard at the fifth costal cartilage on the right side a comparatively soft 
systolic murmur due to this secondary leak, but in some instances the 
mitral murmur completely obscures the tricuspid murmur. In others the 
tricuspid murmur can be heard only at the ensiform cartilage. 

It is of vital importance for the physician to recall the fact that a murmur 
so slight as to be almost inaudible is not an indication of the presence of 
a small and unimportant lesion of the mitral valve. On the contrary, the 
presence of a faint murmur often, but not always, indicates that the heart 
is too feeble to drive the blood with sufficient force to make the murmur 
clearly audible. 
32 



498 DISEASES OF THE HEART 

The pulse of mitral regurgitation varies, of course, with the extent of 
the lesion and the degree of compensation. It is usually nearly normal, 
though lacking somewhat in volume even when compensation is complete. 
It is irregular and small when compensation is insufficient. When com- 
pensation is ruptured, it is very small and hobbling. 

Diagnosis. — It is desirable to separate mitral regurgitation due to dila- 
tation of the mitral orifice from mitral regurgitation due to true valvular 
disease. This is in many cases impossible if the action of the heart is 
already seriously impaired, the more so because in many instances the 
secondary dilatation produces some widening of the orifice. While the 
physical signs may not be distinctive the absence of any history of rheu- 
matism or other infection which affects the valves, and the presence, or 
history of the presence, of any exhausting illness which weakens the heart 
muscle, or of any strain which has dilated the orifice, would indicate that 
dilatation rather than true valvular disease is present. This is particularly 
true if the strain, though moderate, has occurred during convalescence, 
while the heart is weak. This differentiation is important because in some 
cases with returning health and strength the leak may cease and perfect 
recovery ensue, whereas if the valve is actually diseased good health can only 
come from compensatory hypertrophy and the murmur will probably 
always persist. 

The possibility of a murmur being due to ansemia is also to be recalled, 
but hsemic murmurs are usually very soft and are best heard near the 
base rather than at the apex. 

The diagnosis of mitral regurgitation is therefore chiefly based upon the 
presence of a murmur heard most clearly with systole at the apex and trans- 
mitted to the axilla. 

Prognosis. — The prognosis in a case of mitral regurgitation depends upon 
the age of the patient, his occupation, the general condition of his vitality, 
and the severity of the lesion. When a child develops mitral disease it often 
does not survive puberty, chiefly because dilatation in such a case is 
usually excessive and because the constantly increasing demands of its 
growth require of its heart more than it can provide. In young adults who 
will rest after damage to the valves during an attack of rheumatism until 
compensation is really established, the prognosis is good, provided that the 
subsequent occupation is not too strenuous, although with the onset of 
old age vascular changes will probably cause breakdown. In feeble 
persons, however, the prognosis may be unfavorable from the onset, 
particularly if hypertrophy is lacking and dilatation is marked. In old 
persons the prognosis is bad for obvious reasons, since the heart 
cannot, at this time of life, readily gather new strength to meet new 
demands. 

If syphilis or alcoholism are factors in the case the prognosis is grave, and 
if the kidneys are diseased the prognosis is, of course, very bad. So, too, 
the presence of arteriocapillary fibrosis with high arterial tension is a 
serious or grave factor, in that it gives the heart so much work to do. (For 
the relationship of this lesion to age and mortality, see page 490 in article 
on Chronic Valvular Disease.) 



CHROXIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 499 

Treatment. — (This is discussed at the end of the articles on Valvular 
Disease.) 

Mitral Stenosis. Definition. — By mitral stenosis we mean a condi- 
tion of the tissues composing the mitral valves or surrounding the left 
auriculoventricular orifice whereby the blood is prevented from passing 
with normal ease from the left auricle to the left ventricle. It is some- 
times called ''mitral obstruction." 

Etiology and Pathology. — Mitral stenosis is far more common in females 
than in males, although the reason for this is not clear. Sir Dyce Duckworth 
found that out of 264 cases of this disease 177 were females, and other 
statistics are practically in accord with Duckworth's. It is due in the great 
majority of instances to gluing together of the mitral valves as the result 
of acute endocarditis arising from acute rheumatism. 

With this adhesion of the valves there is often associated a growth of 
vegetations on their edges and not uncommonly thickening and sclerosis of 
the chordse tendinese, the papillary muscles and the leaflets themselves, so 
that the parts lose their elasticity and are so stiffened that they are unable 
to move out of the way of the blood stream when it seeks to pass into the 
ventricle. This sclerotic process is so marked in some cases that the 
tissues may seem almost cartilaginous in character, and in advanced life 
lime salts may be deposited to such an extent that the fibrous tissue is 
calcareous and even the walls of the ventricle are infiltrated by calcareous 
masses. In some instances the adhesions are so complete that the valves 
form a funnel-shaped tube through which the blood must find its way. In 
other instances the edges of the valves are adherent and their margins 
thickened, leaving only a small orifice between them, forming the so-called 
" button-hole" mitral orifice, and in still other cases the conjoined edges of 
the valves are so drawn or puckered that the orifice when the auricle is 
opened looks like the normal anus. 

The funnel-shaped opening is most commonly seen in children, but it 
is not always, as some have thought, a congenital lesion; the button-hole 
orifice is much more common in adults. Sansom states that the proportion 
is one button-hole to eight funnels in children, and that as adult life is 
reached the proportion changes to twenty-five button-holes to one funnel. 

There can also be no doubt that chronic contracted kidney with associated 
arteriocapillary fibrosis not only causes mitral stenosis, but that even the 
funnel-shaped opening just described may be developed in this type of 
cases. The studies of Duroziez and Huchard in France, and of Goodhart, 
Sansom, and Pitt in England prove this fact. In 542 autopsies in cases of 
interstitial nephritis, Pitt found mitral stenosis 33 times. 

The results of mitral obstruction are overdistention of the left auricle 
and scanty blood supply to the left ventricle. The engorgement of the left 
auricle results from its inability to empty itself, and leads to dilatation and 
to some degree of hypertrophy. In some instances the growth of muscle 
fibres is so scanty that no true hypertrophy ensues, in others they seem to 
become actually atrophied, but in other instances very complete compen- 
satory hypertrophy develops, so that the auricular wall is distinctly thicker 
than normal. Indeed, it may appear as a firm, muscular mass which does 



500 DISEASES OF THE HEART 

not collapse at autopsy as the ordinary auricle is wont to do. Whether 
hypertrophy exists or not, dilatation is always present. When such an 
auricle is opened the endocardium is often found to be thickened and a 
laminated clot may line its cavity. In other instances polypoid or globular 
coagula are attached to the auricular walls, and these globular thrombi may 
almost fill the auricle. At times the thrombus is free, acting as a ball 
valve in the auriculoventricular orifice. 

The wall of the left ventricle in these cases is often thinner than usual, 
but dilatation and hypertrophy may be present. 

The accumulation of blood in the auricle leads to the engorgement of 
the lung, and the same changes occur in its vessels and tissues that have 
been described under "Pulmonary Congestion" and " Mitral Regurgitation. " 
So, too, the right ventricle undergoes hypertrophy and dilatation from similar 
causes, and the tricuspid valves, even more frequently than in mitral regurgi- 
tation, give way, so that pulsation of the jugular veins, pulsation of the 
liver, and oedema of the lower extremities finally develops. Embolism 
often occurs in mitral stenosis, and, as in all cases of embolism arising in 
the heart, the embolus usually lodges in the left hemisphere of the brain. 

If the narrowing of the auriculoventricular orifice is not progressive, and 
if the auricle undergoes compensatory hypertrophy, the signs of advanced 
disease may not ensue. It is only when auricular hypertrophy fails that 
the malady becomes manifest and causes the symptoms of cardiac failure 
which in all respects resemble those described under mitral regurgitation, 
save that the venous and hepatic pulsation just described are more fre- 
quently present. 

Physical Signs. — The physical signs of mitral obstruction are as 
follows : Inspection of the chest may reveal pulsation at the apex of the 
heart near the nipple, and also near the base of the heart close to the 
sternum, in the second or third left intercostal spaces. Not rarely there 
may be, in addition, epigastric pulsation. If a straw, or piece of card- 
board, be placed over the pulsating spots at the apex and base, it will be 
found that they do not move synchronously, but the lower one moves with 
the ventricle and the upper one with the auricle. It has been claimed 
that the auricle does not produce this upper pulsation, and that it is due 
to the movement of the conus arteriosus of the right ventricle, but this is 
seemingly disproved by the fact that the two movements are not syn- 
chronous with systole. If the patient be a child these pulsations are much 
more noticeable than if he be an adult, at which time of life pulsation may 
be absent. In children bulging of the chest wall close to the sternum and 
near the epigastrium may be quite marked, and if pulsation be well defined 
in this area and absent from the region of the nipple, indicating hyper- 
trophy of the right ventricle, the diagnosis of mitral stenosis is strength- 
ened, provided that adherent pericardium can be excluded. 

Palpation does not always give us much information, but sometimes it 
practically decides the diagnosis, for there are three signs on palpation 
which are noteworthy in this lesion. There is a thrill which is pre- 
systolic in point of time and is felt in the fourth or fifth interspace inside 
the nipple line. It is characterized by sudden arrest at the moment of 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 501 

systole. This sign may be considered diagnostic of mitral stenosis provided 
we have excluded the possibility of aortic regurgitation, which sometimes 
causes a similar sign. This thrill may be present at one time and 
entirely absent at another, and it may be absent when the patient is 
in the dorsal decubitus and present when he is erect, or, again, it is pres- 
ent after exercise and absent after rest. The second sign of some im- 
portance in the diagnosis of this disease by palpation is the heaving 
impulse, felt just below the margin of the last costal cartilage on the left 
side without such impulse near the nipple. This has already been spoken 
of under inspection as indicative of hypertrophy of the right ventricle. 




MO shows area of greatest intensity of a mitral obstructive murmur; TR shows area of greatest 
intensity of a tricuspid regurgitant murmur. The fine lines indicate the area in which is felt the 
characteristic thrill of mitral stenosis. 

Care must be taken, however, that signs of hypertrophy of the left ven- 
tricle are really absent, for it sometimes happens that an overlapping of 
the lung covers the left side of the heart so that it does not transmit its 
impulse to the chest wall. The third sign on palpation is the discovery 
of the edge of the enlarged liver, which pulsates, below the level of the 
floating ribs on the right side. Here, again, care is necessary, for it often 
happens that the liver is moved by a transmitted impulse from the heart 
muscle through the diaphragm. 

Percussion of the prsecordium may reveal, in cases of mitral stenosis, a 
distinct increase in the area of cardiac dulness to the right, with comparatively 
little extension of dulness to the left. This is due to the enlargement of the 



502 DISEASES OF THE HEART 

right ventricle. When, however, the disease is far advanced and the heart 
is greatly dilated or hypertrophied the left margin of dulness is distinctly 
extended, and in such cases the area of cardiac dulness to the left of 
the nipple line may be very great. 

Auscultation is, of course, the most important aid in the diagnosis of 
mitral stenosis, since it presents no less than six points of interest. The 
first of these is the presence of a murmur which occurs just before sys- 
tole, a presystolic murmur, and is best heard between the nipple and the 
sternum, on the nipple level (Figs. 71 and 72) . In most cases the murmur can 
only be heard in this area, but in some instances it is so loud as to extend 
all over the chest. The murmur is usually harsher than that of mitral 
regurgitation, and is vibratory in character. It is due to the passage of 
the blood through the obstructed auriculoventricular orifice, and it ceases 
with the close of auricular systole. In some cases the murmur may ex- 
tend all through ventricular diastole. At times it is so metallic as to be 
musical rather than purring. 

Another sign of importance is the accentuation of the pulmonary second 
sound, which is best heard at the third left interspace, and is due to the high 
pressure in the pulmonary artery, produced by back pressure on the column 
of blood in the lungs. This accentuation is, however, not so constant in 
stenosis as in regurgitation because of the greater irregularity of the heart 
in stenosis. 

A third sign is the reduplication of the second sound of the heart so 
that it appears as a " tap-tap," or resembles the "postman's knock." It 
is very characteristic of mitral stenosis and is heard at two places: at 
the apex and at the base of the heart. It is, however, supposed to be due 
to different causes at each spot. At the apex Sansom believes it is due to 
the sudden rush of the blood into the ventricle through the narrow orifice 
under the pressure of the hypertrophied auricle. In other words, this sound 
is associated with the normal pulmonary and aortic second sounds. When 
this reduplicated second sound is heard at the base, and this is where it is 
usually heard, it is most diagnostic, and is supposed to be due to an asyn- 
chronous closure of the aortic and pulmonary valves, but in all probability 
the cause is similar to the sound at the apex. This is sometimes called the 
"gallop rhythm." 

The fourth sign of importance is the loud and sudden snapping sound 
which is heard at the close of systole of the ventricle. It is supposed to 
be due to forcible snapping to of the bicuspid or mitral valves. 

The fifth sign is not only somewhat indicative of stenosis, but much more 
of cardiac breakdown, namely, absence of the first sound of the heart at 
the apex. 

Still a sixth sign of mitral stenosis is sometimes of value, namely, great 
irregularity as to rhythm and force. In no form of valvular lesion with 
rupture of compensation is the heart so tumultuous as in this disease. 
As already stated, the absence of a murmur may be more indicative of 
grave valvular disease than its presence. 

When cardiac breakdown ensues it not infrequently happens that the 
presystolic murmur itself disappears because the auricle is too feeble to drive 



CHROXIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 503 

the blood through the auriculoventricular orifice with enough force to make 
a murmur. 

Diagnosis. — Mitral stenosis is at times the most difficult of all the cardiac 
lesions to diagnosticate, chiefly because when compensation is ruptured no 
murmur may be present, and the action of the heart being exceedingly 
irregular its sounds are confused. Again, stenosis is so frequently associated 
with mitral regurgitation that the double murmur may cause confusion, the 
more so as only one murmur may be present at one time and both at another 
time, and also because the regurgitant murmur is often so loud that it 
covers the stenotic murmur, with the result that unless the physician is on 
the qui vive to discover the less noticeable sound it is overlooked. In cases 
which are manifestly ones of mitral stenosis the physician need not hesitate 
to express an opinion, but in the obscure forms of the disease he should 
always reserve his statement until he has had an opportunity of examining 
the heart several times under conditions of rest and exercise, and, perhaps, 
after the use of digitalis or some other drug to strengthen the muscle. 

As the physical signs have already been thoroughly described, it is only 
necessary, at this point, to differentiate mitral stenosis from those con- 
ditions which resemble it. 

The most important of these is the so-called "Flint's murmur" first 
described in 1862 by Dr. Austin Flint, of New York. It occurs in some 
cases of aortic regurgitation, and is supposed to be due to the regurgitating 
blood striking upon the mitral valves and chordae tendineae in such a way 
that they vibrate and so cause a sound. This sound is diastolic in point 
of time because it occurs after the blood has been sent out into the aorta and 
while the ventricle is receiving more blood from the auricle. Its time of 
occurrence is, therefore, practically identical with the murmur of mitral 
stenosis. 

The following points make the differentiation between mitral stenosis 
and "Flint's murmur" in most cases, although in some cases the sepa- 
ration may be impossible. In cases with aortic regurgitation auscultation 
at the second right costal cartilage and along the sternum will reveal a 
diastolic murmur which will not be well defined in these areas in mitral 
stenosis unless the mitral murmur is so loud as to be heard pretty much 
everywhere in the chest. The pulse in aortic regurgitation is characterized 
by a full wave followed by a sudden fall — the "Corrigan pulse" — whereas 
the pulse of mitral obstruction is a fine thread, irregular and feeble. 
Again, in cases of aortic regurgitation with "Flint's murmur" there are 
rarely, if ever, those well-developed signs of pulmonary, hepatic, and splenic 
engorgement which have been described as occurring in mitral stenosis, 
nor does the patient so frequently suffer from haemoptysis due to pul- 
monary congestion or infarction. Further than this, the sharp, snapping 
first sound of the heart characteristic of mitral obstruction is not present 
with "Flint's murmur." 

A second condition resembling mitral stenosis is tricuspid stenosis. On 
general principles, this latter lesion can be excluded on the rule of probabili- 
ties, for tricuspid stenosis is an exceedingly rare lesion. If it exists it is 
usually heard best in the tricuspid area (the area of the fourth right inter- 



504 DISEASES OF THE HEART 

costal space), but it may be clearly heard in the mitral area, and as tricuspid 
stenosis and mitral stenosis exist together in some cases and occur simul- 
taneously, they may not be separable and nothing be known of the lesion on 
the right side of the heart until autopsy. 

At times children suffering from adhesive pericarditis present a presystolic 
sound like that of stenosis. It is to be discovered by the signs of adhesive 
pericarditis (which see). In every case of valvulitis due to rheumatism we 
should bear in mind the possible if not the probable, presence of adherent 
pericardium. The presence of this condition is rendered likely if the liver 
is not only enlarged, but very firm, and if ascites develops in excess of 
that seen in cardiac dropsy. This point is of importance, because if the 
pericardium is adherent we cannot expect very good results from digitalis 
nor from any other method of treatment. 

When a patient presents himself with a disordered circulation and con- 
fused or irregular heart sounds, and no murmur, it must be recalled that while 
such a state may be due to tobacco heart, it may also be caused by mitral 
stenosis with no murmur. 

Prognosis. — The prognosis of mitral stenosis is not as favorable as is that 
of mitral regurgitation or aortic stenosis, and children nearly always suc- 
cumb to it before they reach adult years. Adults who have a severe lesion 
also rarely survive for many years after it begins, but there are very marked 
exceptions to this rule. Thus, I have under observation at present a case 
of mitral stenosis which I examined twenty-two years ago, and who was told 
thirty years ago that the lesion existed. During all these years (he is now 
sixty-nine years of age) he has led a very active life, both physical and 
mental, with no cardiac embarrassment, although he had an attack of 
hematuria when I first saw him, which was due to an infarction of the 
kidney. During this time he has taken no treatment, except at rare 
intervals, his compensation being complete. 

In young women with mitral stenosis, marriage and consequent child- 
bearing often cause rupture of compensation and death. 

The average age at death in cases of this disease is stated by Sansom to 
be about thirty-two and seven-tenth years. (See General Discussion of 
Valvular Lesions and Their Effect on Mortality, page 490.) (For treat- 
ment see close of these articles.) 

Aortic Stenosis. Definition. — Aortic stenosis, often called " aortic obstruc- 
tion, " is a condition in which the left ventricle finds it more difficult than 
normal to expel the blood through the aortic orifice, because this orifice is 
narrowed by disease. The murmur which is produced by the blood under 
these circumstances is systolic in point of time, for it occurs as the left ven- 
tricle expels its contents. It is best heard at the second right costal cartilage 
or under the sternum, at its upper portion. It is of vital importance, how- 
ever, to recall the fact that the presence of a systolic murmur at this point 
is not necessarily indicative of actual obstruction of the aortic orifice. An 
aortic systolic murmur does not necessarily mean an aortic valvular lesion. 
The murmur is usually due to roughening of the lining of the aorta by 
atheromatous plaques. Aneurysm may also be provocative of such a sound. 
So rare is true simple aortic obstruction that it may be said that the presence 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 505 

of a systolic aortic murmur is in most cases probably not due to this lesion, 
unless it is found associated with aortic regurgitation. Some clinicians of 
repute assert that they have never seen pure aortic stenosis without regurgi- 
tation. Cabot states that in 252 autopsies made at the Massachusetts 
General Hospital on persons with valvular disease, there was not a single 
instance of uncomplicated aortic stenosis. 

Etiology. — The causes of aortic obstruction are multiple. In the first 
place, it may be the result of rheumatic endocarditis of so severe a type that 
not only the mitral but the aortic valves are involved, for it is only in rare 
cases that rheumatism attacks the aortic valves and leaves the mitral valves 
untouched. In such a case the endocardium covering the valves is roughened 
in patches, and upon these patches is deposited fibrin from the blood stream, 
which, with proliferated cells, forms granulations and vegetations, fibrous 
thickening, and, finally, the deposition of lime salts. If the inflammation is 
severe the edge of the valves may become glued together, and so a funnel- 
shaped opening is formed, which is much narrower than the normal aortic 
orifice. In rare instances, instead of the valves being adherent and thickened, 
they are adherent and thinned, so that they appear atrophied. Such a condi- 
tion is found at times in children and is thought to be congenital, but even 
in young children the cause may be rheumatism, and Sansom asserts that> 
the condition may be due to rheumatic endocarditis in intrauterine life. 
Rheumatism may be considered the usual cause of aortic obstruction in 
children or in those w T ho have not as yet reached advanced years. 

The cause of aortic obstruction is often not acute in character, as in the 
types just described, but chronic, being due to a gradual atheromatous 
change, which, having involved the aorta itself, spreads to the aortic valves, 
and causes a slowly progressive thickening and calcification of their tissues. 
This is the form of stenosis which is often of a very advanced type, so that 
the orifice may be but a small slit or chink through which the blood escapes. 

From what has just been said, it is easy to understand how it is that 
obstruction to the flow of blood in the area of the aortic valve is exceedingly 
rare as a single lesion. The very nature of the morbid changes which take 
place in the tissues at this point renders the simultaneous existence of aortic 
obstruction and regurgitation probable, for the valves at the aortic orifice 
are either glued together as a result of rheumatic endocarditis, or, more 
commonly, are thickened by chronic endocarditis and calcareous deposits. 
In either instance they are not only in the way of the blood as it passes out 
of the ventricle, but they are incapable of preventing its regurgitation, since 
they are too thick and too stiff to approximate their edges. In other instances 
the presence of vegetations on the valves, in addition to these changes, adds 
to the impairment of their functional activity. 

The secondary changes produced by aortic obstruction are chiefly con- 
nected with the left ventricle. Under favorable conditions this portion of 
the heart usually develops a satisfactory compensatory hypertrophy, the 
muscle fibres gaining in strength and size as the process of narrowing in the 
aortic area gradually progresses. As a consequence, it not rarely occurs that 
even an extreme degree of aortic obstruction is accompanied by such a com- 
plete compensatory hypertrophy that the presence of the lesion is only dis- 



506 



DISEASES OF THE HEART 



covered at autopsy. It is interesting to note that the hypertrophy of aortic 
obstruction differs somewhat from that of aortic regurgitation in the fact 
that the ventricular walls increase in thickness without undergoing any 
great dilatation, whereas, in aortic regurgitation they both dilate and 
hypertrophy, causing eccentric hypertrophy. 

So long as the compensatory hypertrophy of the left ventricle in aortic 
obstruction is adequate, practically no changes occur in the other parts of 
the heart. It is only when compensation ruptures that symptoms of impaired 
circulation ensue, or the mitral valves give way under the strain, and con- 



FlG. 73 




Showing area of greatest intensity and the direction of transmission into subclavian and carotid 
arteries of the aortic obstructive murmur. 



gestion of the left auricle and of the lungs develops. This may in time 
increase the labor of the right ventricle and lead to its hypertrophy. 

Symptoms and Physical Signs. — Patients suffering from aortic obstruction 
rarely present or complain of any symptoms which are in any way charac- 
teristic of the lesion. At times a sense of constriction or oppression is felt 
over the aortic area, as it is in cases of aortitis or atheroma of the aorta, 
and as it is felt in some cases of true angina pectoris. When there is an 
associated aortic regurgitation, the symptoms are of that lesion. (See 
Aortic Regurgitation.) 

The physical signs vary considerably with the type of patient exam- 
ined and with the stage of the disease. In old men whose chest walls are 
thickened and rigid and whose lungs are often emphysematous, so that the 



CHROXIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 507 

edge of the left lung projects between the heart and the chest wall, it may 
not be possible to either see or feel an apex beat, even though the heart 
be considerably hypertrophied. On the other hand, if the patient be 
young, or the chest wall pliable, the apex beat may be seen and felt dis- 
tinctly and forcibly, and it is usually a little below and a little outside the 
nipple because of the hypertrophy. If the action of the heart is forcible 
and the fingers are placed over the second right intercostal space, a dis- 
tinct thrill can be felt. This thrill is in the nature of a vibration and is 
often transmitted down the sternum and even up into the carotids. This 
thrill felt in the area described is very characteristic of aortic obstruction, 
but it is also felt in aortic aneurysm. 

The area of cardiac dulness on percussion is not materially enlarged, unless 
associated regurgitation has caused its well-known secondary cardiac changes. 

Auscultation reveals a murmur which is loudest at the second right 
costal cartilage near the sternum. 

This sound is transmitted in most cases into the vessels of the neck, and 
not infrequently it is heard over the sternum as low as the ensiform cartilage. 
It occurs with systole of the heart, and it is usually loud if compensation is 
preserved. Not only is it loud, but it is apt to be harsh and even musical, 
and it is long and blowing in character. The aortic second sound is 
usually absent. 

When rupture of an aortic valve takes place the murmur is usually widely 
diffused, very loud and musical. I showed a patient to the College of Physi- 
cians of Philadelphia in 1902 that possessed a murmur capable of being 
heard when the ear was eighteen inches from the chest. It could be heard 
on top of his head, in his radial arteries, and if the stethoscope was placed so 
that his lips encircled it the murmur could be heard in his mouth. There 
was also a loud aortic regurgitant murmur in his case. The patient was a 
brakeman who suffered from sudden and severe dyspnoea and syncope on 
lifting a heavy weight, and who had a history of syphilis. 

The pulse in aortic obstruction is small (pulsus parvus) because the 
heart cannot expel a large wave of blood through the narrow aortic opening. 
The wave rises gradually and then falls gradually, unlike the sharp upward 
jerk felt in aortic regurgitation. 

Diagnosis. — Sufficient emphasis has already been placed on the fact that 
a systolic murmur at the second right costal cartilage does not mean, neces- 
sarily, aortic obstruction, but if the time of the murmur, the thrill, the 
peculiar pulse and atheromatous vessels are present in an old person 
the diagnosis is fairly certain. When the murmur is due to atheroma 
of the aorta alone the aortic second sound is usually sharp and clear 
instead of being impaired as it is in true obstruction. Aneurysm is 
excluded by the absence of the characteristic signs of that state. (See 
Aortic Aneurysm.) 

Sewall asserts that an aortic stenotic murmur heard at the apex disappears 
on pressure of the stethoscope, and so separates itself from the systolic 
murmur of mitral regurgitation. 

Prognosis. — The prognosis in a case of aortic stenosis is generally con- 
sidered as more favorable than in any other valvular lesion, but in each 



508 DISEASES OF THE HEART 

individual case the physician must base his prophecy as to life upon the 
age of the patient, the state of his arteries, and the condition of the 
kidneys. The mere presence of far-advanced atheroma in aged per- 
sons who have an aortic stenotic lesion is not necessarily of evil import. 
As Clifford Allbutt well says, "We see well-to-do old ladies leading tran- 
quil lives up to four-score years or more with systolic aortic murmurs of a 
quarter of a century's standing." On the other hand, in somewhat younger 
persons, who have more fibrous and less calcareous arterial changes, the 
prognosis is not so good, either because they are at a period of life when 
they are prone to resort to exercise and so strain the heart, or because there 
is a tendency to fibroid heart as well. Allbutt's view that " a person who in 
young or middle life begins to suffer overtly from the symptoms of aortic 
stenosis has but a few years to live" is certainly correct. (For treatment 
see end of article on Valvular Disease.) 

Aortic Regurgitation. Definition. — Aortic regurgitation is often called 
" aortic insufficiency" or " aortic incompetency," and consists, as its names 
indicate, in a condition of the aortic leaflets, or of the aortic orifice, whereby 
the blood after being expelled by the contraction of the left ventricle into 
the aorta is permitted to return. 

Etiology and Pathology. — By far the most common cause of this lesion is 
acute rheumatism, which causes the same changes in the valves at the 
aortic orifice as have already been described as taking place in the mitral 
leaflets, namely, distortion, retraction, stiffening, and the development of 
vegetations. As a rule, when rheumatism is the cause the mitral valves also 
suffer seriously, so that the aortic and mitral lesions coexist. A second 
common cause is aortitis, or atheroma of the aorta, which extends to the 
valves and causes sclerotic and degenerative changes which alter the position 
and functional ability of the aortic cusps. This atheroma may be due to 
mere senility, or to syphilis, gout, or even malarial infection. It is remark- 
able how many of these cases have a history of excessive toil, excessive 
venery, and excessive drinking, with the result that the bloodvessels and 
heart have had to stand strain, toxaemia, and infection. The cases of aortic 
regurgitation which are due to these causes suffer the greatest destruction 
of the valves, for their surfaces may ulcerate or the deposition of an excess 
of lime salts causes necrosis to such an extent that only stumps of the valves 
exist. 

A third cause, which is much more rare, does not primarily involve the 
valves, but the aortic orifice. The aortic ring undergoes dilatation and as 
a result the valves cannot become approximated. In other words, the open- 
ing is too large for them to close it. This condition is met with in cases of 
aneurysm of the aorta. It is not by any means as frequent as dilatation of 
the mitral orifice, because the ring around the opening of the aorta is largely 
made up of fibrous and fibroelastic tissues, whereas that which supports 
the mitral orifice is largely muscular. 

A fourth cause is rupture of an aortic leaflet as the result of violent strain. 
This accident rarely, if ever, occurs unless the valve has already been 
weakened by disease. 

A fifth cause is the presence of vegetations on the aortic valves, developing 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 509 

in the course of the acute infections or chorea. Some of these lesions differ 
from those due to ordinary endocarditis in that they are not always per- 
manent, but may entirely disappear. 

A sixth cause is ulcerative endocarditis, in which great destruction of the 
valves may take place or abundant vegetations develop. This is usually 
due to the pneumococcus. (See Croupous Pneumonia.) 

A seventh cause is congenital malformation, which is exceedingly rare. 
Indeed, aortic regurgitation due to this cause is more rare than are con- 
genital defects themselves, for congenital defects in the valves may not be 
severe enough to permit leakage. 

Finally (eighth) a functional relaxation of the aortic orifice occasionally 
is met with in which temporary regurgitation takes place for the same 
reasons as have been described elsewhere. I saw a case of this character 
while on duty at St. Clement's Hospital some fifteen years ago, in a young 
girl who had a loud, aortic regurgitant murmur and apparently a fusiform 
aneurysm of the innominate artery. At the autopsy the vessels seemed 
perfectly normal in size, but on testing them they were found to be unusually 
yielding and elastic. 

The secondary effects of aortic regurgitation upon the left ventricle are 
most important and interesting. The left ventricle no sooner expels its 
contents into the aorta and begins to dilate in order to receive the blood from 
the auricle, than it also receives part of the blood it has just sent into the 
aorta by reason of the fact that the aortic valves permit regurgitation. The 
ventricle, therefore, contains not only the normal amount of blood from 
the auricle, but an additional quantity from the aorta, and so it becomes 
dilated to contain this excess and also undergoes hypertrophy in order to 
expel this excess into the aorta and empty itself. Any strain upon the heart 
increases the dilatation, and as a result we often see, particularly in those 
who live by manual labor, an extraordinary increase in the size of the 
heart, which is both greatly dilated and greatly hypertrophied, the so-called 
eccentric hypertrophy of aortic regurgitation resulting in the "ox heart" 
or cor bovinum. 

The rapidity and degree of the hypertrophy is extraordinary in some cases. 
Sansom speaks of a case in which the heart was thought to have gained an 
ounce each week for four or five weeks, and Dulles has recorded a case in 
which the heart weighed forty-eight ounces. When the ventricle is much 
dilated the ring guarding the mitral orifice may yield and insufficiency of 
the mitral valves ensue and thus cause dilatation of the left auricle, con- 
gestion of the lungs, and hypertrophy of the right side of the heart. In 
some cases of aortic insufficiency, when the cause is atheroma, the patho- 
logical process of fibrosis and calcification gradually extends to the tissues 
around the opening of the coronary arteries, which are then unable to 
properly supply the heart with blood, or the coronary arteries themselves 
become atheromatous. Under such conditions compensatory hypertrophy 
may never be established, or if established rapidly fails, is ruptured, and 
death ensues. 

Symptoms and Physical Signs. — The symptoms of aortic regurgitation are 
more characteristic than are those of any other form of valvular disease, 



510 DISEASES OF THE HEART 

and are more constantly met with in such cases, although compensation 
may be adequate in many cases for a time at least. Dizziness and partial 
syncope often appear on suddenly sitting up or on standing up, and at 
times are present even when the patient lies down. Palpitation and dyspn&a 
on exertion are pressing symptoms if the heart is feeble, and even when 
compensation is adequate pain in the region of the heart is often a severe 
symptom, being radiated into the arms or into the neck. At this time the 
attacks may be identical with those of true angina pectoris. Sudden death 
occurs more frequently in this form of valvular disease than in any 
other. 

When compensatory hypertrophy is lost the patient is forced to sleep 
sitting erect or nearly erect in an easy chair; he is usually very pallid, but 
at times cyanotic. Cough and pulmonary complications do not ensue until 
the mitral valves give way. 

When the cardiac failure is well marked, and it is evident that death 
cannot be many days away, distressing mental symptoms often appear. 
Hallucinations are pressing and even an active maniacal delirium may 
develop. At times the patient becomes suicidal in his insanity. In some 
cases these mental disturbances are due to disordered and inadequate cere- 
bral blood supply, and at times they are due to a complicating nephritis 
arising as a late lesion of the general breakdown. 

Physical Signs. — The physical signs are characteristic when well devel- 
oped. On inspection the carotid arteries are seen to pulsate markedly, and 
even the head may be moved by the impulse transmitted to it by the heart. 
The thorax, in the prsecordium and neighboring parts, heaves with each pul- 
sation of the heart and is often bulging, owing to the cardiac hypertrophy and 
dilatation. An ocular examination of all the superficial arteries will show a 
characteristic throbbing or jerking, and if a glass slide be lightly pressed 
against the lower lip capillary pulsation is readily seen, in that the color of 
the mucous membrane rises and falls with the movements of the heart. 
Such capillary pulsation, often called " Quincke's pulse," can be seen under 
the thumb-nail when it is gently pressed upon, and in the red line produced 
on the skin of the forehead by drawing the end of a pencil over this part. 
As the arteries are often elongated, and therefore more tortuous than in 
health, the impulse of the wave of blood which tends to straighten the 
curves makes the vessels move laterally as they beat, and this increases the 
pumping effect which is produced by the so-called "Corrigan pulse. " 

The apex beat is always far below and far outside the nipple because 
of the dilatation and hypertrophy of the left ventricle, and also because of 
the elongation of the aortic arch. On palpating the heart the impulse on 
systole is powerful and diffuse except when compensation is ruptured, when 
it is feeble. 

The pulse when felt by the finger-tips or when recorded by the sphygmo- 
graph feels as it looks on inspecting the arteries. With each systole of the 
heart the almost empty artery suddenly gives to the finger a short, sharp 
impulse, which equally suddenly disappears, the vessel being in an instant 
apparently as empty as before. The hypertrophied and dilated heart expels 
a large wave of blood into the aorta, of which a part at once falls back into 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 51 1 

the ventricle, so that what might be called the tail of the pulse is lost. 
This is the so-called " Corrigan pulse," sometimes called the " water-hammer 
pulse/' or " trip-hammer pulse." It can be emphasized in the radial 
arteries by raising the hand above the head. This pulse is usually regular 
as to rhythm and force. If it becomes constantly irregular, it is a sign of 
grave cardiac failure. 

On percussion the area of cardiac dulness is found to be greatly enlarged, 
so that it extends far over to the anterior axillary line in some instances, 
and three inches below the nipple. Dulness due to the enlarged heart is 
also found even as far as the right edge of the sternum. 




Showing the area in which the murmur of aortic regurgitation can be most clearly heard. 



Auscultation. — Auscultation reveals a diastolic murmur, due to the return 
of the blood from the aorta after the systole has expelled it into the vessel, 
and while the ventricle is once more opening for a new supply from the 
auricle. This murmur is heard in its greatest intensity at the fourth left 
intercostal space, or at the second right costal cartilage in the so-called 
aortic area. It is heard at the fourth left intercostal space because the 
reflux of blood carries the murmur back into the ventricle, and because 
the aortic opening as a matter of fact is nearer this area than the second 
right intercostal space (Fig. 74). In still other cases the diastolic mur- 
mur may be very clearly heard at the cardiac apex as well as at the second 
right intercostal area, although between the two no murmur at all, or only 
a very faint sound, can be discovered. The explanation of this is that 



512 DISEASES OF THE HEART 

the right ventricle occupies the anterior surface of the heart, except at the 
extreme left edge, where the left ventricle protrudes and where the apex 
comes closely in contact with the chest wall. 

The murmur of aortic regurgitation is not widely transmitted, but 
is limited, as a rule, to the area described, although when it is very loud 
it may be heard everywhere in the chest. The quality of this murmur 
is blowing or purring. There is no accentuation of the pulmonary second 
sound at the third left costal cartilage, unless there is an associated mitral 
regurgitation or stenosis. The first sound of the heart is loud or pro- 
longed owing to the large amount of blood which has to be expelled at 
systole. In some cases a diastolic sound near the apex may mislead the 
physician into a diagnosis of mitral obstruction, but it is in reality the 
so-called "Flint's murmur." (See Mitral Stenosis.) 

If the stethoscope is placed over any one of the large superficial arteries 
there is sometimes heard, in cases of aortic regurgitation, a sharp systolic, 
"pistol-shot" sound, which is said to be due to sudden filling of the vessel, 
This sound is not transmitted from the heart, but is local in origin. It is a 
modification of the arterial sound which can be elicited in most persons 
with a strong pulse, if the artery is occluded by pressure with a stetho- 
scope. Very rarely a diastolic arterial sound can be heard, the so-called 
"Duroziez sign," which is thought to be due to a transmitted cardiac 
sound. 

The question as to whether a diastolic aortic murmur can be present 
without disease of the aortic valves has been much discussed, particularly 
of late, by Cabot and Locke, of Boston, and Gibson, of Edinburgh. As is 
well known, the aortic ring is so firm that it seems impossible that it can 
yield as do the rings of the pulmonary and mitral orifices. Cabot and Locke 
believe that diastolic aortic murmurs are not uncommon in connection with 
diffuse or localized dilatation of the aorta, but in view of the evidence pre- 
sented by Gibson, we must, I think, agree with him that diastolic murmurs, 
without valvular lesions, are rare at the aortic orifices, and that when they 
occur they are due to defective approximation of the different aortic cusps 
rather than to yielding of the aortic ring. 

Diagnosis. — The symptoms and physical signs of aortic regurgitation 
having been described, it remains to separate them from those conditions 
which possess a resemblance. Occasionally in some persons a diastolic 
cardiopulmonary murmur is heard, but it disappears with change in posture 
and is dissipated or is accentuated by forced expiration and inspiration. At 
the level of the second and third rib there is heard at times a hsemic murmur 
or hum due to anaemia, but this is systolic in time. Cabot has, however, 
reported cases in which diastolic murmurs were hsemic and due to anaemia. 

Finally, it is to be recalled that the aortic regurgitation murmur is often 
inconstant, and if not heard at one examination may be at another, or when 
the patient exercises or changes his posture. 

Prognosis. — Facts in regard to the relative fatality of aortic regurgitation 
have already been given. Allbutt says ten years constitute a long time of life 
in any case of aortic regurgitation. It is not only a serious lesion, but it is 
the valvular lesion above all others which produces sudden death; but death 



CHROXIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 513 

in aortic regurgitation is not always sudden. A majority of cases gradually 
" play out " with dyspnoea, dropsy, and cardiac distress. Much depends on 
the age of the patient, his previous habits, and the cause of the disease. 
In a young adult with a good history, and in whom the lesion has followed 
rheumatism without great injury to other parts, compensatory hypertrophy 
may carry him along for many years unless he ruptures it by severe strain, 
or it is dissipated by illness. When the lesion comes on as the result of 
atheroma it is more serious because it is evidence of general cardiovascular 
degeneration, and the coronary arteries, through which the heart is chiefly 
nourished, no sooner share in the degenerative change than feebleness of 
the heart ensues. If perchance the kidneys share in the cardiocapillary 
fibrosis, the outlook is all the more grave. When fast living and debauchery 
are factors in the case, and an old syphilitic infection is impairing the myo- 
cardium, the outlook is worse still. (For treatment see end of article on 
Valvular Disease.) 

Tricuspid Regurgitation. Definition. — Tricuspid regurgitation, or insuf- 
ficiency, is a condition in which the blood flows backward into the right 
auricle from the right ventricle, upon the contraction of the latter. 

Etiology and Pathology. — This is a rare lesion and is due to two chief 
causes. It occurs most commonly as a result of disease on the left side of 
the heart, whereby the blood is dammed back into the lung and so, by 
preventing free pulmonary circulation, an undue strain is throwm on the 
tricuspid leaflets. In other instances the primary obstruction exists 
in the lungs, as in pulmonary emphysema, fibroid phthisis, and bronchiec-r 
tasis. 

As indicating the relative frequency of these causes, Newton Pitt reports 
from Guy's Hospital that out of 405 cases of tricuspid regurgitation examined 
at autopsy, in a period of twenty-five years, 200 cases were due to left-sided 
failure with valvular disease. Of this number 64 were cases of mitral 
regurgitation with mitral endocarditis or adherent pericardium, 66 were due 
to mitral stenosis, 61 to mitral with associated aortic disease, and 9 had 
valvular lesions not named. In 71 cases the tricuspid condition was due 
to left-sided failure without valvular disease, in 56 cases the cause lay 
in muscular failure of the whole heart, and in 55 the lesion was not 
left-sided, but was right-sided alone. Seven cases were due to disease of 
the pulmonary valves, of which 5 were stenosis and 2 pulmonary regurgita- 
tion. In 4 cases no cause could be found, and in 12 the reports as to the 
exact state of the heart were too imperfect for analysis. 

The valves in these cases are usually healthy and fail to close the right 
auriculoventricular opening because the orifice is enlarged as a result of 
dilatation of the ventricle. 

The second cause of this lesion lies in the heart itself, that is, an endo- 
carditis involving the right side of the heart. This is generally stated to 
be very rare, although in fetal life endocarditis is more commonly on the 
right side of the heart than the left. Bramwell, however, combats the 
statement that acute endocarditis rarely affects the tricuspid valves, and 
believes that endocarditis of the right heart often exists and is overlooked. 
Out of 28 cases of recent simple endocarditis he found disease of the tricuspid 
33 



514 DISEASES OF THE HEART 

valves in 14, or 50 per cent. Nevertheless, the lesions are not so pronounced 
as those due to this cause on the left side of the heart. In ulcerative 
endocarditis Osier found the tricuspid valves affected in 19 cases out of 
238 instances of that disease. 

A case in which tricuspid disease was discovered during intrauterine life 
is reported by Peter, of Paris! 

Symptoms and Physical Signs. — When the cause exists in the left side of 
the heart the symptoms are those naturally arising in cases of pulmonary 
congestion and engorgement. A low-grade bronchitis, with some dulness 
at the bases of the lungs posteriorly from hypostatic congestion, with cough 
and occasionally blood-stained sputum, is discoverable. The jugular veins 
become distended and "pulsate, the liver becomes enlarged and may pulsate, 
and there is marked cyanosis. It is a noteworthy fact that the presence of 
jugular pulsation, while a sign of well-developed regurgitation, is not by 
any means as grave a sign as is its absence in the presence of other evidences 
of cardiac embarrassment, because if the right ventricle is strong it may 
drive the regurgitating blood with sufficient force to cause jugular pulsation, 
whereas if it be weak no jugular pulsation can ensue. On the other hand, 
the presence of jugular pulsation shows that the regurgitation is a grave 
one, because it does not occur until a considerable quantity of blood flows 
into the auricle and distends the veins sufficiently to interfere with the 
valves, so that they cannot prevent auricular regurgitation as they do in 
health. 

A distinct impulse in the upper epigastrium is often present. 

The pidsation of the liver is best discovered, if not seen, by placing the 
finger-tips or hand against the floating ribs at the side, and the other hand 
near the ensiform cartilage, and then exerting gentle pressure upon the 
liver from both directions. Care must be taken that a directly transmitted 
impulse from a hypertrophied heart is not taken for true expansile pulsation 
of the liver. 

On percussion, increase in the area of cardiac dulness to the right of the 
sternum is demonstrable. 

On auscultation at the apex a soft systolic murmur, or purr, can be 
heard, which is found to be loudest at about the fifth interspace, to the right 
of the sternum or at the base of the ensiform cartilage, and which may be 
in a few cases transmitted to the right axillary area. The murmur of 
tricuspid regurgitation has been said to resemble the sounds made by a 
small jet of escaping steam, and it may be singing or musical. Duroziez 
says that venous blood " sings" more than arterial blood. 

Diagnosis. — True tricuspid regurgitation must be differentiated from 
regurgitation at this orifice, which is temporary and not constant. These 
valves not rarely give way from severe strain, as in athletes during exer- 
tion. They act in this way as a "safety-valve" to relieve undue pressure, 
and as soon as the strain ceases the heart gradually returns to its normal 
size and the murmur disappears. So, too, a similar murmur may develop 
in cases of profound asthenia resulting from prolonged fevers, particularly 
if the heart is strained by the patient attempting to do too much. Such a 
murmur may or may not pass away with rest. 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 515 

Prognosis. — The prognosis depends entirely upon the exciting cause, the 
age of the patient, and his general state and manner of life. In those who 
have to do manual labor the prognosis is usually bad. 

Tricuspid Stenosis. — This condition sometimes arises as the result of an 
attack of endocarditis involving both sides of the heart, and is usually asso- 
ciated with mitral stenosis. In other instances it is congenital. In the vast 
majority of cases it is found as an associated lesion, and it is exceedingly 
rare. 

In 1899 Newton Pitt collected 87 cases of tricuspid stenosis from the 
post-mortem records of Guy's Hospital extending over a period of twenty- 
six years, and comprising a total of 12,000 autopsies. Leudet, in his Paris 
thesis on tricuspid stenosis, gives the following figures, based on 114 post- 
mortem examinations which were collected from various sources, and which 
include the cases collected by Fenwick: 

Stenosis of the tricuspid valve alone . . . . . .11 

Stenosis of the tricuspid and of the orifice of the pulmonary artery 3 
Stenosis of the tricuspid, mitral, and pulmonary .... 1 

Stenosis of the tricuspid, mitral, and aortic . . . . .21 

Stenosis of the tricuspid and mitral ...... 78 

F. W. Griffith, of Leeds, has examined Leudet's tabulation of cases and has 
shown that probably only two of them were unassociated with lesions of the 
other valves. These figures show the rarity of uncomplicated tricuspid stenosis. 

Diagnosis. — The diagnosis of the lesion during life is usually very difficult, 
but it can be made. The murmur, if present, is presystolic in time and has 
its greatest intensity at the fifth right interspace near the sternum. As 
already stated, this murmur is usually associated with that of mitral stenosis, 
and its existence may be completely masked by the presystolic murmur at 
the mitral orifice. Additional physical signs of tricuspid stenosis are dis- 
tention of the jugular veins without pulsation, or with very slight pulsation 
due to the feeble auricular regurgitant impulse. 

As dropsy is a late symptom of severe mitral stenosis, the early develop- 
ment of dropsy in a case with a presystolic murmur which is not aortic 
strongly indicates tricuspid obstruction. 

Disease of the Pulmonary Valves. — Lesions of the pulmonary valves are 
so rarely met with that many practitioners of large experience have never 
seen a case presenting them. When actual lesions occur they are nearly 
always congenital, and the usual lesion is that of pulmonary stenosis or 
obstruction, for pulmonary regurgitation is the rarest of cardiac lesions. 
On the other hand, there is no area at which we listen, for the purpose of 
determining the state of the heart valves, in which murmurs are so con- 
stantly found as the so-called pulmonary area, at the second and third left 
intercostal space. These murmurs are not due to actual disease of the 
pulmonary valves or of the pulmonary artery, but they arise from causes of 
a non-organic character and are usually systolic in point of time. These 
functional murmurs may be due to one of several causes, as, for example, 
anaemia and chlorosis, producing the so-called hsemic murmur. They also 
occur in pregnant women and in women after childbirth. In other instances 



516 DISEASES OF THE HEART 

they are present as a sign of Graves' disease or of nervous tachycardia, and 
in still others they arise from some abnormal position of the heart, caused 
by conditions which alter the relationship of the heart muscle to its great 
vessels. These conditions all produce a pulmonary murmur which* may be 
considered as within the area of the pulmonary artery or near its valves 
In addition we sometimes hear at this point a so-called, cardiopulmonary 
murmur, which is supposed to be due to the effect of the bloodvessel upon 
the lung, or vice versa, in that the murmur occurs during forced inspiration, 
or expiration. This murmur is not rarely seen at this point in early tuber- 
culosis of the apex of the left lung. 

Pulmonary Stenosis. — The systolic murmur which is due to actual 
organic disease at the pulmonary valve is due to stenosis, as already 
stated, and is commonly due to gluing together of the cusps of the pul- 
monary valves in antenatal life. This murmur is more harsh than the soft 
purring murmurs of the functional type just described. The patient usually 
has a history of having been cyanotic all his life, with dyspnoea on the 
slightest exertion. Percussion and palpation will usually reveal a distinct 
increase of cardiac dulness to the right from hypertrophy of the right ven- 
tricle. Palpation also will reveal a distinct systolic thrill over the area of 
the pulmonary valves. 

The points by which the true systolic murmur is to be separated from 
the functional murmurs already described are the absence of systolic thrill 
in the case of the functional murmurs, the harshness of the true murmur, 
and the hypertrophy of the right ventricle in cases of actual pulmonary 
disease. From aneurysm of the descending portion of the aortic arch the 
true pulmonary murmur is separated by the fact that in such a case the 
hypertrophy chiefly involves the left side of the heart, by the additional 
fact that there is a bruit, not a murmur, and by the presence of a bruit 
posteriorly on the left side between the vertebrae and scapula. There are 
also pressure symptoms in aneurysm in many cases. Finally, if it be 
aneurysm, percussion of the third left costal cartilage will reveal dulness, 
which is absent in pulmonary stenosis. The murmur of aortic stenosis is 
heard louder at the second right costal cartilage than at the second or third 
left cartilage, and is transmitted into the carotids, but the pulmonary mur- 
mur is not. 

Pulmonary regurgitation, the rarest of all valvular lesions, is usually 
fetal in origin, but cases have been recorded in which it has arisen as a 
result of ulcerative endocarditis. The murmur due to this cause is, of course, 
diastolic, and is produced by the blood falling back from the pulmonary 
artery into the right ventricle. It is to be separated from aortic regurgitation 
by the fact that it is heard best to the left of the sternum instead of to the 
right, and by the absence of the Corrigan pulse of aortic disease. There 
are signs of dilatation and hypertrophy of the right ventricle, and the pul- 
monary second sound may be accentuated. It is by no means uncommon 
for the existence- of pulmonary regurgitation to be unsuspected until autopsy. 

Treatment of Chronic Valvular Disease. — It is of vital importance that the 
physician remember the fact that the mere presence of a valvular lesion 



CHRONIC VALVULAR DISEASE ASA RESULT OF EXDOCARDITIS 517 

in the heart does not indicate drug treatment. On the contrary, much harm 
is frequently done by the administration of cardiac stimulants to patients 
who are found to possess a valvular lesion, with the result that natural 
compensation is disturbed and cardiac symptoms may be noted by the 
patient for the first time in his history. It is only when the patient presents 
symptoms which indicate failure of cardiac function that the pnysician 
should think of administering remedies which have a direct influence upon 
the heart. In other words, when compensation is complete, no cardiac 
treatment is indicated, but when it is ruptured therapeutic measures should 
be instituted. I have again and again seen patients who have presented 
some ailment involving other organs in the body than the heart, in whom 
the physician, on examination, found a mitral regurgitant murmur, and im- 
mediately proceeded to administer digitalis, forgetting that the presence of a 
murmur in the absence of evidences of circulatory failure is not an indica- 
tion for the use of the drug. 

Another important point to be borne in mind when the physician is 
called upon to treat a case in which compensation is failing is that, far and 
above all drugs in value, is rest for the patient; not only rest of the body, 
but rest of the mind. The heart is an organ which, of course, cannot have 
complete rest at any time; but its work can be diminished one-half if the 
patient can be made to take no exercise, and if he will carefully abstain from 
business worries and cares. It is a remarkable fact that disease of the 
coronary arteries and of the heart muscle is more common in brain-workers 
than in those who gain their living by manual toil, and this is an indication 
of the fact that mental labor throws a severe strain upon the heart. Care- 
ful observation will promptly prove that patients who are not benefited 
by digitalis and other cardiac stimulants, when suffering from ruptured 
compensation, will at once improve if rest is insisted upon; for, manifestly, 
the rupture of compensation is largely the result of cardiac fatigue, and this 
fatigue cannot be put aside by the mere administration of stimulants. In 
order that the juices of the body may be kept moving, it is useful in these 
cases, when they are made to rest in bed, to use more or less vigorous massage 
daily, its vigor depending upon the strength of the individual. If the massage 
is too vigorous, it may produce very considerable fatigue, and it should not 
be employed to this extent. 

In all cases of ruptured compensation the patient should be warned of 
the danger of sudden, severe effort, since, even if death does not ensue under 
these circumstances, the heart may be so dilated or fatigued that irreparable 
damage is done to it. 

Digitalis is without doubt facile princeps the best of cardiac stimulants. 
I have proved that it actually increases the muscular development of the 
heart, and the manner in which it acts results in an increased nerve and 
blood supply to this viscus which is not equalled by the results obtained 
from the administration of any other remedy. Digitalis is, in a large number 
of cases, given in too large doses. Xot infrequently as much as 10, or even 
20 minims of the tincture are given three times a day, with the result that in 
the course of a few davs the heart is overstimulated by the drug; its cumu- 
lative effect is produced, and instead of doing good it may do serious harm. 



518 DISEASES OF THE HEART 

I have known of cases in which the use of full doses of digitalis, persisted 
in for a considerable period of time, have resulted in the sudden death of 
the individual. 

When digitalis is given in overdoses it produces a curious irregularity of 
force and rhythm in the heart, with imperfect systole, followed by wide 
diastole, and this causes a hobbling pulse. The urine may also be reduced 
in amount instead of increased, as it should be, under the influence of the 
remedy. 

It has been my experience that if the patient is made to rest, small doses 
of digitalis produce satisfactory results, not more than 5 drops of the tincture 
being given three times a day. The only conditions in which I think that 
the use of large doses is justified are when the condition of the heart is 
found to be exceedingly feeble, and the patient's condition so critical that 
immediate stimulation is necessary; and again, when because of idiosyncrasy 
or other cause the heart is found not to respond to smaller doses. In the 
first class of cases it has been my experience that it is better to overcome 
pressing cardiac weakness by more rapidly acting and diffusible stimulants 
such as Hoffmann's anodyne, strychnine, and caffeine for the first twenty- 
four of forty-eight hours until the digitalis has a chance to act; for it must 
always be remembered that digitalis is a drug which produces its effects 
very slowly, and maintains these effects for some time after its use has been 
stopped. When large doses are given, it has been my experience that they 
may be decreased to about one-half or one-quarter the original quantity at 
the end of a few days, and their effects maintained by the use of smaller 
quantities. I do not think that I am exaggerating the case when I state 
that digitalis, through its abuse, does almost as much harm as it does good. 
(See my Text-book of Therapeutics, article "Digitalis.") 

The fluid extract of digitalis may be given in the dose of from J to 5 
minims, according to the needs of the case. One-half to 1 minim every 
eight hours is usually sufficient. A physiologically tested preparation should 
always be employed. 

When dropsy is present it has been held that the infusion of digitalis is 
the best preparation on the ground that it is more diuretic. But any slight 
increase in diuretic power is, I think, counterbalanced by the fact that it is 
much more apt to disorder the stomach, which is in a disturbed condition 
in any case of grave disease, and particularly so in heart disease. 

When digitalis has been given in full doses to a patient suffering from 
ruptured compensation, he should be warned against getting up suddenly, 
and particularly against evacuating the bladder when in a standing posi- 
tion, as dangerous syncope may occur under these circumstances. 

Before deciding upon the administration of any cardiac stimulant in 
a case with ruptured compensation, the physician should make a careful 
study of the state of the bloodvessels, and if the arterial tension is higher 
than normal he should remember that the use of nitroglycerin to reduce 
this tension, and thereby diminish the work of the heart, is a more important 
therapeutic procedure than the administration of a stimulant which simply 
urges the heart to do more work in the face of vascular obstruction. 
In such a case the fact that digitalis stimulates the vasomotor system and 



CHRONIC VALVULAR DISEASE AS A RESULT OF EXDOCARDITIS 519 

raises arterial tension should also be remembered. Nitroglycerin can often be 
given to advantage to prevent this arterial effect of the drug. Strophanthus, 
which is a much less powerful stimulant than digitalis, possesses the advan- 
tage that it does not raise arterial pressure by stimulating the vasomotor 
system, and can often be given in the dose of 5 to 10 minims of the tincture 
every eight hours with advantage. Large doses of strophanthus are prone 
to produce an irritative diarrhoea. 

There is a host of drugs which have been recommended for ruptured 
compensation, but none of them approach these three in value, and often 
when these fail the failure is due to a mistake in the dose rather than to 
a fault of the drug. Should there be any tendency to hypostatic congestion 
of the lungs or pulmonary cedema, digitalis may be freely given, and strych- 
nine and atropine administered as vasomotor stimulants. Two or three 
dry cups over the base of each lung are also useful under these circum- 
stances, and sometimes a sharp purgative may do good if dropsy is present ; 
but the possibility of the purge weakening the patient must always be borne 
in mind. 

Attacks of acute cardiac failure are to be combated by Hoffmann's anodyne 
in the dose of 1 or 2 drachms every hour or two, or aromatic spirit of ammonia 
in the dose of \ to 1 drachm. If, associated with the cardiac failure, there 
is high arterial tension, the nitroglycerin should be used hypodermically 
in the dose of yw'S ^° TTo" °^ a g ram > an d repeated every half-hour until the 
tension is lowered. 

When marked dropsy is present, the use of magnesium sulphate in con- 
centrated solution, a heaping teaspoonful to one-half glass of water taken 
before breakfast, will often do good by removing large quantities of fluid 
from the patient's body. A very useful remedy in cardiac dropsy, both 
by reason of its action on the heart and because of its diuretic effect, is 
apocynum cannabinum given in the dose of from 5 to 30 minims of the 
tincture twice or thrice a day until it produces slight purgation. Care 
should be taken that a fluid extract of real apocynum cannabinum is obtained. 
Much of that on the market is apocynum androsimsefolium, which has no 
such therapeutic properties, but which so closely resembles apocynum canna- 
binum that its leaves are often unintentionally substituted for the true drug. 

Another very useful prescription in cardiac dropsy is a tablet composed of 

Extract of sourwood leaves ...... 2 grains. 

Extract of elder flowers ....... 2 grains. 

Extract of squill ........ ^ grain. 

Take one or two tablets three times a day. 

For generations physicians have been in the habit of employing a pill 
composed of — 

Powdered squill ........ 1 grain; 

Powdered digitalis leaves ...... 1 grain; 

Calomel .......... 1 grain; 

three times a day in the treatment of cardiac dropsy, for its stimulant and 
diuretic effect. If free diuresis is not produced by this pill at the end of 



520 DISEASES OF THE HEART 

the third day it should be stopped, and a saline purgative administered 
to sweep out the calomel from the alimentary canal. 

In many cases of cardiac disease, particularly if the presence of ansemia 
is marked, iron and arsenic are indicated, both on general principles and 
because we cannot expect to improve the nutrition of the heart when it is 
supplied by impoverished blood. 

It is important to remember that in nearly every case of failing compensa- 
tion there is a certain amount of hepatic congestion. This is best relieved 
by the use of 5 or 10 grains of blue mass given every week or ten days. 
Frequently digitalis and other stimulants will act much better after the 
liver has been unloaded by the mercury than they will when this gland is 
congested. 

When the rupture of compensation has resulted in dyspnoea and anxiety, 
morphine proves itself a most valuable remedy. It should not be given except 
in cases in which there is dire need of rest, since if used too frequently it 
loses its good effects, and frequently causes constipation and disorder of 
digestion. On the other hand, the quiet and rest produced by ■§- to j of a 
grain of morphine will often cause marvellous improvement. It has seemed 
to me that it is most satisfactory in mitral lesions. If dropsy is present, it 
cannot be given hypodermically because it will not be absorbed. 

When there is great engorgement of the jugular veins, and manifest dis- 
tention of the right side of the heart with pulmonary congestion, vene- 
section to the extent of about 8 ounces to a pint, according to the size 
of the individual, is often very valuable as a means of relief. It also 
is a remedy which is to be reserved for somewhat desperate conditions, as 
manifestly it is not proper to bleed frequently. 

It is generally considered that digitalis does less good in cases of aortic 
regurgitation than in other valvular lesions, and I believe this opinion is 
correct. Some have taught that it is contraindicated in aortic regurgitation. 
While this may be the general rule, every now and then we meet with cases 
in which cautious use of the drug in this state produces excellent results, 
provided compensation is ruptured. 

In some instances when the heart's action is very irregular and excitable 
an ice-bag applied over the prsecordium is advantageous. 

When the patient has had syphilis, chronic rheumatism, or gout, or 
manifests evidences of arterial capillary fibrosis, iodide of sodium or iodide 
of potassium in the dose of 10 or 15 grains a day is advantageous. 

The diet in cases of valvular disease should be simple, but nutritious. 
The patient had better eat four or five small meals a day than two or three 
hearty ones, and the greatest possible care should be taken that foods 
which are prone to produce gaseous distention of the stomach and bowels 
are avoided. Fatty substances are very apt to produce such symptoms, as 
are also the starches, when they remain in the stomach undigested for a 
considerable period of time. This, however, can be put aside in the case 
of the starches by the use of taka-diastase or pancreatin and by the use 
of powdered capsicum, either in pill or upon the food, for the purpose of 
stimulating the gastric mucous membrane, which is often atonic or catarrhal 
as a result of the impaired hepatic circulation. 



NEUROSES OF Till:' HEART 521 



NEUROSES OF THE HEART. ' 



Definition. — By neuroses of the heart it is meant to include a number 
of conditions widely separated in their actual causes, but depending upon 
a disorder of the nerve supply of this organ, so that, without there being 
necessarily present any grave organic lesions, its functional activity is 
impaired or perverted. 

Palpitation. — Palpitation of the heart may be due to any of the valvular 
or other lesions that cause the heart to beat rapidly or irregularly when 
the individual takes exercise. In other cases it arises from the accumulation 
of gas in the stomach or colon, which by its pressure causes cardiac dis- 
turbance. In other instances it is due to intense nervous erethism, and in 
still others it arises from the excessive use of tobacco or of coffee or tea. 
So, too, sudden nervous shock may cause repeated attacks of this character. 
Probably the most frequent cause of cardiac palpitation is not connected 
with the nerves supplying the heart, but is due to irregularities in the nervous 
control of the vasomotor system, whereby the tension of the vessels is 
relaxed and as a result the heart beats rapidly because the ordinary pressure 
in the arteries is suddenly removeol. It is remarkable how cases of palpi- 
tation get well if attention is paid to the state of the bloodvessels rather than 
the heart. The so-called "irritable heart of soldiers," first described by 
J. M. Da Costa, is due in all probability to this cause as well as to the 
imperfect action of the vagus. Associated with the disordered cardiac action 
it will often be found that the peripheral capillaries suddenly become 
dilated, so that the blood can flow more rapidly than normal into them. 
Profuse diuresis, in which the urine is found to be pale and clear, shows 
that a similar relaxation of the renal vessels has ensued. These symptoms 
often cause the patient great alarm and bring him at once to the physi- 
cian w T ith the statement that heart disease is feared. It is usually the 
case that a patient who says he has heart disease has only a neurosis, 
unless some physician has found a real lesion and told him of its existence. 

Tachycardia. — Many cases of neurosis are closely allied, if not identical, 
with that condition of rapid heart called tachycardia. This may be due 
to vasomotor palsy, to a deficient action of the vagus nerves, or to some 
central nervous lesion. (The tachycardia of exophthalmic goitre is not 
considered here.) 

Such attacks occur in young hysterical women and are called "pseudo- 
angina," because a sense of cardiac expansion is often present with the 
rapid beating of the heart. They also appear in women near the menopause, 
and in men who have been guilty of excessive sexual abuse. A few cases 
in men are apparently due to some organic nervous lesion. The pulse may 
rise as high as 220. The tachycardia may be paroxysmal or continuous. 
In a case under my care in 1890, a woman w T ho had seen her husband and 
sons drowned in the great Johnstown flood, and had been swept from the roof 
of her floating cottage, presented a pulse rate which was uncountable, it 
was so fast. This persisted for months and was present two years after 
the catastrophe. 



522 DISEASES OF THE HEART 

Rapid, feeble heart sounds, in which the first and second sounds appear 
alike, are met with in prolonged exhausting fevers such as severe typhoid 
fever, and to this state is given the name "fetal heart sounds" or "em- 
bryocardia." 

Bradycardia. — Great slowness of the heart's action (bradycardia) is caused, 
to some extent at least, by conditions which are the antithesis of those that 
cause tachycardia. A sudden or persistent rise of arterial pressure may cause 
a very slow pulse, as the heart endeavors to force blood through tightly 
contracted vessels. This may be called vascular bradycardia. Again, it 
occurs as the result of irritation of the vagus nerves by poisons such as 
digitalis and opium, or in chronic lead poisoning, or again in cases of jaun- 
dice when the slowing is due to the biliary salts in the blood. It is also 
met with in cases of apoplexy, cerebral tumor, and in the coma following 
epilepsy. 

A pulse below 60, or even as low as 40, is sometimes felt after a woman 
has given birth to a child. 

Occasionally cases are met with in which the bradycardia becomes 
extraordinary „ The late D. W. Prentiss reported to the Association of 
American Physicians in 1889, 1890, and 1891 the case of a man whose 
pulse at times fell to 11 per minute and rarely rose over 40 per minute 
for two years. In this case no very distinct morbid lesions were found at 
autopsy, although the patient died suddenly in an attack. (See Stokes- 
Adams Disease. 

Arhythmia. — There are other cases met with in which cardiac 
arhythmia — that is, irregularity as to the speed and the force of the 
heart beats — occurs. In many cases this is due to a neurosis of the 
vagus. It is very commonly met with in persons who have taken 
excessive doses of digitalis, and it is also a common symptom in mitral 
stenosis with ruptured compensation. The so-called gallop rhythm may 
appear in these cases. (See Mitral Stenosis.) Occasionally arhythmia is 
a notable symptom in cases of myocardial degeneration, but cases are 
recorded in which arhythmia has lasted for several decades in seemingly 
healthy men. 

Treatment of Cardiac Neuroses. — In the treatment of the various cardiac 
neuroses it is essential that the physician shall first determine what portion 
of the circulatory system is chiefly affected by disordered innervation. Not 
infrequently, however, it will be found that both the heart and vasomotor 
system are out of order, and therefore the treatment will have to be devoted 
to regulating the nerve supply of the functions of both of these important 
vascular areas. 

When it is believed that attacks of tachycardia have their origin in a 
condition in which the pneumogastric nerve fails to control the action of 
the heart, digitalis is, of course, a valuable remedy in that it exercises a 
powerful stimulating influence upon the pneumogastric nerves. In some 
instances, however, the action of the heart is already sufficiently vigorous 
and the administration of digitalis, while stimulating the pneumogastric 
nerve, also stimulates the heart to such an excessive degree that its action 
becomes too violent. Under these circumstances it is well to combine with 



ANGINA PECTORIS 523 

the digitalis a little aconite, which drug also stimulates the pneumogastric 
nerve, and thereby aids the digitalis in controlling the heart, and at the 
same time combats the influence of the digitalis upon the heart muscle 
itself, thereby preventing overstimulation. A prescription made up as follows 
will often be of advantage, the quantities of the ingredients being varied 
to suit the needs of the individual case: 

R. — Tinct. digitalis (physiologically tested) . . . f^j (4.0). 

Tinct. aconiti . . . . . . . . f gss (2.0). 

Tinct. belladonnse f^ij (8.0). 

Tinct. cardamom, comp. . . . . q. s. ad f ^iij. 

A teaspoonful to a dessertspoonful three or four times a day. 

The efficiency of this prescription may be increased by the application of 
a belladonna plaster over the heart. 

In those cases in which the cardiac irregularity depends chiefly upon 
alternate spasm and relaxation of the bloodvessels, so that they are at one 
moment offering too much resistance and at another too little resistance 
to the flow of blood, much benefit can be produced by hydrotherapeutic 
measures, such as directing that the patient shall take an alternate hot and 
cold sponging in the morning on getting up ; first, drenching himself with a 
sponge dipped in as hot water as he can bear, and next drenching himself 
with a sponge dipped in cold water. In this way he does not become chilled, 
but the elasticity and tone of the bloodvessels is much improved. The 
prescription just recommended is also beneficial in many of these cases, and 
not infrequently moderate doses of tincture of nux vomica are advantageous. 
When the disorder depends upon the excessive use of tobacco, this drug 
must, of course, be prohibited; and if the patient is overworked, and suffer- 
ing from nervous strain, he must be sent away on a vacation; or, if his con- 
dition is grave, be given a " rest cure." When a disordered circulation is 
associated with pain in the neighborhood of the heart, small doses of 
antipyrin, 2 to 3 grains, are often useful; and if the tension is high, 
nitroglycerin should be given. 



ANGINA PECTORIS. 

Definition. — By angina pectoris is meant a condition in which a patient, 
usually in or past middle life, is seized by a severe, agonizing pain in the 
cardiac area, which extends in most cases down the left arm even to 
the wrist, and suffers from intense mental anxiety and a sense of im- 
pending dissolution. It is important that pseudoangina be not confused 
with it. 

Etiology and Pathology. — The cause of true angina pectoris is usually 
atheromatous change in the coronary arteries, although this is by no means 
always the case. Thus, Potain found stenosis of both coronary arteries in 
20 out of 45 cases at autopsy, and Huchard in 38 out of 70 cases. It is 
distinctly a disease of the brain-worker rather than of him who gains his 
bread by manual labor. The laborer and artisan present to us very com- 



524 DISEASES OF THE HEART 

monly the most surprising degenerative changes in their arteries in the 
way of calcification of their radials and temporals, but they rarely have 
true angina. On the other hand, the man who is subjected to nervous 
strain rarely shows extraordinary calcareous changes, but he is the unfortu- 
nate victim of this terrible malady. Physicians are peculiarly prone to it. 
The number of deaths among the leaders of the profession in Philadelphia 
during the last decade from this cause is extraordinary. Mental strain 
with a sedentary life are, therefore, causes. Gout, syphilis, and renal disease 
are also causes. The disease affects men much oftener than women. Out 
of 65 cases collected by me only 4 occurred in women, and out of 290 cases 
collected by Forbes, Huchard, and Lartigue only 47 occurred in women. 
Aside from the narrowed and thickened coronary arteries and the fibroid 
changes in the heart which result from their state, there are no characteristic 
lesions of true angina pectoris. Among the exciting causes of an attack 
are to be named nervous wear and tear, anger, or muscular exertion, par- 
ticularly if it be made in the face of a cold wind, which contracts 
the capillaries and so increases still more the labor of the heart. So, too, 
errors in diet, by causing gastric disorder, may reflexly cause an attack. 

Sir Douglas Powell and Merklen give the age incidence for true angina 
at twenty to forty years. This is probably too young. The actual age is 
forty to sixty years. 

Symptoms. — When angina pectoris is well developed there is no symptom- 
complex so characteristic and dramatic. Seized on a sudden or with 
but a few moments' warning, the patient stands or sits transfixed with 
pain and fear. It is difficult to tell whether his arrested respiration is 
controlled by the disease or his own will-power. The sense of dissolution 
or of impending death is so real that the patient expresses the belief that 
death is at hand, if he can find breath to speak. The expression of the face 
is one of intense anxiety or horror, the skin is pallid to the degree of cadaveric 
hue, and the brow is marble white and perhaps bedewed with sweat as 
the attack advances. The pulse during an attack is usually slow, small, and 
very tense, becoming feebler and more relaxed as the paroxysm passes 
away. The pain is often beyond the patient's power of description after 
his recovery, both as to severity and character. Some patients say that the 
heart feels as if it were being crushed in a vice; others that a huge stone 
is crushing the ches,t wall; others that a heavy bar of steel is laid across the 
thorax. At times the pain not only extends down the left arm to the fingers, 
but to the right arm as well. As the attack passes off the patient's expression 
of keen suffering is modified. A flush may supplant the pallor and a sigh 
reveals that the seizure has passed. At this time the patient not rarely 
belches up large volumes of gas, and this seems to give much relief. It is 
this which gives rise to the euphemistic diagnosis of "acute indigestion" in 
some of these cases. Sometimes more than one attack may occur in an 
hour, but this is rare. 

Modified forms of severe angina are constantly met with in which the 
pain is not so severe as in the cases just described. The degree of modifica- 
tion may be so great that little or no pain is felt, this form being called 
angina pectoris sine dolore. 



ANGINA PECTORIS 525 

Diagnosis. — When angina pectoris presents itself in its well-developed 
form, there cannot be much doubt as to its true character. The question 
of the character of an attack is, however, often in doubt when the symptoms 
are not all present. While it is a rule that valvular disease of the heart 
rarely causes pain, it is a fact that attacks of anginoid pain are occasionally 
met with in cases of aortic regurgitation, particularly if dilatation of the 
heart is marked. This state can be determined by the diastolic murmur 
and the "Corrigan pulse." Again, aortitis may cause symptoms practically 
identical with those of true angina, and it may be impossible to separate 
the disease of the aorta from that of the coronary arteries because the lesion 
spreads from the aorta to the openings of these vessels. 

It is of some importance to differentiate the angina pectoris due to 
ordinary coronary sclerosis and secondary myocardial change from that due 
to syphilis. This is probably impossible by the physical signs in the 
circulation, but can be made if a history of late syphilis can be obtained, 
or if the patient is prematurely aged. While these changes, when due to 
syphilis, cannot be treated as successfully as can secondary syphilis, for 
they are of the nature of parasyphilitic affections, more aid can be given 
by the use of the iodides than in those cases which present changes in the 
coronary arteries from other causes. 

A form of pseudoangina is occasionally seen in nervous women and in 
men who resort to wine, tobacco, and women to excess. It differs from true 
angina pectoris in the facts that the man is usually under thirty years 
rather than over forty years of age; his vessels are usually in fair con- 
dition; there is a history of neurosis or excessive venery and of the 
excessive use of tobacco, and the sensation about the heart is that of 
distention instead of constriction. 

Prognosis. — From what has been said as to the state of the vessels and 
the heart muscle in true angina pectoris it must be evident that the prog- 
nosis is most grave, for death may ensue in any attack and an attack may 
come on at any time. On the other hand, patients sometimes go long 
periods without an attack, particularly if the mode of life can be quiet and 
the pulse tension can be reduced by the iodides and nitroglycerin. Much 
depends in prognosis upon the degree of vascular and myocardial change 
which can be found. In many of these cases the feeble first sound shows 
how weak and dilated the ventricles have become. 

Treatment. — The treatment of angina pectoris may be divided into that 
which is devoted to the improvement of the circulatory condition with the 
object of preventing paroxysms of the disease, and to that which is devoted 
to the relief of the patient during the paroxysm. As the treatment of a 
paroxysm requires very active procedures, it will be considered first. If 
seen as a paroxysm is commencing, the patient should inhale from 3 to 
5 minims of nitrite of amyl, or if this drug is not at hand a few whiffs 
of chloroform should be used. Nitroglycerin should also be given hypo- 
dermically in the dose of yj-g- or even -£$ of a grain. If the patient has 
become accustomed to this remedy, larger doses are indicated. Sometimes 
it is advantageous to give simultaneously with the nitroglycerin j of a grain 
of morphine ; but in those cases in which the paroxysm is not of long duration. 



526 DISEASES OF THE HEART 

the attack commonly passes away before the morphine has an opportunity 
to exercise its pain-relieving influences. If the patient can swallow, a very 
useful remedy is 1 or 2 drachms of Hoffmann's anodyne given in a little 
cracked ice and water; or, if this is not at hand, J to 1 drachm of spirit 
of chloroform may be given in a similar manner. The employment of 
nitrite of amyl, nitroglycerin, and chloroform is useful in direct proportion to 
the degree of arterial spasm which is present. In that somewhat unusual 
class of cases in which attacks of angina occur with a state of low arterial 
tension, these drugs, manifestly, cannot be of the same value as in those 
patients in which the systemic arteries are tightly contracted. Should the 
patient be seen in a paroxysm and the physician possesses none of the 
remedies just named for his relief, a drink of hot water, containing some 
capsicum, or some brandy, may be given, since this not infrequently causes 
the belching up of a considerable quantity of gas followed by some degree 
of relief to the patient. 

The treatment between the paroxysms is dietetic, hygienic, and medicinal. 
The patient must take a sufficient quantity of food for the purpose of 
maintaining his nutrition, and must be forbidden to eat anything more 
than is absolutely necessary for this purpose. Sweet and fatty articles of 
diet should be entirely avoided, as should be champagne and all sweet 
wines. If any alcoholic stimulant is required, Scotch or rye whiskey, or 
a dry gin with lime-juice and sparkling water should be ordered. There 
is no objection to the diet being largely one of meat, if the kidneys are in 
a fairly healthy state; the more so, as starchy foods are prone to cause the 
formation of gas in the stomach and bowels, which may reflexly upset the 
cardiac balance and precipitate an attack. 

The hygienic treatment consists in having the patient take as much 
sunshine and fresh air as possible; in forbidding him to expose himself 
to blustering winds, and to warn him that if his peripheral circulation is 
chilled the consequent contraction of his capillaries may result in an attack 
of heart pang. Flannel should be worn next the skin both winter and 
summer. Sudden effort, as going up stairs rapidly or running for a car, 
or entering into any heated debate, either in court or in a business argument, 
should be avoided. 

As distention in the stomach sometimes causes an attack, it is often 
necessary to feed the patient with small quantities of food four or five 
times a day rather than to permit him to eat two or three hearty meals. 

Care must be taken that the bowels do not become overloaded with 
feces, and that they be moved every day by some vegetable laxative or one 
of the mild saline waters. 

The medicinal treatment consists in the administration of iodides in as 
large doses as the patient can readily bear without danger of disordering 
his digestion. If there is a history of syphilis in the case, larger doses are 
needed than if the history is not specific. The patient should take at least 
60 grains a day of the iodide of sodium or iodide of strontium if possible, 
divided into four doses, which should be taken one hour after food. In 
some cases syrup of hydr iodic acid, in the dose of h to 2 drachms three or 
four times a day, may be given with advantage, well diluted with water. 



CONGENITAL CARDIAC DEFECTS 527 

The iodides under these circumstances lower arterial tension and do what- 
ever can be done toward arresting the process of fibroid overgrowth in the 
bloodvessels. The patient will also be much benefited if he receives nitro- 
glycerin in the dose of y-J-g of a grain four or five times through the twenty- 
four hours, the dose being controlled, not by the number of doses admin- 
istered, but by the effects which it produces upon arterial tension. In 
some instances it is wise to alternate the nitroglycerin and iodide. If the 
heart muscle is very feeble, full doses of nux vomica, 10 or 20 drops of the 
tincture, or moderate doses of digitalis — say, 5 minims of the tincture — 
may be given three times a day; the nitroglycerin being actively employed 
at the same time to prevent these drugs from raising arterial tension while 
they are stimulating the heart. The patient should be instructed to carry 
glass pearls of nitrite of amyl in his pocket and to crush one and inhale 
its contents if at any time he feels threatened by an attack. 

Symptoms of gastrointestinal dyspepsia are to be relieved not only by 
regulating the diet in the way indicated, but by the use of pancreatin and 
taka-diastase to aid digestion. A very useful capsule under these circum- 
stances is one which contains 2 grains of taka-diastase, 2 grains of pancreatin, 
1 grain of capsicum, and \ grain of extract of nux vomica. This should 
be taken thrice daily. 



CONGENITAL CARDIAC DEFECTS. 

Two abnormal conditions may arise in the heart of the fcetus and persist 
after birth, namely, defects of development and defects produced by an 
attack of endocarditis. In some instances the endocarditis is responsible 
for the defect in development. The most common of these defects is the 
persistence of the foramen ovale, which permits the blood to make a short 
circuit through the interauricular septum instead of passing into the right 
ventricle and thence through the lungs. Sometimes this opening is partly 
guarded by a membrane, but in other cases no such membrane is present. 
If the opening is large and entirely unguarded by a membrane the patient 
is apt to present intense cyanosis, particularly if any effort is made; but 
in some cases the defect does not produce this symptom and the patient 
lives to adult years, no one suspecting the presence of such a defect, the 
existence of which is revealed only at autopsy. Thus, my colleague, 
Coplin, made an autopsy upon a woman, dead of croupous pneumonia. 
During her life and in her final illness there were no signs of cardiac dis- 
ease, but at the autopsy a twenty-five-cent piece could be dropped flatwise 
through the foramen ovale. More or less oblique communications between 
right and left auricles are present in about 2 to 5 per cent, of adult hearts. 

A much more rare condition is that in which there is an absence of the 
septum between the right and left sides of the heart, and as a result "biloeular 
heart" is present. In others again the absence of an interventricular septum 
produces a "trilocular heart." At times a condition is met with in which 
a perforation exists in the upper part of the ventricular septum, in the 
so-called ''undefended space." 



528 DISEASES OF THE ARTERIES 

Valvular anomalies also occur. The three aortic semilunar valves may be 
replaced by two leaflets. This state while not at all incompatible with life 
is, nevertheless, prone to become grave, in that the semilunar valves usually 
become thickened and distorted. The pulmonary valves are much more 
rarely abnormal, and the valves protecting the auriculoventricular orifices 
on both sides of the heart are even more rarely anomalous from defective 
development. These valves may, however, be the subject of endocardial 
disease prior to birth, and the result is, in one sense, not very different 
from that met with in the heart of the ordinary individual who suffers 
from rheumatic endocarditis; for we find the auriculoventricular valves 
thickened and the chordae tendineae broadened and shortened so that they 
interfere with the free action of the valves. That form of acute or chronic 
endocarditis which results in the production of granular or warty nodules 
on the valves is rarely encountered in fetal endocarditis. 

The orifice of the pulmonary artery is very commonly found to be in a 
state of stenosis, as a result of gluing together of the valves and contraction 
of the ring around the orifice itself. The agglutination of the segments 
may be so perfectly accomplished as to leave a smooth, funnel-like open- 
ing, or the valves may be roughened by vegetations. Patients with this 
defect may live for years, but it is a curious fact that they are very prone 
to die of pulmonary tuberculosis. 

Stenosis of the right conus arteriosus, of the pulmonary artery, and 
of the pulmonary orifice are often associated, and form a large propor- 
tion of the congenital lesions seen at autopsy in persons who have suffered 
from these defects, but lived for years. It is a noteworthy fact that these 
lesions are not rarely complicated by a patulous interventricular septum, 
an open foramen ovale, and an open ductus arteriosus. Considerable 
hypertrophy of the right ventricle is naturally found in these cases if life 
is prolonged. 

Narrowing of the aortic orifice is a rare congenital defect. Malposi- 
tion or transposition of the heart is sometimes seen. Transposition is 
always associated with transposition of the other viscera. 

Occasionally ectopia cordis, a state in which the heart is not protected 
by the chest wall, is met with. The heart has also been found in the abdom- 
inal cavity. Peacock reported one such case in a man of forty-seven 
years, and Rezek one in a man of thirty-two years. 



DISEASES OF THE AETERIES. 

The tubes carrying blood are subject to many alterations, some of which 
depend upon changes in the perivascular tissues, including with these 
para-arterial inflammations, infection, trauma, etc. The most important 
group of vascular changes, however, result from alterations in stress and 



ARTERIOSCLEROSIS 529 

tension under which the circulation is maintained, and, to a greater degree, 
are the results of the irritant action of poisons circulating in the blood. The 
intravascular irritants may be bacterial or of bacterial origin (toxins), 
unusual quantities of normal salts, or the presence of abnormal compounds 
that irritate the endothelium. 

Of the acute and subacute inflammations involving the intima (end- 
arteritis), and the relation of this change to later alterations in the vessels, 
we are at present, through the studies of Thayer and others, becoming 
more familiar. The clinical importance, however, of these alterations is 
not as yet fully appreciated. Hyaline and fatty degenerative changes occur 
in the intima and subintimal tissues in a number of pathological processes. 
The deposit of pigment in the vessel walls, infiltration by lime salts (calcifi- 
cation), and amyloid disease are rarely, if ever, primary in the vessels, but 
depend upon a number of primary conditions, and therefore are rarely, if 
ever, recognized independently of the conditions by which they are caused. 
Infections acting within the vessels give rise to proliferative or necrotic 
changes in the endothelium with the formation of thrombi (thrombo- 
arteritis and thrombophlebitis), which, by mechanical interference of the 
circulation, influence the nutrition of the organs, or, by causing embolism 
and distribution of infectious material through the system at large, constitute 
the basis of septicaemia and pyaemia as already considered. 

ARTERIOSCLEROSIS. 

Definition.- — Arteriosclerosis, as we understand it to-day, evidently com- 
prises a number of pathological processes, the exact relation of which, one 
to the other, is still somewhat uncertain. Two important processes, often if 
not constantly associated, are, first, an affection involving particularly the 
smaller arteries (arterioles) , and commonly termed arteriocapillary fibrosis ; 
and, second, a type of arterial change involving particularly the larger vessels 
and called atheroma, or, on account of the changes in the conformation of 
the affected vessels, arteritis deformans. Writers are not agreed that these 
two processes are independent, but they are very constantly associated, and 
the clinical picture embraced under the term arteriosclerosis includes them 
both. 

Etiology. — Certain individuals, and often whole families, seem peculiarly 
liable to arteriosclerosis. The change is often a manifestation of age, and 
the trite but true saying "that a man is as old as his vessels" indicates the 
belief in preliminary aging of those in whom arterial change occurs in early 
life. Alcohol, and intemperance in work and eating, and overexertion, 
mental or physical, are also causes. The autointoxications, lead poisoning, 
syphilis, and gout are important factors in the production of arterial 
disease. Certain forms of chronic interstitial nephritis may precede, ac- 
company, or follow arterial change. (See Etiology of Chronic Interstitial 
Nephritis.) 

Recent studies, experimental and pathological, seem to indicate that 
possibly arteriosclerosis may bear some definite relation to morbid processes 
affecting the adrenals. Josue, Ziegler, Erb, Pearce, and others have 
34 



530 DISEASES OF THE ARTERIES 

produced atheroma, or a closely allied lesion, by the intravenous injection 
of adrenalin. Vaquez reported an instance of adenoma of the adrenal asso- 
ciated with heightened arterial tension, and Josue* and Bernard, and, more 
recently, my colleague, Coplin, have shown that in patients having arterio- 
sclerosis the adrenal is rarely, if ever, a normal organ. The observations 
are not, however, as yet conclusive. 

The relation of heightened stress to arteriosclerosis is one of the problems 
upon which authorities are not agreed. Allbutt recognizes a mechanical 
arteriosclerosis depending upon prolonged high tension of whatsoever origin. 
There can be no doubt that in some cases prolonged stress is an important 
etiological factor, as is shown by the fact that typical arteriosclerosis is rare 
in the pulmonary artery and its branches, except when mitral disease or pul- 
monary lesions increase the tension in this vessel, under which circumstance 
sclerotic changes are not of infrequent occurrence. Heightened stress in the 
veins also tends toward the development of phlebosclerosis, as is shown by 
the occurrence of this lesion in the veins of the lower extremity, when for 
any reason the tension in these tubes is heightened, and also by the develop- 
ment of similar changes in the portal area in cirrhosis of the liver with 
venous obstruction. 

Pathology and Morbid Anatomy. Lesions in the Terminal or Small 
Arteties. — The change in the arterioles is characterized by proliferation of 
the endothelium and subendothelial tissues, fragmentation of the elastica, 
and alterations in the media. There has been much dispute as to the 
primary alteration in the muscle layer, some holding that there is evidence 
of a distinct hypertrophy, which others fail to recognize. Whether or not 
there be an initial increase in the muscle layer of the arteriole, there is, 
sooner or later, if the condition persists, a degenerative change, hyaline in 
tendency, with loss of elasticity, thickening of the intimal and subintimal 
tissues, and narrowing of the lumen, and hence increased peripheral 
resistance. 

Lesions in the Larger Arterial Trunks. — Tn the second conspicuous alter- 
ation of arteriosclerosis there develops in the larger arteries a succession of 
changes greatly influencing the elasticity of these structures. Councilman 
recognizes at least three divisions of this type of arterial change. In the 
nodular form a cellular infiltration occurs around the vasovasorum, as 
originally pointed out by Martin, extending into the media and subintimal 
layers. Fragmentation of the elastica with efforts at production of new 
elastic tissue occurs. Later necrotic and degenerative changes weaken the 
wall and, as pointed out by Thoma, endothelial proliferation tends to 
restore the smooth lumen. The cells forming the node undergo hyaline 
and fatty degeneration, giving rise to a mass of cellular detritus constituting 
the so-called atheromatous abscess. Should the overlying endothelium give 
way an atheromatous ulcer is formed; these areas are particularly prone 
to develop around smaller branches given off by relatively large trunks, 
and lessen the blood-carrying capacity of the affected branches. 

The nodules, seen on the vascular surface of the larger arteries, are elevated, 
yellowish, and often soft from degenerative changes, and, later, are infil- 
trated by calcareous material, becoming rigid so that they break when bent. 



A R TERIOSCLEROSIS 



531 



Often associated with this nodular form is a diffuse arteriosclerosis, which 
may also occur independently. The affected vessels are dilated, thin- 
walled, with irregular elevations at points, taking on more or less fully the 
character of the nodules already described. Sometimes the intima is almost 



unchanged. 



Fig. 75 



. '»/, 




Left coronary artery. Advanced arteriosclerosis, from a case of fatal angina pectoris. Magnified 30 
diameters. But little of the adventitia is shown. The media is thinned and at points encroached 
upon, but the most conspicuous change is in the intima, beneath the endothelial layer of which there 
has been extensive proliferation and leukocytic accumulation, most marked in the upper segment, 
greatly altering the lumen of the vessel, lessening its carrying capacity, and rendering it practically 
inelastic. There was a marked fibroid myocarditis in the area supplied by the vessel. 



The senile arteriosclerosis so classified by Councilman would appear to 
represent that late stage of the nodular type in which so-called atheromatous 
ulcers and abscesses form with calcareous scales, giving rise to rigid " pipe- 
stem" or "slate-pencil" vessels that can be rolled under the fingers as 
tortuous, inelastic, rigid tubes. The blood-carrying capacity of such vessels 
is materially diminished, and the resistance offered to the circulation pro- 
portionately increased. 

These briefly described alterations in the arteries may be associated with 



532 



DISEASES OF THE ARTERIES 



similar, though usually much less marked, changes in the veins (phlebo- 
sclerosis), the combined arterial and venous lesions constituting what 
Thoma has called angiosclerosis. 

The thoracic aorta is the large vessel of all others which usually presents 
the greatest atheromatous change. Its entire inner surface may be so 
roughened that it no longer presents any of the appearances seen in health. 
In other cases, in which the process has not gone so far, we find patches, 
or plaques, of atheromatous change all over its lining. These patches 
may cover areas of softening or areas of calcification, and on them thrombi 

Fig. 76 




Atheromatous plaques on the lining of the aorta. (Graupner and Zimmermann . ) 

may form. They are particularly prone to appear about the origin of 
branch vessels, and this is the reason that fatal disease of the coronary 
arteries so often occurs as part of the aortic changes. 

In vessels of the intermediate class and in the aorta these changes may 
so weaken the resistance of the vessel wall that it yields to pressure and 
an aneurysm develops. 

When changes occur in the small vessels their intima becomes thickened 
by an outgrowth of the endothelial cells, and the connective-tissue cells 
in the media also proliferate, so that the vessel becomes fibroid, the elastic 
coat being rendered rigid and the calibre of the vessel diminished. If this 
process proceeds far it causes an obliterative endarteritis. 

The secondary effects of these vascular changes have already been largely 
considered when discussing the causes of cardiac hypertrophy and myo- 
cardial degeneration. The heart, if its own tissues are not invaded, under- 



ARTERIOSCLEROSIS 533 

goes hypertrophy to enable it to pump blood through rigid, unyielding 
vessels, and finally, when the pressure becomes too high, develops a leak 
at the mitral valve to relieve pressure, or breaks down and fails, suddenly 
or gradually, under the strain thrown upon it. The hypertrophy chiefly 
affects the left ventricle, because it is upon this part that the strain falls. 

Symptoms. — If the heart is examined the apex will be found displaced a 
little downward and to the left, and palpation will show that the impulse 
against the chest wall is forcible if hypertrophy is present. 

A symptom of equally great importance is the accentuation of the aortic 
second sound at the second right costal cartilage, and, indeed, wherever 
it is heard elsewhere in the chest. If the radial or temporal arteries 
are palpated they are found thickened and corded, often elongated and 
tortuous and so rigid it is difficult to extinguish the pulse by pressure. 
This high arterial tension is one of the most important clinical condi- 
tions that can be estimated by the physician. 

A patient presenting these signs and symptoms may continue in ap- 
parently excellent health for several years, but as life progresses the cardio- 
vascular changes also progress, and cardiac failure, attacks of angina pec- 
toris, or renal disease ensue. Much depends in these cases upon how 
widespread the lesions are and where they are most developed. If the 
coronary arteries are the parts chiefly affected, anginoid attacks soon 
come on. If the cerebral arteries are calcareous apoplexy ends existence, 
or, if the stroke be mild, it were better for the patient if death ensued. 
Not rarely attacks of vertigo, of fleeting monoplegia or hemiplegia, and 
aphasia may take place as the result of the arteriocapillary fibrosis, with- 
out being due necessarily to rupture of a cerebral vessel. If, again, the 
renal vessels are involved, then the general manifestations of chronic con- 
tracted kidney are produced. 

Among the complications may be named cerebral and pulmonary embolus, 
and gangrene of the extremities from the same cause. 

Treatment. — The treatment consists in the use of the iodides, whether 
there be a history of syphilis or not, in the administration of nitroglycerin 
to lower arterial tension and relieve the heart of labor, and in the use of 
gentle exercise and warm bathing in moderation to flush the capillaries 
with blood. After the circulation begins to fail in the advanced stages of 
the disease strychnine and digitalis may be urgently required. Alcohol in 
any form must be avoided as if it were poison. Highly seasoned dishes 
are also to be avoided. If the heart is tired, strophanthus is to be given 
to support this organ. High altitudes are dangerous for such patients. Great 
muscular and mental strain are dangerous because the increased arterial 
pressure may rupture a vessel or weary the heart. 

As chronic interstitial nephritis is nearly always present the treatment for 
that state should be instituted if any sign of renal disease can be discovered. 
(See Chronic Interstitial Nephritis.) 



534 DISEASES OF THE ARTERIES 



ANEURYSM. 

Definition. — An aneurysm is a localized dilatation of an artery and depends 
upon a weakening of its wall so that it is unable to withstand the pressure 
of the blood. This dilatation may involve the entire circumference of the 
vessel, forming a cylindrical or fusiform aneurysm, or it may chiefly affect only 
a part of the circumference, forming a sacculated aneurysm. The walls 
of the aneurysm are composed of the thinned coats of the vessel, but as the 
sac develops some of these may in part disappear. 

The term ''dissecting aneurysm" is applied to that form in which the 
blood escapes through the intima and forces a passage for itself into the 
middle area of the vessel wall, between the media and the adventitia. By 
"false aneurysm" is meant a state in which all the coats of the vessel give 
way so that the blood escapes into the surrounding tissues, where a pulsating 
sac usually forms, owing to the development of fibrous tissue around it. 
An "aneurysmal varix," or "varicose aneurysm/' is one in which the 
artery communicates with a vein through an abnormal opening, so that 
the vein and its neighboring veins are distended with pulsating blood. 
An "embolic aneurysm" is one in which a vessel is plugged by an embolus 
and then undergoes dilatation in its proximal part. "Mycotic aneurysm" 
is often multiple and occurs as a result of the infection of the vessel by 
micro-organisms, as in ulcerative endocarditis. 

Etiology. — Aneurysm is due to arterial degenerative changes whereby the 
normal elasticity of the vessel is impaired and its lining membrane injured. 
(See Arteriosclerosis.) The primary causes of aneurysm are, therefore, identi- 
cal with those of ordinary arterial disease, and consist in syphilis, alcoholism, 
and excessive toil or sudden strain. Thus syphilis, for example, weakens 
the vessel and a strain causes it to give way. There are also cases, not so 
commonly met with, in which congenital defects seem to exist in the vessel 
walls. Thus, I saw a few years ago a young man of about twenty-eight 
years, who developed a popliteal aneurysm and then a thoracic aneurysm 
and finally died of cerebral aneurysm, but who at no time suffered from 
syphilis or from strain. It may also arise from injury, as when a vessel 
is damaged by a stab wound or by a bullet, and these injuries may result 
in the development of the aneurysm many years after the injury, and only 
when the arterial changes of advancing age still further weaken the area 
which was damaged. In other cases the acute infectious diseases, without 
acusing general or widespread arterial change, may produce localized 
vascular inflammation and necrosis. 

Pathology and Morbid Anatomy. — In fusiform aneurysm the wall of the 
vessel dilates in its full circumference, but certain spots give way more 
rapidly than others, so that the surface of the dilated vessel is slightly nodular 
or uneven. As it increases in size its walls become thinner, but if an inflam- 
matory process is set up in the surrounding tissues the actual thickness of 
the wall may be increased, and finally a marked deposit of lime salts may 
take place. 

In sacculated aneurysm the dilatation may originate in at least two ways. 



ANEURYSM 



535 



In one, the entire vessel having become weakened, dilates, and the middle 
coat atrophies. This process of atrophy becomes further advanced in one 
area than in another, and here bulging rapidly progresses. In other cases 
the low-grade inflammatory process results in degeneration of the tissues 
lying under the intima, thereby greatly weakening the sustaining lamina, 



Fig. 77 




2 cm/ 

Double sacculated aneurysm of the thoracic aorta, the upper sac rupturing into the pleura. On the 
right is the aorta, in which can be seen the two oval openings communicating with the aneurysmal sacs . 
The inferior margin of the lower sac has been pushed! upward, showing the erosion of the body of the 
vertebra, which, above the point shown, has exposed the spinal canal, but had not, in this case, com- 
pressed the cord. 

which eventually yields, so that the fibrous sheath of the vessel may be 
all that is left of the arterial wall. In either case, however, a process 
of compensation or repair may develop and the sac become filled with 
a clot which is usually laminated and remarkably tough. Such aneurysmal 
sacs often grow to an enormous size, becoming as large as a child's head. 

Frequency. — The relative frequency of aneurysm as compared to other 
diseases is not of much interest, and there are no very large statistics which 



536 DISEASES OF THE ARTERIES 

deal with this point. There is, however, interesting information at hand 
in regard to the relative frequency of the most frequent and important 
forms of aneurysm. Thus, at St. Bartholomew's Hospital, Browne found 
that in thirty years there were 468 cases of aortic aneurysm, 80 of popliteal 
aneurysm, 21 of femoral aneurysm, 14 of subclavian aneurysm, 8 of carotid 
aneurysm, and 6 of external iliac aneurysm. 

Aneurysm of the Thoracic Aorta. — Not only is aortic aneurysm the most 
common lesion, but it is, by reason of the importance of this vessel and of 
the tissues about it, capable of causing very characteristic and also very 
obscure symptoms, both by disturbing the circulation and by pressure on 
neighboring organs. 

For convenience of study the aorta is usually divided into three parts : 
the ascending, the transverse, and the descending. Each of these may be 
the seat of an aneurysm, but the ascending portion is most frequently 
affected. Some years ago one of my assistants, Holder, and myself studied 
the statistics derived from 953 cases of aortic aneurysm, and obtained the 
following results. No less than 570 of these were cases of aneurysm of 
the ascending portion of the arch. Of these, 544 were sacculated and 466 
occurred in males and 78 in females. The remaining 26 cases were fusi- 
form, and all of these 26 cases occurred in males. These statistics em- 
phasize very forcibly the far greater frequency of sacculated aneurysm than 
the fusiform variety. When we consider that of nearly 1000 cases analyzed, 
aneurysm of the ascending aorta occurred no less than 570 times, while 
aneurysm of the transverse portion occurred only 104 times, and of the 
descending portion 110 times, the great difference in the relative frequency 
of the lesion in different parts of the aorta is also marked. 

Of the 466 cases of sacculated aneurysm occurring in males, it is inter- 
esting to note that the great majority of them occurred in persons between 
thirty-five and forty-five years of age, that the next greatest frequency was 
in persons between twenty-five and thirty-five, then between forty-five and 
fifty-five. 

When we come to the consideration of aneurysms involving the second 
or transverse portion of the aorta we find, once again, that the most com- 
mon age for the development of this lesion is between thirty-five and 
forty-five; for out of 88 males suffering from this lesion 37 were between 
these ages, 21 between forty-five and fifty-five, 14 between twenty-five and 
thirty-five, 10 between fifty-five and seventy, and 2 between fifteen and 
twenty-five. The same facts as to age also hold true for aneurysm of the 
descending arch. It is evident, therefore, that aneurysm is not a disease 
of old age, but of the middle period of life. As Coats has well expressed 
it, ''aneurysm occurs when the period of greatest bodily vigor overlaps 
the period of occurrence of atheroma." 

Symptoms. — Aneurysm of the aortic arch not infrequently lasts for some 
time before producing any symptoms, and is then spoken of as a "latent 
aneurysm." In other instances it causes symptoms almost as soon as it 
develops, and the difference in the promptness with which the signs 
appear depend largely upon the site of the growth and the parts pressed 
upon. 



ANEURYSM 537 

'When the convex surface of the ascending arch is involved we find the 
patient presenting engorgement of the veins of the head, neck, and arm 
on the right side, and the voice is often altered or lost from the pressure 
upon the recurrent laryngeal nerve of the right side. The pupil of the 
right eye may be dilated, due to irritation of the sympathetic; or it may 
be contracted because the ciliospinal nerves are paralyzed by pressure. 
There is often severe pain due to pressure, and attacks of anginoid pain 
may be present. 

The physical signs are dulness on percussion over the second right inter- 
space, a bruit, or roaring sound, produced by the passage of blood through 
the sac, and perhaps bulging of the first, second, or third interspace on the 
right side. If the hand is placed over the area of bulging, a distinct, expansile, 
heaving movement is» felt. Some displacement and hypertrophy of the 
heart is often present, and, if the sac is a large one, the apex beat of the 
heart may be far below and outside the normal spot near the nipple. If 
the sac develops on the concave part of the arch, then the downward dis- 
placement of the heart is still greater, for obvious reasons. 

Hypertrophy of the heart is by no means a constant sequence to aneurysm. 
Not rarely the heart is not increased in size at all, but its apex may be 
displaced and the impulse transmitted to the chest wall more markedly 
than normal because of the pressure produced by the aneurysmal sac. 

When we come to the consideration of the direction in which sacculated 
aneurysms of the ascending arch most commonly rupture, or, in other 
words, when we study the neighboring tissues into which the blood forces 
its way when the wall of the aneurysm bursts, we find that the vast majority 
rupture into the pericardium. Thus, out of 289 cases in which death was 
stated to have been due to rupture in males, 75 ruptured into the peri- 
cardium and 58 into the pulmonary artery; 23 ruptured into the right 
auricle, 3 of these taking place some time before death; 23 ruptured exter- 
nally; 14 ruptured into the superior vena cava; 11 into the oesophagus; 
9 into the left auricle; 8 into the right ventricle; 8 into the trachea; 6 into 
the left ventricle; 6 into the left pleura, and 5 into the right lung; 3 burst 
in the posterior mediastinum and 1 burst simultaneously into the trachea 
and oesophagus; in 20 others no statement was made as to the direction of 
the rupture. It is, however, a fact that death is much more commonly due 
to pressure symptoms than to rupture. 

Aneurysm of the transverse portion of the arch usually causes a ringing, 
brassy cough, dysphagia, expansile pulsation in the suprasternal notch, and 
dulness on percussion on the first and second left intercostal spaces. Its 
pressure on the innominate vein may cause congestion of the left side of 
the face and neck. Dyspncea from tracheal pressure may be present, and 
there may be aphonia from paralysis of the left vocal cord, arising from 
pressure on the left recurrent laryngeal nerve. If the growth is so situated 
that it passes from the left bronchus it may cause bronchiectasis and even 
bronchial suppuration by preventing drainage. Again, if the sac be a large 
one, it may involve the innominate artery, the left carotid, and even the 
subclavian, and in this manner the radial pulse may be absent on one side. 
Even the pulse in the arteries of the trunk and lower extremities maybe greatly 



538 



DISEASES OF THE ARTERIES 



lessened in vigor. The bruit may be loud and angry, but if the laminated 
clot be large it is often absent. The aortic second sound is usually accent- 
uated or ringing in character unless aortic regurgitation is present. 

When the descending arch is affected it often occurs that the aneurysm 
extends posteriorly, and the bruit and pulsation are found in the back, 
between the scapula and the spinal column on the left side. In these 
cases severe pain due to pressure on the intercostal nerves is often present, 
and the pressure on the vertebrae may cause erosion and even paraplegia 
by destroying the spinal cord. 

Fig. 78 




Aneurysm of the ascending and transverse part of the aortic arch, with erosion of the chest wall. 



Aneurysms of the ascending and transverse portion of the aorta often 
produce an extraordinary degree of erosion, and so pass through the wall 
of the chest by causing the absorption of the bony tissues, and by pushing 
the fragments of the ribs to one side. This is well shown in the accompany- 
ing cut. The surface of this tumor is often shining from distention of the 
skin, it is discolored by blood, and the surface may weep bloody serum for 
days as the end approaches. 

Under the name tracheal tugging a symptom of aortic aneurysm, which 
consists in the transmission of a tugging sensation to the trachea, has been 



ANEURYSM 539 

described by Oliver and studied by MacDonnell. To make this test, the 
patient stands erect with his head slightly tipped backward, so as to stretch 
the tissues of the front of the neck. The cricoid cartilage is now grasped 
by the thumb and finger and drawn toward the chin, when if aneurysm is 
present a tugging sensation will sometimes be felt with each beat of the 
heart. Sewall has shown that this sign is present in cases which have 
adhesions in the left pleura, and in some healthy persons when they take a 
deep inspiration. 

Occasionally in aortic aneurysm incurvation of the finger-nails and 
clubbing of the finger-tips on one side may be present. 

Blood-spitting is due to the formation of an erosion of the mucosa at the 
spot in the bronchial tube where the tumor causes pressure. Such a cause 
produces only a slight blood stain of the sputum. When the blood passes 
by a process of leakage through the wall of the sac and escapes into a 
bronchus it may be in considerable amount, and death may be due to a 
free hemorrhage of this sort. 

Very rarely there develops in the chest, as the result of aortic aneurysm, 
an adhesion between the sac and the superior vena cava, so that on the 
development of ulceration a communication between the two vessels is 
established, forming on a large scale an arteriovenous aneurysm. The 
most exhaustive study of this state has been made by Pepper and Griffith, 
and was reported to the Association of American Physicians in 1890. They 
could find only 28 cases in literature in addition to the one they observed. 
Less commonly the aneurysm communicates with the pulmonary artery. 

Diagnosis. — The symptoms of aneurysm, on which the diagnosis must 
be chiefly based, have already been mentioned. They may be briefly 
named as follows: The presence of bruit, expansile pulsation, pressure 
symptoms, dulness on percussion over the second and third interspace 
anteriorly on either side, unilateral sweating, and mydriasis or myosis, and 
thoracic pain. Swellings due to aneurysm nearly always are expansile, 
but care must be taken that swellings which pulsate by reason of transmitted 
impulse are not mistaken for a true dilated vessel. 

Nothing is more difficult to diagnosticate correctly than the early mani- 
festations of aortic aneurysm. Scarcely a physician of experience can look 
back and not recall cases in which its early signs completely misled him. The 
inconstant pain in the chest is often thought to be rheumatic or neuralgic. 
In other instances dyspnceic seizures are thought to be asthmatic, or attacks 
of severe cardiac pain are considered to be due to true angina pectoris. 
The persistence of symptoms like these, despite treatment, the age of the 
patient, the degenerated state of the palpable arteries, the sounds of the 
heart, and the history of syphilis, of alcoholism, and of strain or blow or 
wounds, are all at least capable of arousing suspicion of the real condition. 
The pain of aneurysm is often dull, gnawing, and constant, but in some cases 
pain may be absent. Occasionally an unsuspected aneurysm may cause 
an attack of stridor or paroxysmal dyspnoea, resembling somewhat a laryngeal 
crisis in locomotor ataxia. This should excite suspicion of aneurysm causing 
pressure on the recurrent laryngeal nerves. A hemorrhage from the lungs 
in the absence of tuberculosis should also be regarded as significant. This 



540 DISEASES OF THE ARTERIES 

haemoptysis may be frothy and mucoid, or rusty, like that of pneumonia, 
or prune-juice in hue. 

A very valuable aid in the diagnosis of thoracic aneurysm is the use of 
the arrays, either the fluoroscope being used or cc-ray pictures being taken. 
The advantage of the fluoroscope is the fact that the physician can see 
the expansile movement of the mass. 

Prognosis. — The prognosis of aortic aneurysm is, in the vast majority of 
cases, inevitably fatal, but in some cases life is preserved for many years 
if nature succeeds, by the deposition of laminated clot, in walling off the 
sac. An old scrub-woman has presented herself to my clinic during the 
past thirteen years, each season, with a massive aneurysm of the aorta 
which eroded the sternum years ago, and which has not grown since 
to any extent. She works hard for her living and has little discomfort. 
Her case is the exception that proves the rule, however. If the growth is 
of any size, life rarely lasts more than a few months. Even when it is small 
a rupture may occur. As already stated, death from aortic aneurysm is 
usually due to pressure on adjacent parts, and not most commonly to 
rupture, as is generally thought. 

Treatment. — Aneurysm of the peripheral arteries is best treated by 
compression and ligation, and the methods to be employed will be found 
discussed in works devoted to surgery. 

In aortic aneurysm there are two plans of treatment which may be insti- 
tuted, namely, medicinal and dietetic, on the one hand, and operative on 
the other. 

The medicinal treatment depends to some extent upon the underlying 
cause of the aneurysm. If it be due to syphilis, in the sense that this disease 
is chiefly responsible for the vascular degeneration, it is hardly necessary 
to state that the iodides in full doses are advisable, not that they can cure 
the aneurysm in the sense of regenerating an old vessel, but that they may, 
by their specific influence, arrest the degenerative influence in the vessel 
wall, and so delay the progress of the malady. Even if there is no history 
of syphilis in the case, the iodides are often of value in that they seem to 
arrest in some unknown manner degenerative changes in the vessels. They 
should be given in sufficiently large dose to produce some evidence of 
iodism, but not in sufficient dose to seriously disorder digestion. 

The second point in the treatment of the case is the institution of the 
greatest degree of rest which is compatible with comfortable existence. 
The patient should be placed in bed and required to use a bedpan in 
order that he may not disturb his circulatory equilibrium by getting up. 
He should also be given small doses of the bromides, if necessary, to 
overcome nervous irritation and restlessness, and if the action of his heart 
is exceedingly tumultuous and fails to become more quiet, by rest in bed, 
I have known small doses of aconite, such as 2 minims of the tincture, three 
or four times a day, to be advantageous. In other cases veratrum viride is 
useful in the same dose. Such a plan of rest treatment is useless unless it 
is carried out for weeks, and sufficient time must be allowed for a laminated 
clot to form in the aneurysm and reinforce its walls. 

The so-called Tufnell treatment of aneurysm consists in a more rigorous 



ANEURYSM 541 

method than that just described. The patient is not only put at absolute 
rest, but he is also given considerable quantities of iodide of potassium and 
as low a diet as is compatible with existence. Indeed, the treatment may 
be called the starvation plan of treatment, for it is the deliberate purpose, 
when this plan is instituted, to lower the activity of the circulation by the 
depression which is associated with semi-starvation. I have seen this plan 
instituted in a few cases only, and I have never seen good results from it. 
Surely, no advantage can accrue except by diminishing the activity of the 
circulation, and this can be obtained by the use of aconite or veratrum viride. 

The use of digitalis in these cases is not advisable because, while the drug 
steadies the heart, it increases arterial tension and so tends to increase the 
pressure upon the aneurysmal sac 

The operative treatment of thoracic aneurysm is only possible when the 
tumor is of the sacculated type. The fusiform type of aneurysm eontra- 
indicates its employment. A large number of operative procedures have 
been suggested, but there is only one which has at the present time received 
general recognition by the profession, namely, the so-called Corradi method, 
in which there is introduced into the aneurysmal sac several feet of fine 
gold wire which has been previously twisted about a glass spool, both the 
spool and the wire being carefully sterilized by boiling before they are 
used. After the skin over the sac has been carefully sterilized, the greatest 
gentleness being used lest it be damaged, a hollow needle, which is insulated 
by being coated with porcelain, is pushed into the sac, and then through it is 
passed from ten to thirty feet of wire, according to the size of the growth. A 
larger number of feet have been used, but ten or fifteen feet will be sufficient 
in the vast majority of cases. As soon as all the wire, save about six inches 
has passed into the sac, the external end of the wire is made fast to an 
electrode which is attached to the positive pole of a galvanic battery. A large, 
wet, clay electrode attached to the negative pole is placed under the back to 
complete the circuit and by means of a "current controller " the electricity 
is gently turned on. At first about 5 milliamperes are used ; at the end of five 
minutes the current is raised to 10 milliamperes, and after this the current 
is increased every five minutes by 5 milliamperes until about 50 milliamperes 
are employed. A higher number of milliamperes have been used, but with 
increasing experience I am confident that they are unnecessary and perhaps 
harmful. As the result of this method of procedure it not infrequently 
happens that by the end of the first twenty minutes or half-hour the sac 
is found to be somewhat more firm than before, and that pulsation in it 
has diminished owing to the fact that the acid reaction produced by elec- 
trolysis about the gold wire has resulted in the formation of a clot, which, 
as time goes by, becomes more and more firm and solid. At the end of 
from thirty minutes to an hour the wire is disconnected from the battery, 
its external end is pushed underneath the skin, and the external wound is 
closed by collodion. Absolute quiet must be maintained for ten days or 
two weeks after the operation, in order that the clot may become thoroughly 
consolidated. 

I have now performed this operation thirteen times, and my experience 
has been that in no instance did the patient suffer much pain. In 



542 DISEASES OF THE ARTERIES 

several instances the patient has stated during the operation that he 
was much improved, and in every instance he has voluntarily expressed 
his pleasure at the subsequent improvement. Unfortunately, the condi- 
tion of the aorta is such that when we close one bulging spot in this way, 
it is not long before another area gives way under pressure, and so another 
aneurysm is formed. In all of my cases this accident has ultimately occurred. 
The greatest duration of life after any one of the operations which I have 
performed has been a little over six months. But in one case operated on 
by Stewart some years ago the patient lived in comparative health for a 
period of three years, and then died from pneumonia following an alcoholic 
debauch, although at the time of operation the aneurysm could be seen as 
large as a fist outside the chest wall. Considering the slight pain of the 
operation, it is indicated in many cases, if only for the temporary relief which 
it gives. 

Aneurysm of the Abdominal Aorta. — Aneurysm of the abdominal aorta 
usually occurs near the diaphragm, and it is far more rare than aneurysm 
of the thoracic aorta. Out of 325 cases of aortic aneurysm collected at 
Guy's Hospital in forty-six years, 54 involved the abdominal aorta. Of these 
63 per cent, occurred between the ages of twenty-one and forty years and 77 
per cent, between twenty-one and fifty years; over 90 per cent, occurred 
in men. The growth usually arises from the neighborhood of the cceliac 
axis. Like that in the thorax, its sacculated form is more common than its 
fusiform type. It usually projects forward, but it may extend backward 
and cause erosion of the vertebrae, followed by pressure on the spinal cord. 
Pain is usually a constant symptom, which is often referred to the region 
of the heart or to the back. On inspecting the abdomen distinct pulsation 
may be seen at once, but care must be taken that the transmitted pulsation 
of the aorta in a state of health is not mistaken for true expansion. These 
two states can be separated by careful palpation. In some instances the 
aorta can be clearly felt through the belly wall; in other cases a morbid 
growth in the stomach or in the omentum can be felt, but although it 
pulsates it is not expansile. If the patient is placed in the knee-elbow 
position so that the growth falls away from the aorta, the diagnosis may be 
readily made. Auscultation may reveal a bruit if aneurysm is present, but 
if a stethoscope is used it is easy by pressure on the aorta to narrow its 
lumen and cause a humming sound, which is not a sign of aneurysm. 
Again, in hysterical persons a very marked pulsation of the aorta may be 
complained of by the patient and felt by the physician. I saw not long since 
an hysterical male who had rhythmical contraction of his abdominal rectus 
muscles synchronous with his pulse. It was only possible to diagnose his 
case by giving him ether to the point of relaxation. 

A larger proportion of these cases end by rupture than is the case in 
aneurysm of the thoracic aorta. Thus, out of these 54 cases no less than 
43 died from rupture. 

Aneurysm of the abdominal aorta may rupture into the retroperitoneal 
tissues, through the diaphragm into the pleural spaces, or into the general 
peritoneal cavity, or more rarely into an intraperitoneal viscus, as, for 



ANEURYSM 543 

example, the stomach. Rarely death ensues from the vessel becoming 
closed by a thrombus. 

Even more rare than aneurysm of the abdominal aorta is aneurysm of 
its branches. Cases have been recorded in which a blow upon the belly 
has caused aneurysm of the hepatic artery, and in a case seen by the writer 
it followed ulceration produced by a malignant growth of the gall-bladder 
That this condition is very rare is shown by the fact that up to 1898 only 26 
cases had been recorded. The symptoms are usually mistaken for hepatic 
colic, and this error is all the more easy because jaundice from pressure 
is often present. In most of the recorded cases the antemortem diagnosis 
has been "gallstones" or " duodenal ulcer." 

Aneurysm of the splenic artery is rarer than aneurysm of the hepatic 
artery, and causes symptoms like those of gastric ulcer. 

Aneurysm of the superior mesenteric artery is also rare. Rolleston has 
collected 20 cases. Embolism is the usual cause, and injury may be respon- 
sible for it. This growth may cause jaundice by pressure on the gall-duct, 
as in a case reported by J. A. Wilson; or it may press on the renal arteries 
and cause uraturia, as in a case recorded by Burney Yeo. Aneurysm of the 
inferior mesenteric artery is practically unknown. 

Aneurysm of the renal artery is also rare, although small multiple sacs 
are sometimes seen. If the sac be very large hematuria may occur, or 
wasting of the kidney may ensue. Sometimes by the sudden rupture of 
an aneurysm of this vessel the retroperitoneal space has been filled with 
blood. In the surgical clinic of the Jefferson College Hospital, my colleague, 
Dr. W. W. Keen, recently cut down on a kidney because of severe renal 
symptoms, and found a large aneurysm of the artery. He was forced to 
remove the aneurysm and the kidney. 



DISEASES OF THE DIGESTIVE TKACT. 



DISEASES OF THE MOUTH. 

STOMATITIS. 

Definition. — As its name implies, stomatitis is an inflammation of the 
mouth. Of the many forms that have been described three are important : 
catarrhal stomatitis, aphthous stomatitis, and ulcerative stomatitis. All 
these forms of stomatitis usually occur in childhood. The catarrhal and 
aphthous forms are more common in early infancy, but the ulcerative type 
is practically never met with in children who have not as yet gotten teeth, 
and is more common in those past puberty than are the other forms. 

Catarrhal Stomatitis. — In catarrhal stomatitis there is hyperemia of the 
mucous membrane of the tongue and cheeks, with an increase in secretion 
on the part of the mucous and salivary glands. It arises from injury, as by 
some foreign body being taken into the mouth which acts as a mechanical 
irritant, or by hot or irritating liquids. These are, however, only predis- 
posing causes. Difficult dentition, or the use of a rubber nursing nipple 
which is dirty, are more common factors. It also occurs as one of the mani- 
festations of the acute eruptive diseases, as in scarlet fever and measles, 
and it may be a symptom of some metallic poisoning, as mercury, lead, or 
arsenic. 

Symptoms. — The symptoms of catarrhal stomatitis are intense hyper- 
cemia of the mucous membrane of the mouth with some swelling which is 
particularly visible on the gums. If the finger be placed in the mouth a 
sense of increased heat is felt. The child evidently suffers a good deal of 
pain. When given the breast or bottle it eagerly seizes it because of hunger 
and thirst, and then, as the nipple touches the tender mucous membrane, 
gives a cry of pain and disappointment. Cool water is usually taken with 
avidity if given from a cup. The flow of saliva is so free that constant 
dribbling on the chin is present or the excess of saliva is swallowed and 
disturbs digestion. If the mouth be very carefully examined it may be that 
tiny blisters at the opening of the mucous glands will be seen and the papilla 
of the tongue will be found enlarged, swollen, and unduly red in hue. Some 
digestive disturbance and diarrhaa are nearly always present. Whether 
these symptoms are the result of the condition of the mouth, or whether the 
state of the mouth is secondary to disturbed digestion, is often difficult to 
determine. 

35 ( 545 ) 



546 DISEASES OF THE MOUTH 

Prognosis. — Recovery from catarrhal stomatitis is usually rapid, the con- 
dition rarely lasting for more than a few days after the disordered digestion 
is corrected and proper cleanliness of the mouth is obtained. 

Aphthous Stomatitis. — The aphthous form of stomatitis, sometimes called 
follicular or vesicular stomatitis or canker, may be considered as a still fur- 
ther development of the catarrhal form. In this condition we not only have 
a diffuse hyperaemia of the mucous membrane of the mouth, but in addi- 
tion small spots appear which look as if the superficial epithelium had been 
snipped off with curved scissors. These spots are, of course, exquisitely 
sensitive. All the symptoms of the catarrhal form are much exaggerated, 
and in addition to more marked digestive disturbance the patient often 
has systemic disturbance, as is shown by some fever and general wretched- 
ness. Nutrition is interfered with materially only by the inability to take 
food. 

Ulcerative Stomatitis. — The ulcerative form of stomatitis, sometimes 
called fetid stomatitis, or putrid sore mouth, is a much more serious type, 
but it is often so mild that the dividing line between it and the aphthous 
form is not readily made. When well developed, the mucous membrane 
is seen to be studded by small ulcers which may coalesce, forming rather 
large areas of superficial necrosis. If the child is badly nourished, or suffer- 
ing from some malady which impairs its general nutrition, ulcerative stom- 
atitis may become a very serious affection, causing great suffering, inter- 
fering seriously with proper feeding and rapidly undermining the strength 
of the patient. The ulcers are situated chiefly along the edges of the gums 
which recede from the teeth, or on the margins of the tongue, on the buccal 
membrane, and even on the lips. The breath is often very foul and the 
corners of the mouth become excoriated from the salivary flow. When the 
patient is a sufferer from scurvy and bad hygienic surroundings, it may be 
an important factor in preventing recovery. 

In many cases the condition arises from carious teeth and occasionally 
the disease occurs epidemically. On the other hand, I have repeatedly 
seen mild ulcerative stomatitis occur in otherwise healthy young girls past 
puberty, in whom none of these causes were apparent. 

In severe cases the ulceration may be very deep and may even cause 
loosening of the teeth or superficial necrosis of the lower jaw. 

Treatment. — The treatment of all these forms of stomatitis may be con- 
sidered simultaneously. All of them are to be treated by careful attention 
to cleanliness of the mouth itself and of all objects entering the mouth, by 
careful regulation of the bowels and the food, and by a mouth- wash of 
chlorate of potash and myrrh in the following formula : 



R. — Potassii chlorat. ....... gr. 

Tinct. myrrhae Tit x. 

Elix. calisayse ........ f ^iij. — M 

Sig. — Dilute one tablespoonful with two of water, and use as a mouth-wash 

When very young children are treated this solution may be applied to 
the mucous membrane by means of a swab tied to a small stick or pencil 
These measures are usually efficient in the catarrhal and aphthous type. 



STOMATITIS 547 

In the ulcerative form it may be necessary in addition to touch each ulcer 
with a solid stick of nitrate of silver or with a solution of this drug of the 
strength of GO grains to the ounce. This is painful, but efficacious. Only a 
few spots should be touched at each sitting. When the teeth are not carious 
peroxide of hydrogen may be used locally. The system should be well sup- 
ported by nutritious foods such as cold consomme or cold chicken-jelly, by 
ordinary foods if they can be taken into the mouth, and, if anaemia is 
present, by the use of iron and quinine in moderate doses. 

When for any reason chlorate of potash cannot be applied locally the, 
physician may give the drug internally in the dose of 2 grains every three 
hours, since, as it is eliminated by the salivary glands, the saliva bathes 
the diseased mucous membrane with the drug. This plan of treatment is 
contraindicated if any renal irritation or marked gastric disturbance is 
present. 

In scorbutic cases fresh vegetables, fruit, and beef-juice are absolutely 
needful in the treatment of the patient. 

There still remains to be discussed in this connection three forms of sore 
mouth which do not, strictly speaking, fall under any of the headings just 
given, since in all of them definite specific causes have been isolated, 
namely, so-called thrush or parasitic stomatitis, gangrenous stomatitis, 
and mercurial stomatitis. 

Thrush. — Thrush, or parasitic stomatitis (Soor or Muguet), is due to 
the presence in the mouth of a parasite variously named Saccharomyces albi- 
cans, Monilia Candida, or Oidium albicans. This parasite has been classed 
with yeasts, and grows with branching filaments at the ends of which egg- 
shaped, torula cells are produced. Thrush is distinctly associated with 
impaired health of the mucous membrane, and in children, in whom it is 
most commonly met with, it is due, as a rule, to the use of dirty nursing nipples 
or nursing bottles, or to general impairment of health. When the latter 
cause is present, thrush may appear in the mouth of adults, and for this 
reason it sometimes aids in increasing the miseries of those whose vitality 
is impaired by tuberculosis, diabetes, and by prolonged exhausting fevers. 
It is also seen in children suffering from marasmus. The parasite can be 
readily conveyed from one person to another by utensils. 

Symptoms. — The subjective symptoms of thrush consist in the same 
discomfort in the mouth which is met with in aphthous stomatitis. The 
objective symptoms are, however, to be carefully separated from that state. 
Instead of denudation or depression of the surface of the mucous membrane 
there is seen on the tongue small particles or specks in the form of tiny yearly 
white spots, which are raised and may gradually coalesce and seem to from 
a membrane that is usually easily removed, although its removal may leave 
a bleeding surface. From the tongue the growth may extend to the entire 
mucous membrane of the mouth and the soft and hard palate. Very rarely 
it even spreads to the pharynx and oesophagus, and even into the stomach 
and small intestines. Holt states that the fungus has been found in the 
lungs of babies suffering from bronchopneumonia. Thrush is separated 
from aphthous stomatitis by the fact that the profuse salivation of the 



548 DISEASES OF THE MOUTH 

latter is replaced by great dryness of the mouth, and by the aid of a 
microscopic examination of the growth. 

Prognosis. — The prognosis depends upon the health of the patient. In 
the robust the condition may last but a few days, but in the feeble and 
impoverished it may persist for weeks. It does not materially influence 
the general health except by interfering with the taking of nourishment. 

Treatment. — The treatment consists in cleanliness, good feeding, the use 
of a mouth-wash of borax in the strength of 10 grains to the ounce, or of a 
mouth-wash of permanganate of potash, 1 grain in 8 ounces of water, 
or by diluting peroxide of hydrogen, 1 part in 5 of water. Any under- 
lying disorder of nutrition should be carefully removed if it be possible. 
All sweets and syrups should be carefully avoided. 

Gangrenous Stomatitis, Cancrum Oris, or Noma. — Noma is a term 
applied to all forms of severe ulceration of a localized character attacking 
mucous membranes, but the state may be present without the mucous 
membrane being broken, the tissues of the cheek being chiefly affected. 
The condition occurs so rarely in those who are past puberty that it may 
be said to be a disease of early childhood. It affects the buccal mucous 
membrane and cheek so constantly that the word "noma" has come to 
mean a malignant and sometimes a perforating gangrenous process involv- 
ing the cheek, although, strictly speaking, noma may affect the ear, the 
vagina, the buttock, the nose, or the external genitalia. 

In the vast majority of cases noma results in the death of the patient, 
not so much because it is in itself a fatal disease as that it is a terminal 
infection; that is, one which develops only in a child or adult whose vital 
resistance is so lowered by disease or poor nutrition that the pathological 
process known as noma is possible. 

The disease is rarely seen in private practice, but has its greatest fre- 
quency in institutions for poor children, where because of mismanagement, 
or of the wretched state of the child on admission, it readily falls a victim 
to infections of all kinds. 

Noma more commonly follows measles than any of the other eruptive 
diseases, but it also sometimes complicates or follows scarlet fever, typhoid 
fever, or whooping-cough. It is practically never a primary lesion at the 
point of development, but begins in a solution of continuity such as an 
1 ulcer due to a carious tooth or as a sequence of ulcerative stomatitis. In 
all probability it is not due to an infection by any single micro-organism, 
but to several organisms which may be associated. Cases have recently 
been recorded in which the ulceration seemed to be due to the bacillus of 
diphtheria, but mixed infection is the rule. An attempt to establish speci- 
ficity for any single organism has been futile. 

Not only has the ulcerative process a tendency to rapidly become deep 
and so to perforate the cheek, but it lacks the sharp line of demarcation 
marking the wall often built by nature to prevent the spread of gan- 
grene. That is to say, the ulcer is bounded by an extending area of 
necrosis, often branching and discolored, which spreads from day to day, 
with no apparent effort on the part of the system to limit its progress. 
The soft parts melt into the fetid ulcer, and cartilage and bone undergo 



ECZEMA OF THE TOXGUE 549 

necrosis. When recovery does occur, which is exceedingly rare, a line of 
demarcation forms, and the extension of the disease is arrested in this way; 
the ulcer clears up and repair slowly takes place. 

Symptoms. — The local symptoms of noma are a foul breath, a state of 
localized ulceration with deep induration of the tissues near by, and the 
speedy development in the centre of the ulcer, of a dirty-looking slough of 
necrotic tissue. The side of the face is usually much swollen and distorted, 
and when felt by the fingers the tissues feel brawny and hard. If the ulcera- 
tion extends to the gums, the teeth become loosened. So great may be the 
destructive process that the teeth and alveoli may be seen through the per- 
forated cheek. 

The systemic symptoms are not characteristic of any specific state, but 
are those of profound systemic poisoning, depression, and exhaustion. The 
pulse is rapid and feeble, the appearance of the patient markedly septic and 
cachectic, and the temperature mildly febrile. The height of the tempera- 
ture depends, however, to a considerable degree, upon the vitality of the 
patient. When the sufferer is profoundly exhausted and the vital state is 
very low marked febrile movement does not occur. 

. Treatment. — From the description just given it is evident that the treat- 
ment of noma, to be successful, must depend upon its early institution and 
thorough character. It must also consist in the use of such nutritious food 
and such medicines as will serve to support the strength of the patient. 
The local treatment consists in the early and complete cauterization of the 
part affected by the electrocautery or its excision by the knife, so that the 
necrotic mass is at once destroyed and removed. The physician must not 
limit the operation to the dead tissues, but extend the excision to the living 
tissues as well in order that none of the infected tissue may remain. The 
local process may be temporarily treated by swabbing the part with peroxide 
of hydrogen or by using permanganate of potash. In cases in which the 
streptococcus or the bacillus of diphtheria are present, the serum therapy 
needed for these specific infections should be used. 



ECZEMA OF THE TONGUE. 

Under this distinctly erroneous term is described a condition in which 
there is a superficial overgrowth and desquamation of the epithelium cover- 
ing the tongue. As a rule, the centre of each spot of desquamation begins to 
heal while the periphery is still spreading, so that the appearance of the 
inflammatory zone is distinctly circinate. Its irregular outline has given it 
the name of " geographical tongue." In other instances the appearance of the 
tongue is that of a worm-eaten leaf. In some patients it produces no dis- 
comfort whatever. In others the patient may have some itching and tingling, 
and on examining the tongue is surprised to find the curious outlines which 
have been described. Not infrequently nervous patients are wont to con- 
sider that it is an evidence of syphilis, or perhaps of a malignant growth. A 
modified form of this condition is very frequently seen in children as a result 
of a catarrhal condition of the stomach and bowels. 



550 DISEASES OF THE SALIVARY GLANDS 

Treatment. — In adults it is best treated by the local application of nitrate 
of silver, 20 grains to the ounce. In children the correction of the gastrointes- 
tinal disorder usually results in a normal growth of epithelium, so that the 
condition is relieved. As a rule, such children require some simple bitter 
such as tincture of gentian with 5 or 10 grains of bicarbonate of soda. 



LEUKOPLAKIA BUCCALIS. 

Leukoplakia buccalis is sometimes called smoker's tongue, ichthyosis lin- 
gualis, and buccal psoriasis. It is characterized by the development of white 
spots of considerable size on the mucous membrane of the mouth and tongue, 
which are due to cellular infiltration of the subepithelial connective tissue 
and a thickening of the epithelium. When the spots occur on the edge of 
the tongue and are indented by the teeth they sometimes look like the scars 
or puckerings which are seen on the edges of the tongue in cases of advanced 
syphilis. Occasionally these areas may be slightly ulcerated, and in some 
cases are thought to be the seat of epitheliomatous degeneration. In the 
majority of instances, however, they are benign, and after removal of the 
cause require no treatment unless the surface is ulcerated, in which case they 
may be touched with nitrate of silver and the patient directed to avoid taking 
hot, irritating substances into the mouth, and particularly to avoid smoking 
or chewing. Leukoplakia is sometimes looked upon as a precancerous 
condition, and this is probably true in the sense that the state if per- 
mitted to continue may lead to cancer. 



MUCOUS PATCHES. 

Mucous patches are opaque, white, flattened swellings on the mucous 
membrane of the mouth and lips, and are characteristic of secondary syphilis. 
(See Syphilis.) From them the virus of syphilis is readily communicated. 
Not infrequently their surface is somewhat ulcerated. 

Treatment. — The treatment, of course, consists in the active employment 
of mercury internally and the use of nitrate of silver locally. 



DISEASES OF THE SALIYAEY GLANDS 

FUNCTIONAL DISORDERS OF THE SALIVARY GLANDS. 

Ptyalism. — Ptyalism, or salivation, occurs as the result of poisoning by 
mercury or the iodides. It is also produced by such drugs as jaborandi, 
and occasionally occurs because of irritation of the mucous membrane of 



INFLAMMATION OF THE SALIVARY GLANDS 551 

the mouth by the development of stomatitis in one of its several forms. 
Rarely a form of idiopathic ptyalism is met with in young children. Under 
these conditions the salivation is probably the result of a neurosis. 

When due to the influence of a drug, the condition is to be arrested by 
stopping the use of that substance and aiding in its elimination by the 
employment of sodium bicarbonate if the iodides have been taken, and mild 
saline purgatives if mercury has been used. A mouth-wash containing 10 
grains of chlorate of potassium and 2 drachms of fluid extract of rhus glabra 
in an ounce of water will be useful to improve the condition of the mucous 
membrane and arrest the flow of saliva. Sometimes moderate doses of 
atropine are useful. In other cases, 10 to 15 grain doses of camphoric acid 
given thrice a day may be used. 



DRY MOUTH. 

Dry mouth, or xerostomia, is frequently met with in all fevers, but some- 
times occurs as an independent condition. Under these circumstances the 
tongue is seen to be red and dry, with lessened superficial epithelium, so that 
it is smooth and shiny. It is said to be most frequent in women after great 
nervous excitement or in those suffering from hysteria. 

Treatment. — Temporary relief from dryness of the mouth may be pro- 
duced by washing it with a mixture of 1 part of glycerin to 2 of water, to 
which has been added a little lemon-juice. 



INFLAMMATION OF THE SALIVARY GLANDS. 

The most important and most common inflammation of the salivary glands 
is the swelling of the parotid gland in mumps, which has already been con- 
sidered. The next most frequent cause of inflammation of the salivary 
glands is a septic condition of the mouth in the course of one of the prolonged 
adynamic fevers, such as typhoid fever, and in persons who are suffering 
from cerebral softening. In these cases it would seem that infection may 
pass through the salivary duct, and so cause inflammation of the gland itself. 
Occasionally a similar accident occurs in pyaemia, pneumonia, syphilis, and 
scarlet fever. In some of these diseases the infection undoubtedly enters 
the glands by way of the bloodvessels and lymphatics. Pyogenic infection 
of the parotid, whether haemal, lymphatic, or by a duct, produces a suppura- 
tive interstitial parotitis, or parotid abscess, also called " parotid bubo." A 
curious form of inflammation of the parotid gland with stenosis of Steno's 
duct is sometimes seen in cases of sulphuric acid poisoning. While it is pos- 
sible for the sublingual and submaxillary glands to be involved, the parotid 
is the gland which nearly always suffers. 

The inflammation may be treated in its early stages by cold compresses, 
by the application of leeches, and by the administration of circulatory 
sedatives like aconite, provided the patient is not already depressed by dis- 
ease. So far as possible the treatment should also be addressed to the relief 



552 DISEASES OF THE PHARYNX 

of the underlying cause of the condition. If the gland is suffering from 
a subacute inflammation, mercurial ointment, iodine ointment, or ichthyol 
ointment may be thoroughly rubbed into the skin over it, unless perchance 
the gland is swollen as the result of mercurial or iodide influence. When an 
abscess forms it must not be forgotten that it should be opened promptly, 
but with great care. Not infrequently a parotid abscess is so closely asso- 
ciated with an important bloodvessel, or indeed with the external carotid 
artery, that a careless incision may produce disaster. Such an abscess should 
always be opened by careful dissection. 

Chronic indurative or sclerosing parotitis is a well-known pathological 
condition the clinical features of which are still obscure. It has been observed 
in diabetes with and without pancreatic disease, but the exact relationship, 
if any, is not known. 

Ludvig's Angina. — This condition, sometimes called Angina Ludovici, is 
a cellulitis of the neck which begins as an inflammation of the floor of 
the mouth, usually in the area of the submaxillary gland. As a rule it begins 
on one side and then spreads to the opposite side. In malignant cases it 
rapidly involves not only the floor of the mouth, but the tissues about the root 
of the tongue and under the angles of the jaw, so causing oedema of the 
glottis. In some cases these tissues slough, forming what is known as 
cynanche gangrenosa. In still others, an abscess points externally. 

Symptoms. — The symptoms are brawny swelling, great pain, rigors, fevers, 
and, if the infection is severe, general septicaemia and death. 

Treatment. — In the very early stages the use of cold and of leeches to the 
skin under the jaw may be of advantage. After the inflammation is well 
developed, drainage should be established by the surgeon. 



DISEASES OF THE PHAEYNX. 

ACUTE PHARYNGITIS. 

Definition. — Acute pharyngitis is an acute catarrhal inflammation of the 
mucous membrane lining the pharynx in which there is hyperemia and 
congestion, with some infiltration of the submucous tissues, and, later, an 
increased secretion of mucus. 

Etiology. — Acute pharyngitis is caused, as a rule, by simultaneous exposure 
to cold and infectious dust. Cold and damp air first impair the vital resist- 
ance of the pharyngeal mucous membrane, and then dust, laden with micro- 
organisms, falling upon it speedily produces infection. There can be no 
doubt that systemic conditions also favor the development of this state. 

Aside from the fact that lowered vitality always permits infection to take 
place readily, there can be no doubt that the excessive use of alcohol, 



ACUTE PHARYNGITIS 553 

tobacco, or rich foods, or the presence of a torpid liver, or a catarrh of 
the nose, mouth, or stomach aid materially in permitting the condition 
to arise. Pharyngitis also arises as a result of lithsemic states. Sometimes 
infection seems to come from a chronic tonsillitis or is an extension from 
the nares. The condition is particularly prone to arise in those who work 
for a number of hours a day in imperfectly ventilated rooms. Sometimes 
irritating fumes and dust seem capable of producing this condition. 

Pathology. — After a preliminary dry stage the engorgement of the blood- 
vessels of the mucous membrane and the inflammation of the mucous glands 
results in the pouring out of considerable quantities of mucus, marked 
epithelial desquamation, and in severe cases some fibrin. If pyogenic 
organisms are present the secretion may be distinctly mucopurulent. In 
some instances the swelling of the submucous tissues is very marked. In 
others, although severe, it may be superficial. In very rare cases the exudate 
may be so fibrinous as to form a false membrane which is not always due 
to the presence of the bacillus of diphtheria. Not rarely in such cases the 
uvula and the tonsils are also involved. 

Symptoms. — Acute pharyngitis usually comes on suddenly, with the symp- 
toms of what is popularly called "sore throat" so that the patient feels that 
the mucous membrane is swollen and sore, and there is some pain on swal- 
lowing. On inspection it will be found that the posterior wall of the pharynx 
and neighboring parts are dry and red, with the capillaries injected. After 
secretion is established the parts are thoroughly moistened by serum and 
mucus. In some instances, if the infiltration of the submucous tissues is 
marked, the patient may complain of a sense of constriction in the throat, 
and at times a good deal of pain may extend along the Eustachian tube into 
the ear. If the pain is not too. great, the patient may continually clear his 
throat in an effort to relieve the irritation. Constitutional symptoms are 
usually mild, but the tongue is coated and the patient may be somewhat 
depressed. 

Prognosis. — Recovery always ensues unless some unforeseen complica- 
tion arises. 

Treatment. — The treatment consists, if the patient is seen in the early 
stages, in the application of a cold compress to the neck below the angle 
of the jaw. This compress is made by dipping cloths in ice-water, wringing 
them out, and then binding them against the part. They should not be 
allowed to become warm and so produce the relaxing effects of a poultice. 
Internally, if the patient is an adult, he may be given from 1 to 5 drops of 
the tincture of aconite with a drachm of sweet spirit of nitre in a glassful of 
hot lemonade. Before taking this he should be put to bed in order that when 
perspiration develops he will not catch cold. Small pieces of ice may be held 
in the mouth, but, as a rule, better results will be obtained if the patient gar- 
gles with as hot water as he can bear. This water may be fortified by adding 
to it an equal quantity of the distilled extract of witch-hazel. If the bowels 
are at all constipated, saline purgatives, such as citrate of magnesia, should 
be used to unload them. If there is any rheumatic or gouty tendency, the 
patient will do best if, in addition to the purgatives, he is given 20 grains of 
bicarbonate of potash in large draughts of water every four or five hours; 



554 DISEASES OF THE PHARYNX 

or, instead, 10 grains of salol may be given every three hours until 40 grains 
have been used. 

Local treatment aside from the use of the gargle is usually unnecessary. 
If the condition is due to a gouty tendency, the use of any one of the oily 
substances commonly employed in atomizers produces increased discomfort, 
in the writer's experience. If it is not due to this cause, some relief may 
be obtained by spraying the parts with 3 drops each of oil of sandal-wood 
and oil of sassafras in an ounce of liquid albolene. In other cases, when the 
oils cause discomfort, my colleague, Dr. Kyle, strongly recommends apply- 
ing hydrochloric acid, in the proportion of 5 to 10 drops of the dilute acid 
in an ounce of water, for the purpose of contracting the dilated bloodvessels. 

The salicylates are useful if lithsemia is present. 

When the second stage is reached 5 to 10 grains of chloride of ammonium 
may be given in equal parts of fluid extract of licorice and water four or 
five times a day. Or, instead, 10 grains of benzoate of ammonium may 
be given in capsule four times a day. 



ULCERATIVE OR PHLEGMONOUS PHARYNGITIS. 

Etiology. — This condition, sometimes called ulcerated sore throat, or 
phlegmonous pharyngitis, is due to an infection of the mucous membrane 
of the throat by micro-organisms. It is not uncommonly seen in physicians 
and nurses who are attending children suffering from scarlet fever and 
diphtheria. Many years ago it was frequently met with in medical students 
who were dissecting cadavers which had been imperfectly preserved. This 
form of pharyngitis is exceedingly painful in its early stages, and is charac- 
terized by changes much like those just described in acute catarrhal pharyn- 
gitis, except that a superficial necrosis of the mucous membrane rapidly 
occurs, so that in a few hours small, irregular ulcers may be seen upon the 
soft palate, the half arches, and the pharyngeal wall. If the infection is 
severe, so that the submucous tissues are involved, it becomes a phlegmon- 
ous pharyngitis. 

Symptoms. — A patient with infectious pharyngitis usually complains of 
much pain in the throat and in the muscles of the neck. This is greatly 
increased when he attempts to swallow. There may be slight febrile move- 
ment and depression. 

Treatment. — The treatment consists in spraying the inflamed mucous mem- 
brane with a normal salt solution, and following this by a gargle or spray 
of 1 per cent, solution of carbolic acid and water or albolene. This in turn 
is followed by a spray of menthol, 4 grains to the ounce. Cold compresses 
applied under the jaw are advantageous. If one or two ulcers are par- 
ticularly active, they may be touched with nitrate of silver. Usually it is 
advisable to give the patient a moderate purgative dose of calomel and to 
follow it by a saline purge, such as a Seidlitz powder. 



CHRONIC PHARYNGITIS 555 



CROUPOUS PHARYNGITIS. 

Etiology. — Croupous pharyngitis occurs in two forms as diphtheria, which 
has already been described, and as a simple membranous pharyngitis, which 
commonly is due to infection by the pneumoeoccus or Streptococcus pyogenes. 
The chief difference between this form of pharyngitis and diphtheria is that 
the mucous membrane is not deeply involved, that true ulceration never 
occurs, and the Klebs-Loeffler bacillus is absent. The inflammation is, 
however, of such a character that a false membrane develops with desquama- 
tion of the epithelium. If the membrane is removed, the tissues beneath 
may bleed, very much as they do in diphtheria. Although there is usually a 
slight chill and some fever, the degree of systemic disturbance is by no means 
as marked as in the well-developed case of true diphtheria. 

Treatment. — The treatment consists in washing the infected parts thor- 
oughly by a spray of normal salt solution, and following this by a solution 
of hydrogen peroxide and water half and half, and this in turn by gargling 
and spraying with distilled extract of witch-hazel. Usually this treatment 
is sufficient. If the condition persists, LoefBer's solution may be applied 
locally. Antitoxin is to be used if diphtheria is present. (See Diphtheria.) 



CHRONIC PHARYNGITIS. 

Etiology. — A condition of chronic inflammation of the pharyngeal mucous 
membrane is frequently met with in certain climates, particularly that of 
the Atlantic seaboard. It is also found in persons who continually use the 
voice, and so it has obtained the name of " auctioneer's " or "clergymen's" 
sore throat. It is also met with in persons who use tobacco to excess, and 
sometimes in those who take too much alcohol. Obstructions in the nasal 
passages seem distinctly to predispose to this state. 

Pathology. — The pathological condition consists in a thickening of the 
mucous membrane of the pharynx and an increase in the connective tissues 
of the mucous membrane itself, and of the submucous tissues. This may 
result in a secondary atrophy of the glands in the mucous membrane. 

Symptoms. — The symptoms consist in a thickening of the pharyngeal 
secretions and irritation of the mucous membrane, so that the patient is 
continually attempting to clear the throat, which often feels dry and harsh. 
The cough is spasmodic, unproductive in its result, and is made much worse 
by exposure to cold and dust. 

Treatment. — The treatment consists in a regulation of the digestive sys- 
tem, in giving tone to the circulation if it is feeble, in rest for the nervous 
system if the patient is overworked, and in the internal administration of 
benzoate of ammonium in 10 grain doses several times a day. Before going 
to bed at night the patient should gargle his throat with hot water or with 
hot salt solution, and if the bloodvessels are much dilated a spray of dilute 
hydrochloric acid, 10 drops to the ounce of water, should be used. 



556 DISEASES OF THE TONSILS 



FOLLICULAR PHARYNGITIS. 

Etiology. — Under the name of follicular pharyngitis a closely related 
condition to that just described exists, in which an annoying cough is per- 
sistent, and in which a considerable number of enlarged follicles, surrounded 
by an injected mucous membrane, can be seen on the posterior wall of the 
pharynx. 

Treatment. — The treatment is of the same character as that just described 
for chronic pharyngitis. Occasionally it is necessary to cauterize the follicles. 
An excellent application is tincture of iodine 1 part in 2 parts of glycerin. 



DISEASES OP THE TONSILS. 

ACUTE TONSILLITIS. 

Definition. — As its name implies, this disease consists in an acute inflam- 
mation of the tonsils, accompanied by great swelling of their tissues, and 
an associated pharyngitis. It occurs in two forms, the follicular and 
diffuse. The follicular form is distinctly infectious. 

Etiology. — Acute tonsillitis is the result of an infection by pathogenic 
micro-organisms, which are practically always present in the crypts of 
the tonsils, but do not penetrate the mucous membrane until its per- 
meability is increased by congestion, or by general causes affecting perhaps 
the vital resistance of the entire body. In many instances the suppurating 
form arises because the organisms attempt to enter the general system by 
way of the tonsils, and the suppurative process is the result of an effort to 
prevent such an entrance. The streptococcus is a cause in some cases. 
In other cases the organism which Poynton and Payne think is the cause of 
acute articular rheumatism is responsible, and the bacillus of diphtheria is 
also a common factor. 

Follicular tonsillitis is more common in the period of life from five to 
twenty years than at any other time, and is rare in infancy. Some indi- 
viduals suffer from frequent attacks until they reach forty or fifty years 
of age. After this time of life it is very rare. 

Although follicular tonsillitis is rare in adults, the suppurating form is 
frequently met with in this class of patients. Persons who have a lymphatic 
temperament are far more susceptible than persons of the wiry type, and it 
is particularly prone to occur in those who, because of obstruction of the 
nasal passages, are "mouth breathers," or who suffer from subacute or 
chronic hypertrophic catarrh of the nasopharynx. One attack distinctly 
predisposes to another. My experience leads me to believe that it is dis- 
tinctly infectious, for I have repeatedly seen healthy persons develop the 



ACUTE TONSILLITIS 557 

malady after being exposed to the breath of those who were ill with it. 
Another predisposing cause is the breathing of vitiated air, and air that is 
contaminated by sewer gas or smoke. How much these influences act 
directly as sources of infection and how much as agents which, by dimin- 
ishing vital resistance, make infection possible, is difficult to determine. 

Pathology and Morbid Anatomy. — In acute follicular tonsillitis there is an 
inflammatory swelling of the parenchyma of the gland. The mucous mem- 
brane covering the gland is intensely hypersemic and may even show vesicles 
on its surface. Each follicle exudes a cheesy-looking mass, and these masses 
dot the surface of the tonsil or coalesce and produce a tonsillar coating, 
which at first glance closely resembles the false membrane of diphtheria. 
If some of this material is examined microscopically it is found to consist 
of dead epithelial cells, micro-organisms, and pus cells. In addition to 
these superficial changes there is hyperemia of the tonsillar capillaries, and 
proliferation of the lymphoid cells in the deeper tissues of the glands. In 
the more deeply situated and intense inflammations of the gland, sometimes 
called quinsy, there is a necrosis of the tissues, suppuration takes place, and 
the pus escapes from the tonsillar abscess, either by the aid of the surgeon's 
knife or by rupture of the abscess wall. In any of these conditions the 
passage of bacteria or their toxins into the lymphatics may produce glandular 
enlargement in the neck. 

Symptoms. — A patient suffering from the earliest stages of acute tonsillitis 
may first feel soreness of the throat, with a sense of local swelling or con- 
striction, or the systemic signs of the infection may first be manifested. 
Creeping, chilly sensations, or even a true rigor, may develop, and there is 
very frequently an amount of aching and pain in the limbs which is extraor- 
dinarily severe, so that the patient complains most bitterly, not only of this 
symptom, but of the degree of illness, so that he fears a serious malady. 
Violent headache is often a prominent symptom, and the temperature 
soon becomes very high, mounting to 103° or 104° or even 105° in a few 
hours. Rarely nausea and vomiting may occur. An examination of the 
throat will show the presence of distinct swellings of the tonsils, which 
not rarely extend as far across the fauces as the uvula, and even press against 
one another. These swellings are intensely congested and frequently covered 
with exudate, and are often very foul in appearance. The breath of the 
patient is exceedingly foul, and unless ventilation is very good the odor may 
fill the room. Owing to the swelling of the tonsils and adjacent glands and 
stiffness of the muscles of the sides of the neck, an examination of the patient's 
throat may be very painful. 

As general svstemic infection often enters the body by way of the tonsils 
it is wise to be on the watch for signs of endocarditis. Doubtless the asso- 
ciation of rheumatism with tonsillitis by many practitioners is due more to 
the development of septic arthritis from the entrance of pathogenic germs by 
these pathways than to any real relationship between acute rheumatism and 
tonsillitis. I have seen several cases of severe ulcerative endocarditis and 
acute arthritis follow an acute tonsillitis. It is a noteworthy fact that acute 
follicular tonsillitis is practically always bilateral, while the deeper form, 
sometimes called quinsy, is often unilateral. 



558 DISEASES OF THE TONSILS 

In the suppurating form of the disease the systemic manifestations are 
often less severe than in the follicular types just described, but the local pain 
is often very severe, and opening the mouth may be very painful. The tonsil 
is often enormously enlarged, but is rarely dotted with follicular spots. 
Instead it may be smooth and shining in appearance. The inflammation 
often extends to the uvula, which may be so swollen and elongated as to 
cause great distress, 

Treatment. — The treatment of both forms of tonsillitis is largely identical. 
To the surface of the tonsil, in the first twenty-four hours of the inflam- 
mation, there is nothing better to arrest the process and relieve pain than 
pure guaiacol applied by a cotton applicator. This often causes great pain 
for the moment, but it is remarkably efficacious. Externally, over the 
gland, a small ice-bag is a valuable application. It should be kept con- 
stantly applied for several days. Internally in the very early stages the use 
of biniodide of mercury is very useful in the dose of -g-J-g- of a grain every 
half -hour till fa grain has been taken. 

After the stage of onset is past the best internal treatment is 10 to 20 
minims of tincture of iron chloride well diluted with water every three or 
four hours and potassium bicarbonate, or citrate, in copious draughts of 
water to flush the kidneys and diminish the backache. 

Many practitioners rely largely on salol or salicin at this time, giving them 
in full doses. They are efficacious, but they increase headache, disorder 
the digestion, and may irritate the kidneys, wmich are prone to irritation in 
this disease. 

Some cases get relief from gargling with very hot water or by holding ice 
in the mouth. 

When the tonsils are chronically enlarged and repeated attacks of tonsil- 
litis occur they should be removed between attacks by the tonsillotome. The 
application of caustics like nitrate of silver often makes them larger than before. 

In the suppurating form the pus should be evacuated as soon as it is 
formed, the tonsils being punctured by a bistoury or a tenotome, the tip of 
which is exposed after being run through a small cork so as to guard it and 
prevent any movement of the patient from causing the physician to injure 
an important bloodvessel. 

In all cases of follicular tonsillitis cultures of the secretions from the throat 
should be examined for the Klebs-Loeffler bacillus, for in all cases before 
making a diagnosis of follicular tonsillitis the physician should carefully 
exclude diphtheria. (See Diphtheria.) When children are in the household 
the patient should be carefully isolated. 



CHRONIC HYPERTROPHIC TONSILLITIS. 

Definition. — Chronic hypertrophic tonsillitis is a condition of overgrowth, 
or hyperplasia of the tonsils, which affects all parts of both tonsils and 
usually involves the so-called pharyngeal tonsil. In some instances the 
lymphoid texture of the glands is chiefly affected, while in others the connec- 
tive tissue undergoes the greater part of the overgrowth. In the one instance 



CHRONIC HYPERTROPHIC TONSILLITIS 559 

the enlarged tonsils present themselves as projecting masses, soft in texture. 
In the other they are remarkably hard and cut with a resistance almost 
cartilaginous in character. In some instances there is overgrowth of the 
tonsils without the adenoid of the pharynx being involved. Nearly always 
patients with this affection suffer from associated nasal catarrh, often from 
secondary middle-ear disease, and they present a peculiar expression of 
stupidity or lack of intelligence. 

Symptoms. — Aside from organic disease of the great viscera there is no 
chronic malady which produces such extraordinary changes in the physical 
appearance, growth, and mental development as does this one. The obstruc- 
tion to free nasal breathing results in mouth breathing, and this in turn 
causes the child to hold the mouth open in a silly manner, which detracts 
from its facial appearance. So, too, the lack of free respiration results in a 
failure of physical development, so that the chest is often poorly developed, 
and even the entire body is dwarfed. Finally, this same cause produces 
restless nights and so causes loss of physical rest, which may be empha- 
sized by attacks of spasmodic croup or night screaming. Constant cough 
at night on lying down is also often a troublesome symptom and is due 
to undue dryness of the nasopharynx or to tickling of the uvula by the 
edges of the projecting tonsils. 

After the disease has lasted for years the child is often stupid, morose, 
and apathetic to a degree, and the open mouth, stunted nose, and heavy eyes 
make a diagnosis of the tonsillar state easy. When the child is stripped 
the chest is often found to be barrel-shaped or the patient is pigeon-breasted, 
or it presents the Trichterbrust of the Germans, or the so-called funnel chest 
of English writers, in which there is a deep depression of the lower part of 
the breast -bone. These thoracic changes are due to two chief causes: first, 
the general impairment of nutrition produces malnutrition of the thoracic 
walls as in rickets, and, second, in the effort at sufficient respiration the 
chest walls undergo faulty development. The breath is often quite fetid, 
due to retained secretions and particles of food in the crypts of the tonsils, 
and if the tonsils be pressed upon a surprisingly large amount of material 
can be expelled from their cavities. 

The nasopharyngeal spaces of such children are first-rate culture fields for 
the growth of bacteria of all sorts and for acute infections, such as diphtheria 
and scarlet fever. 

Treatment. — If we except the effects produced by the use of thyroid gland 
in cretinism it is not possible to find any state in which the physician can 
cause such a complete metamorphosis in his patient as to health of mind 
and body as in this malady. The removal of the enlarged tonsils by tonsil- 
lotomy and the scraping away or curetting of the pharyngeal adenoid 
results in free and easy breathing and in an extraordinary change in growth 
and spirits. Children who have been stunted in mind and body for years 
gain, it may be, thirty pounds in a few months, become rosy and bright- 
looking, and are able for the first time to keep up with their fellows in 
school and in sport. 

The use of cod-liver oil and syrup of the iodide of iron after the operation 
is a great aid to speedy recovery. 



560 DISEASES OF THE (ESOPHAGUS 

Physicians and parents should regard it as a duty to see that children are 
relieved from this trouble, which threatens health and mental power, and 
which exposes the patient as a fair mark to infectious disease. Chronic middle- 
ear disease and deafness often ensue if these growths are not removed. 

While it is true that operation often gives permanent relief, it sometimes 
has to be repeated, as the tissues redevelop after removal of the primary 
hypertrophy. 

As an anaesthetic ether is far safer than chloroform during the performance 
of the operation of tonsillotomy or curetting the pharyngeal tonsil. 



DISEASES OF THE (ESOPHAGUS. 

OESOPHAGITIS. 

An acute inflammation of the oesophagus often ensues after the ingestion 
of irritant poisons, such as concentrated lye, ammonia- water, carbolic acid, 
and similar substances. Under these conditions it is but a part of the 
general inflammation of the gastrointestinal tract which all irritant poisons 
induce, and has little interest except from a toxicological standpoint and 
the strictures that commonly follow. When oesophagitis is due to disease 
it may arise from an extension of a diphtheria from the pharynx or from 
an extension of the inflammation in the pharynx in cases of scarlet fever. 
So, too, in certain cases of typhoid fever the oesophagus may undergo inflam- 
matory changes, and these may progress to such an extent that ulceration 
ensues. (See Typhoid Fever.) Sometimes, too, the oesophagus is involved 
in cases of aphthous stomatitis and in thrush. 

A membranous oesophagitis occurs, but it is rare. It may follow the swal- 
lowing of escharotics and is occasionally seen after prolonged alcoholic 
excesses. A cast of the entire oesophagus may be expelled. 

The mucous membrane in ordinary inflammations of the oesophagus is 
reddened and hypersemic. There may be some pain beneath the breast- 
bone, which is increased by the swallowing of food or drink, but in the milder 
types no symptoms are present, and unless ulceration is followed by cica- 
trization, neither the physician nor the patient may be aware of the fact that 
the oesophagus has suffered from an inflammatory process. 

Should symptoms of pain and discomfort exist, they may be relieved by 
the use of demulcent drinks, of which perhaps the best is emulsion of 
sweet almonds, or milk with arrowroot. Sometimes swallowing small 
pieces of ice gives relief. 

In cases of heart disease and cirrhosis of the liver a form of chronic 
oesophagitis sometimes develops, in which the mucous membrane suffers 
from a chronic catarrh and the smaller bloodvessels become varicose and 
rupture, causing the vomiting of blood. 



DILATATION OF THE (ESOPHAGUS 561 



ORGANIC STRICTURE OF THE OESOPHAGUS. 

As has already been intimated, stricture of the oesophagus usually follows 
the healing of an ulcer which is produced by the ingestion of some corrosive 
substance, or by ulceration developing in the course of typhoid fever or 
syphilis. Stricture may be cylindrical or annular, symmetrical or asym- 
metrical, single or multiple. The usual sites are behind the cricoid cartilage, 
opposite the bifurcation of the trachea, and at the hiatus cesophagei. 
Occasionally inflammation of a lymphatic gland, the pressure of a tumor in 
the mediastinum, or of an aneurysm, causes a narrowing of the gullet, and, 
more rarely still, a polypoid tumor may grow from the mucous membrane. 
Malignant stricture will be discussed later. 

Symptoms. — The symptoms consist in difficulty in swallowing food, the 
patient stating that it lodges part way down to the stomach, and that if 
any considerable quantities are taken regurgitation takes place, the regurgi- 
tated materials containing no trace of gastric juice or the products of 
digestion. If an oesophageal bougie is passed it is found to be arrested at 
the level of the stricture, and it may be impossible to push it past this point. 

Treatment. — The treatment consists in the use of a small bougie to dilate 
the stricture, followed by the employment of larger, graduated bougies. If 
the stricture is so tight that food cannot pass and the life of the patient is 
endangered by inanition, and if the use of a bougie fails to overcome the 
obstruction, surgical interference will be necessary. Sometimes stricture 
of the oesophagus is a congenital condition, in which case the child rarely 
lives, and little can be done for its relief. 



DILATATION OF THE (ESOPHAGUS. 

Etiology. — Dilatation of the oesophagus occurs in two forms, namely, 
the diffuse and the localized. In the diffuse form the entire tube is dilated, 
and there may be some overgrowth of the muscular fibres, which has occurred 
in an endeavor on the part of the oesophagus to force food past an obstruction 
which exists near the cardiac orifice of the stomach. 

When a localized dilatation occurs it takes the form of a diverticulum, 
which may be divided into two types, namely, "pressure diverticula" and 
"traction diverticula." The pressure diverticula are very rare and are 
found usually at the junction of the pharynx and the oesophagus, where 
the muscular fibres are weakest. Their origin is supposed to depend upon 
pressure upon this point of the gullet in deglutition, and they are thought 
to develop in those who are in the habit of bolting their food. The diver- 
ticulum arising from this cause is lined with mucous membrane, its sub- 
mucous tissues are thickened, and the muscular coat is atrophied so that 
the mucous coat bulges through it as a hernia-like projection. The lesion 
always occurs in the posterior or posterolateral wall of the oesophagus. 

Traction diverticula occur more frequently than the type just mentioned, 
but are very seldom recognized during life. They are thought to be due 
36 



562 DISEASES OF THE (ESOPHAGUS 

to contraction of tissues which have become attached to the oesophagus by 
inflammatory adhesions, as in cases in which inflammation of the bronchial 
lymph glands has taken place. This lesion is usually found in the anterior 
wall of the gullet, and a number of diverticula may be present in a single 
case. 

Atonic dilatation of the oesophagus is occasionally observed; the dilated 
tube may be fusiform or flask-shaped, the part of the organ corresponding 
to the neck of the flask being upward. Such dilatation occurs indepen- 
dently of organic disease below, and has been attributed to spasm of the 
cardia. The dilated oesophagus may be extremely capacious, holding a 
pint or more of fluid. 

Symptoms. — The symptoms of diffuse dilatation of the oesophagus due to 
stenosis are those produced by stricture of the gullet, and consist chiefly in 
difficulty in swallowing. It is a condition rarely recognized during life. The 
small diverticula due to traction by adhesions are also rarely recognized, 
unless one of them becomes so large that it forms a pocket in which food 
accumulates, until by reason of its decomposition or fermentation it pro- 
duces so much irritation and inflammation that the stomach, oesophagus, and 
all the muscles of the chest and abdomen endeavor to expel it by a process 
akin to that of vomiting. Sometimes a diverticulum of this character is 
capable of holding a very considerable quantity of fluid. 

Diagnosis. — The diagnosis of a diverticulum is reached by the use of a 
stomach tube, which is passed as far as it will go and then used as it would 
be in lavage, or as a stomach pump would be employed. Under these 
circumstances milk or other liquids which have been swallowed are brought 
up when the tube has not been passed far enough to make it possible that 
the liquids are obtained from the stomach. Such large diverticula are 
usually of the traction type. A diverticulum or dilatation may be discovered 
by filling the cavity with a mixture of bismuth and syrup of acacia and using 
the a>rays. 

Treatment. — The treatment consists in the use of a stomach tube for the 
purpose of feeding the patient, provided the physician or the patient is suc- 
cessful in passing the tube past the diverticulum. In those cases in which 
the diverticulum is so large that it prevents the ingestion of food, by pressure 
on the oesophagus, and so interferes with the patient's nutrition, the only 
resort is a surgical operation and rectal alimentation. 



SPASM OF THE (ESOPHAGUS. 

This affection, sometimes called " oesophagismus," is rarely met with 
except in persons suffering from hysteria or insanity. It is sometimes 
seen in hydrophobia, and it is this difficulty in swallowing water, rather 
than an actual dread of water, which has given that disease its name; for 
with the thought of swallowing, at the sight of water, the spasm develops. 
The difficulty in swallowing usually points to the presence of spasm or 
stricture, and if there is no history of the ingestion of an irritant some time 
before, or other causes which would be likely to produce ulceration and 



CANCER OF THE (ESOPHAGUS 563 

stricture, the strong possibility of spasm is to be considered. Usually in 
spasm it is much easier to pass an oesophageal bougie than it is in cases of 
stricture. But occasionally the spasm is sufficiently tight to oppose the 
passage of the bougie, and to give to the hand guiding the bougie the sensation 
which is produced by the end of the instrument coming in contact with a 
true organic obstruction. 

Treatment. — The treatment consists in the passage of a bougie once or 
twice a day; in the administration of nervous sedatives if the patient is in a 
condition of nervous excitation; of stimulants, if she is in a condition of 
profound depression, and of measures devoted to the improvement of the 
general health, both mental and physical, if it is impaired. As the spasm 
may be due to a fissure, ulcer, or other tender spot the food should not be 
bulky, but preferably liquid and never taken in large amounts. 



CANCER OF THE (ESOPHAGUS. 

Cancer of the oesophagus usually occurs in the form of squamous epithe- 
lioma, and affects men more frequently than women. Occasionally a medul- 
lary cancer is found in this region. The growth soon undergoes ulcera- 
tion, and not infrequently the entire circumference of the tube may be 
involved, and in this manner a stenosis may be developed with dilatation 
of the oesophagus above the point of growth. The disease is quite rare, for 
of 7290 cases of cancer collected by Williams but 6 per cent, were primary 
in the oesophagus. Tanchon in 9118 cases of cancer found only 13 in the 
oesophagus. Cases have been recorded as early in life as nineteen years, 
but most patients are past forty. The disease is about equally divided as 
to its occurrence in different levels of the tube. Thus, if the statistics of 
Kraus, von Hacker, and Newmann are added together, making 1477 cases, 
we find that '582 were near the cardia, 453 near the middle third, and 440 at 
the upper third. 

Symptoms. — The symptoms, as in cases of ordinary stenosis due to stric- 
ture, consist in difficult deglutition and not infrequently considerable pain, 
both at the time of swallowing and when the oesophagus is at rest. The 
food is often regurgitated almost as soon as it leaves the pharynx, and some- 
times the effort at regurgitation is followed by the appearance of some blood 
and mucus. Blood and mucus also very frequently appear if a bougie is 
used to pass the stricture. The age of the patient, the absence of a history 
of the ingestion of a corrosive poison, the emaciation and weakness, and 
the presence of primary or secondary growths elsewhere render the diagnosis 
possible. Sometimes an aneurysm of the thoracic aorta by pressing on the 
oesophagus may produce somewhat similar symptoms, but under these 
circumstances the physical signs of aneurysm may be found. 

Prognosis. — The prognosis in oesophageal cancer is, of course, exceed- 
ingly bad. Death comes from exhaustion and starvation, from pneumonia 
due to the inhalation of septic materials, or to ulceration of a large blood- 
vessel. Sometimes the lymphatic glands of the neck are secondarily involved. 
Occasionally the physician is chagrined at the autopsy to find that an unsus- 



564 DISEASES OF THE STOMACH 

pected oesophageal cancer has been present for weeks without presenting 
symptoms, and without his having recognized its existence. 

Treatment. — Medicinal measures are of course fruitless except for the 
relief of pain. Surgical measures are of little value, since the patient is 
usually so exhausted by the time that the diagnosis is confirmed and he is 
willing to resort to an operation, that life is prolonged but little by the opera- 
tive interference. Exner has recently reported a case in which improvement 
followed the use of radium in a tube attached to a bougie. 



DISEASES OF THE STOMACH. 

ACUTE GASTRIC CATARRH. 

Definition. — Acute gastric catarrh, or acute catarrhal gastritis, as its name 
indicates, is a state in which the mucous membrane of the stomach becomes 
hyper semic and then swollen, with lessened secretion, followed by excessive 
production of mucus and reduction in the quantity of digestive ferments. 
The term acute gastritis is sometimes employed to describe this state. This 
is unfortunate because a true inflammation of all the coats of the stomach 
is not present except when irritating foods have been taken in excess, or 
when some irritant poison has been swallowed. 

Etiology. — The causes of acute gastric catarrh are very various. In chil- 
dren it is often a sequel to taking cold, with some resulting interference 
with the activity of the liver. It also follows the excessive use of sweets in 
this class of patients. In older persons it is nearly always due to the takingof 
an excessive amount of indigestible food or overloading the viscus with 
ordinary foodstuffs, particularly if alcoholic drinks and highly seasoned 
articles have been swallowed. 

j Symptoms. — The symptoms of acute gastric catarrh in children are quite 
different from those met with in adults in most instances. The child has 
nausea and vomiting, and some epigastric discomfort. Fever, varying from 
100° to 102°, often develops and persists for several days. The bowels 
may be constipated or several loose movements may occur daily. The 
appearance of the tongue in this class of cases is very characteristic. It is 
evenly coated by a thin white fur which is dotted by many tiny red spots 
where the enlarged papilla? exist. The tongue is also somewhat drier than 
normal and the breath slightly foul and hot. The urine is usually decreased 
in amount and high colored. 

In adults acute gastric catarrh presents somewhat different symptoms. 
There is often some pain or tenderness on pressure in the epigastrium and 
a loss of appetite amounting to disgust for food. Nausea may be quite per- 
sistent and vomiting may occur. 

In both children and adults the attacks may last for from one to four days. 



ACUTE TOXIC GASTRITIS 565 

Diagnosis. — When the physician is called to see a child who is suffering 
from moderate fever, a somewhat coated tongue and epigastric distress, 
he must not be hasty in stating that the case is one of acute gastric 
catarrh, because many of the acute infectious diseases begin by moderate 
gastric disorder and a coating of the tongue. Whenever the gastric symp- 
toms persist for more than four or five days, enteric fever should be sus- 
pected as being the cause of the illness, but care must be taken that the 
common error of calling mild typhoid fever "gastric fever" is not made. 
Uncomplicated acute gastric catarrh is so rare in adults, who have not 
abused alcohol, that great care should be taken before the physician is 
satisfied with this diagnosis. 

Treatment. — The treatment consists in unloading the portal and hepatic 
circulation, which is nearly always disordered, by the use of small doses of 
calomel, giving J of a grain every half-hour for eight doses, and following 
this in five hours by a Seidlitz powder or some other mild and cooling saline 
purge. If the stomach is very irritable the Seidlitz powders should be 
divided into fourths and taken at fifteen -minute intervals. After this treat- 
ment has acted the patient should receive small doses of bismuth subnitrate 
and oxalate of cerium. For a child 2 grains of the former and 1 of the latter 
may be given every hour for five or six doses. Adults may take 5 grains of 
the bismuth at a dose. 

The rest of the treatment consists in the use of small quantities of liquid 
food, such as whey or barley-water, or scalded toast. Small quantities of 
milk and lime-water may be used. In some instances total abstinence from 
food for twelve or twenty-four hours gives the best results. Rest in bed is 
also very advantageous for both children and adults. 



ACUTE TOXIC GASTRITIS. 

Etiology. — Acute toxic gastritis is produced, as its name implies, by the 
entrance into the stomach of any poison which is capable of acting as a 
severe irritant or as a corrosive. Some of these irritants act with only suffi- 
cient severity to produce hyperemia and moderate superficial inflamma- 
tion, but others corrode the stomach, and may even perforate it. Most 
of the metallic poisons, such as mercuric chloride and mercuric iodide; 
oxalic acid, carbolic acid, and the ordinary mineral acids, such as sulphuric, 
hydrochloric, and nitric acids, belong to the class of severe corroding irri- 
tants. Other substances, such as phosphorus and chlorate of potassium, 
not only act as irritants, but produce fatty degeneration. Arsenic differs 
in its action on the stomach from that of the mineral acids in that it does 
not coagulate albumin and is not corrosive. It causes, however, a peculiar 
exfoliation of the mucous membrane lining the stomach and bowels, partly 
by its local effect induced by direct contact, and partly by the elimination 
of the arsenic by the gastric walls, whereby the mucous membrane is shed. 
Among the vegetable substances which may cause gastritis may be men- 
tioned croton oil, elaterium, and castor-oil beans. 



566 DISEASES OF THE STOMACH 

Morbid Anatomy. — As the result of the violent inflammation of the stomach 
produced by these drugs death may ensue, or, if the patient survives the 
acute stage, extensive exfoliation of the superficial part of the mucosa 
occurs, or ulcers may form which ultimately cause death. Free and 
interstitial hemorrhages occur. In other instances there is so much destruc- 
tion of the peptic tubules that the . gastric mucosa is largely destroyed and 
cicatricial contractions ensue. 

Symptoms. — The symptoms of toxic gastritis are violent burning fain in 
the stomach, thirst, and vomiting. The vomited matters may be stained 
with blood, and usually contain an excess of mucus and often flakes of 
the mucosa itself. Sometimes diarrhoea develops. The pulse is rapid, the 
patient's expression is anxious, and death may occur within a few hours 
in collapse. 

Diagnosis. — While it is not possible to make a positive diagnosis as to the 
character of the poison which has been taken by the appearance of the 
stomach at autopsy, certain poisons nevertheless produce definite lesions 
which may be considered almost peculiar in themselves. When sulphuric 
acid is taken, the parts are blackened; nitric acid makes them yellow. Most 
of the alkalies stain them brown and the silver salts cause intense redness 
followed by a brown and black hue on exposure to light. It is also stated 
that oxalic acid causes a peculiar gelatinous appearance of the gastric 
mucous membrane and that ammonia may cause a suppurative condition. 

Treatment. — The treatment, of course, depends upon the character of the 
poison. In all instances, except when phosphorus is taken, olive oil may be 
given to protect the stomach; morphine should be used hypodermically 
to relieve pain and irritation, and external heat should be applied to combat 
shock. When one of the acids has been taken, any alkali such as lime- 
water, plaster from the walls suspended in water, very dilute ammonia, or 
even soap and water may be used to antidote the acid except in the case of 
oxalic acid, when only lime or chalk should be used; for while calcium 
oxalate is insoluble, the oxalates of potassium and sodium are not insoluble, 
and are practically as poisonous as the oxalic acid itself. When lead in one 
of its soluble forms, or carbolic acid is taken as a poison the antidote is any 
soluble sulphate, of which magnesium sulphate and sodium sulphate are 
the best. 

The after-treatment of acute toxic gastritis consists in the use of large 
doses of bismuth subnitrate, and in the employment of rectal feeding, so 
that the stomach may be put at rest for as many days as possible. 



PHLEGMONOUS GASTRITIS. 

Definition. — The term "phlegmonous gastritis" is applied to a condition 
in which the inflammation is of such a character that it proceeds to suppura- 
tion, the chief part of the suppurative process developing in the submucous 
tissues, and sometimes extending to the muscular coat of the stomach and 
even to the peritoneum. 



PHLEGMONOUS GASTRITIS 567 

Etiology. — The disease is exceedingly rare, and has appeared with about 
equal frequency at all ages from ten to eighty years. In some instances 
it is primary, the seat of the infection beginning in an ulcer or growth, or 
more rarely from some direct traumatism. The secondary cases are those 
in which the process develops during the course of one of the acute 
infections, such as typhoid fever, puerperal fever, pyaemia, and variola. 
Fifty cases have been gathered by Jacoby and 85 by Leith, but these figures 
of course include many of the same instances of the disease. Phlegmonous 
gastritis is of two kinds: a diffuse form with a rapid course, profound sys- 
temic disturbances, and speedy death, and a circumscribed form in which 
the symptoms are much less severe; the patient living, it may be, for weeks, 
but usually dying as the result of the disease. 

The pyloric portion of the stomach is chiefly affected. Its walls are 
greatly thickened, and the submucous tissues are riddled with pus, having 
undergone almost complete necrosis. Not infrequently many perforations of 
the mucous membrane occur, so that the internal surface of the stomach has 
a sieve-like appearance. 

Several cases of suppurative gastritis have been reported in the United 
States, and they are remarkable enough to demand notice. In Kinnicutt's 
case the disease followed an alcoholic debauch. In Hemmeter's case the 
patient had vomited blood, was treated for gastric ulcer, and did not 
die until two months after the onset of severe symptoms. The infection had 
here occurred through a healed ulcer. In Smith's case violent epigastric 
pain with collapse and death in two and a half days took place, the entire 
submucosa being infiltrated with pus. In Loomis' case abdominal pain, 
bilious vomiting, and a feeble pulse with delirium preceded death, which 
occurred at the end of four days. In Hun's case the gastric walls were 
fully one-half inch in thickness and the tissues between the peritoneum 
and the mucous membrane were purulent. 

In the circumscribed form of phlegmonous gastritis the abscess may be 
single, or multiple abscesses may be present. 

Symptoms. — The symptoms in the diffuse form consist in the sudden 
development of violent epigastric pain, followed by faintness and collapse, 
with incessant vomiting. After the vomiting has continued for some time, 
the vomited matter may be stained with bile. 

When the disease is secondary to malignant growth, it is stated that vomit- 
ing does not often develop. Notwithstanding the severity of the process, 
pus is never found in the vomit in the acute cases. The temperature 
varies from 103° to 105°. The pulse is rapid and feeble, and becomes 
more and more so until death occurs in collapse, preceded by a stage of 
apathy. 

Diagnosis. — There is practically no array of diagnostic symptoms in cases 
of this disease save the onset of violent epigastric pain. 

The pus may escape into the general peritoneal cavity, the patient 
dying with symptoms of perforation and collapse. The most extraordinary 
case of this character so far recorded is the one reported by Callow, in 
which the patient vomited a pint of pus, pus appeared in the stools, and 
there were seven pints of it in the peritoneal cavity. All this pus was 



568 DISEASES OF THE STOMACH 

traced to a large abscess cavity in the wall of the stomach which had, how- 
ever, not been accompanied by pain during its formation. 

Treatment. — When it is possible to make a diagnosis prompt operative 
interference is strongly indicated. So far, this has not been attempted 
early enough in any case to give satisfactory results. The parts should be 
drained and a gastroenterostomy performed. (For an excellent paper on 
this subject see Moynihan in the Medical Chronicle for November, 1903.) 



DIPHTHERITIC GASTRITIS. 

Inflammation of the stomach with the formation of a false membrane due 
to the Klebs-Loeffler bacillus is very rarely encountered. It nearly always 
follows diphtheria in the upper air-passages. Still more rarely in cases of 
septicemia, scarlet fever, and smallpox a false membrane may develop in 
the stomach. The condition is of interest solely from a pathological stand- 
point. 

MYCOTIC GASTRITIS. 

Inflammation of the stomach due to the growth of specific micro-organ- 
isms upon its mucous membrane is very rare. The thrush fungus, Oidium 
albicans, has been found in certain cases. Anthrax of the stomach has also 
followed anthrax of the mouth. The yeast fungus is not infrequently 
present, but rarely produces severe inflammation of the stomach. Cases 
which are in the nature of medical curiosities have been reported in which 
acute inflammation of the stomach was due to the action of maggots deposited 
about the mouth by the common fly, or swallowed with various articles of 
food. In all such instances the condition of the stomach has been profoundly 
depressed, as otherwise the ability of this organ to destroy invading micro- 
organisms and parasites prevents it from becoming infected. 



CHRONIC GASTRITIS. 

Definition. — By chronic gastritis is meant a state in which the gastric 
mucous membrane suffers from prolonged and persistent inflammation of a 
low grade, or repeated acute or subacute attacks, which result in more or less 
well-marked pathological changes. The term "chronic gastric catarrh" is 
often used as a synonym to describe this condition. 

Etiology. — The causes of chronic gastritis are very numerous. In the 
majority of cases they consist in the frequent entrance into the stomach of 
irritating foods or drinks, as in alcoholics, or in persons given to the exces- 
sive use of highly seasoned foods. In these cases a very large part of the 
disorder in the gastric mucosa is also dependent upon the engorged portal 
circulation and the hepatic torpor which such dietary indiscretions induce. 
Cardiac diseases which lead to hepatic congestion very frequently induce 
gastric catarrh. Alcohol, bad food, or badly chewed food, hepatic cirrhosis, 



CHRONIC GASTRITIS 569 

and congestion of the liver are, therefore, the chief causes of this con- 
dition. 

Pathology and Morbid Anatomy. — The changes in the stomach in chronic 
gastritis may be divided into two classes: In the first there is a proliferation 
of the connective-tissue cells and formation of new tissue, which, like similar 
forms of overgrowth elsewhere, results in atrophy or degenerative changes 
in the gastric glands. In other words, the lesions are not limited to the 
superficial portion of the mucous membrane, but extend well down into 
the deeper layers. As the contraction of the overgrown connective tissue 
proceeds, it may cause the projection on the surface of the inner wall of the 
stomach of wart-like masses, so that broad, raised patches of mucous mem- 
brane are discernible, or even polypoid formations appear (gastritis poly- 
posa). The entire gastric mucosa may be contracted or plicated. 

In other cases the lesions appear to be more of a degenerative type; the 
sclerosis or fibrosis is inconspicuous, and the epithelial, or granular, atrophy 
is most marked. In other cases cystic alteration, with little fibrous hyper- 
plasia, may be the dominant alteration. In the pyloric end of the 
stomach the contraction which follows the overgrowth of connective tissue 
may produce stenosis, a condition which is emphasized in some cases by the 
inflammatory process extending to the muscular layer of the stomach, by which 
means still greater thickening takes place. The closure of the pyloric orifice 
is, therefore, due to a true hyperplasia. The cause of the nipple-like projec- 
tions found in the gastric mucous membrane in some of these cases is un- 
known. It may be due to the constricting influence of connective tissue 
formed between the tubules, or it may arise from overgrowth of the submucous 
coat of the stomach. 

The second type of chronic gastritis is that characterized, not by over- 
growth of connective tissue, as has just been described, but by wasting or 
atrophy of the glands. In some cases, however, there is at first some hyper- 
plasia of connective tissue, and this is followed by atrophic changes. The 
mucous membrane becomes thin and smooth and is often pigmented, while 
the epithelial cells lining the gastric tubules suffer from atrophic, fatty or 
necrotic changes. The deeper tissues in some cases escape, but in others 
they also undergo wasting, so that even the submucous coat and the mus- 
cular coat atrophy. To this condition has been given the unfortunate, but 
etymologically correct, name of phthisis ventriculi. In such a case it is quite 
possible for gastric dilatation to develop. 

Atrophic gastritis is much more rare than the hyperplastic type, and is 
often, if not always, associated with another grave condition, pernicious 
anaemia. Finally, in very rare instances, cases of atrophic gastritis may 
develop into ulceration of the gastric mucosa, the ulcers being small, round 
or irregular in shape, and rarely penetrating very deeply (erosive gastritis). 
They are found chiefly near the pylorus and may bleed very freely. 

Symptoms. — The symptoms of chronic gastritis consist in loss of appetite, 
impairment of the sense of taste, and nausea, which is particularly prone to 
be present in the morning and may often amount to actual vomiting — the 
"morning vomiting of the drunkard." The vomited matters are but partly 
digested and are often mixed with much mucus. Most cases frequently belch 



570 DISEASES OF THE STOMACH 

up gas, and with it a mouthful of acid fluid may be brought up which scalds 
the pharynx. Hydrochloric acid may be lacking in the gastric contents, but 
in its place an excess of butyric and acetic acids is often present, particularly 
if the stomach is feeble and is unable to expel its contents into the bowel with 
sufficient promptness. Lactic acid is also present in some cases. It is the 
presence of these acids that causes heartburn, or pyrosis. In some cases, 
however, an excess, or at least a normal amount, of hydrochloric acid is 
secreted. 

The tongue is moderately coated, the bowels are prone to constipation, 
and the general nutrition is slightly impaired, partly because of poor diges- 
tion, but chiefly because of the fact that the patient has cut off from his 
diet list one article after another, with the thought that it " disagrees" with 
him. There is not, however, an impairment of nutrition sufficient to cause 
great loss of weight in many cases, because the digestive function of the 
duodenum is not always impaired. If the liver is diseased, a very consider- 
able loss of weight is usually present. Digestion is, of course, as is clear from 
a consideration of the state of the gastric mucous membrane, greatly delayed 
and very imperfect, and as a result the patient becomes inert, low-spirited, 
and vitally depressed, so that he presents the clinical picture of what is 
commonly called by the laity "a confirmed dyspeptic." 

If the cause of the gastric disorder is alcoholic cirrhosis of the liver, the 
symptoms of cirrhosis are associated with those of gastric catarrh. 

A constant, unproductive cough is often present without any lesions being 
found in the lungs 

When the atrophic form of chronic gastritis is present, a very profound 
degree of anaemia is often developed, as already stated. 

Diagnosis. — The separation of chronic gastritis from gastric cancer is by 
no means easy in many instances, for in many cases of cancer gastritis is 
also present. The presence of a mass, of considerable pain, of coffee-ground 
vomit, and an absence of HC1 in the gastric fluids would point to the diag- 
nosis of cancer; but as pain is not always present in cancer, as ulcers of the 
stomach may be present in chronic catarrh, giving rise to bloody vomit, 
and as HC1 is often diminished or absent in this state, these signs are not 
entirely reliable. Lactic acid is not commonly present in large amount in 
chronic gastritis, but it is usually present in excess in cancer. 

Prognosis. — The prognosis in a case of chronic gastritis must be given 
guardedly, for while one patient may speedily recover under proper treatment, 
other patients remain ill for long periods, even with the most skilful treat- 
ment. Much depends, too, upon the course of the disease and upon the 
general health of the patient. While, on the one hand, the malady does 
not cause death, on the other, complete recovery may seem impossible. 

Treatment. — Theoretically, chronic gastritis may be prevented by avoiding 
the use of irritating and indigestible foods and alcoholic drinks, but, practi- 
cally, patients are not seen until after the condition has been developed by 
the various causes which have been enumerated. After the condition has 
developed the treatment must be devoted to the removal of the habits which 
act as causes, to the relief of the conditions which exist in other portions of 
the body, and to the cure of the symptoms already present in the stomach. 



CHRONIC GASTRITIS 571 

In cases in which errors in diet exist these must be rectified, and if alcohol 
is used it must be stopped. If an examination of the heart shows that it is 
feeble, and that the gastric condition is due to an impaired circulation, rest 
and the use of moderate doses of digitalis must be resorted to, but it must 
not be forgotten that digitalis in full doses is capable of causing gastric 
distress. Usually it is necessary, in order to get the best results, to administer, 
every few days, small doses of blue mass, which not only unloads the liver, 
but seems to increase the efficiency of the digitalis. 

The local treatment of the stomach consists in the employment of lavage, 
by means of which the excessive quantities of mucus and undigested food 
are removed. Emetics should not be employed, as they are too violent and 
apt to increase the inflammatory process. Not infrequently the mucus which 
is secreted is so thick and tenacious that there is some difficulty in removing 
it from the stomach. Under these circumstances, various medicinal sub- 
stances may be added to the water which is employed for the lavage. A salt 
solution may be used, composed of \ ounce of sodium chloride and 1 ounce 
of sodium bicarbonate, placed in a quart of warm water. After the stomach 
has been thoroughly cleansed, it may be washed a second time with boric 
acid, 1:100; salicylic acid, 1:1000; chloroform-water, 1:200; hydrochloric 
acid, 1 : 200. AYhen chloroform-water is used, great care should be taken that 
the chloroform is thoroughly mixed with water and that the mixture is then 
allowed to stand for a sufficient time to permit of the separation of any excess 
of chloroform. 

Lavage should be carried out, as a rule, not oftener than twice in 
twenty-four hours; in many cases once every alternate day is often enough. 
The best time to perform lavage is usually in the evening at about 9 o'clock, 
so that the stomach may have complete rest for the next ten hours. In those 
cases, however, in which the taking of food in the morning produces 
great distress, it is often advantageous to use lavage on first arising, in order 
that mucus may be removed. 

In regard to drags, it may be said that the one which has the greatest 
reputation is the nitrate of silver given in pills containing \ grain, or in solution 
in the dose of from \ to 1 grain to 2 drachms of one of the aromatic waters, 
as cinnamon-water or peppermint-water. Another drug which has a high 
reputation is the subnitrate of bismuth, which should be given in large doses, 
about 1 drachm twice or thrice a day. Both of these forms of treatment 
possess the disadvantage that they are constipating, and therefore the patient 
usually has to take a small dose of one of the mild laxative saline waters on 
first arising in the morning. 

For the relief of loss of appetite and for absence of hydrochloric acid, the 
various simple bitters, such as cinchona, quassia, and cardamom, may be 
given. Of the compound tincture of cardamom, 1 or 2 drachms may be 
given once or twice a day with meals. If, in addition, it is believed that the 
stomach lacks motive power, strychnine may also be used, and the fluid 
extract of condurango may be given in the dose of a drachm three times a 
day. If digestion is delayed because of a lack of hydrochloric acid, 5 drops 
of this dilute acid may be given with each meal, combined with a good 
essence of pepsin. The administration of nitrate of silver one hour before 



572 DISEASES OF THE STOMACH 

meals usually diminishes pyrosis, or heartburn, but, if it does not, magnesium 
carbonate or bicarbonate of sodium may be used for this purpose. These 
alkalies frequently diminish pain by decreasing acidity. 

The diet should consist of easily digested foods, and it is to be remembered 
that small meals given five or six times a day are better than large meals 
given three times a day. Chicken, beef, and mutton broths, free from fat 
and fortified by the addition of barley or rice, are exceedingly useful. If 
solids are taken, the patient must be instructed to chew both the meats and 
starches thoroughly. Often it is advisable to have the meat made tender by 
pounding it, or by cooking it in such a way that its fibres are readily dis- 
solved by the gastric juice. 

The digestion of starches, like baked potatoes, toasted bread, Zweiback, 
and pulled bread, should be aided by the use of taka-diastase or pancreatin. 
Often a capsule containing both of these digestive ferments will be advan- 
tageous in its effect. 

Milk may be given to those with whom it agrees. In some instances, 
when it cannot be taken pure, it can be digested readily if diluted with some 
sparkling water, particularly Vichy water. In other instances the addition 
of a small quantity of salt aids in its digestion, and in still others lime-water 
may be given with it. 

The question as to the use of the light wines by a patient suffering from 
chronic gastritis is debatable. If any fermentation is present, they must 
not be used. If patients are accustomed to drinking wine with each meal, 
it may be advisable to permit small quantities, particularly with luncheon 
and dinner. Champagnes are usually distinctly harmful. 



GASTRIC DILATATION. 

Definition. — By dilatation of the stomach is meant a condition in which 
this viscus loses its propulsive power to a greater or less degree and also 
undergoes a certain amount of dilatation, so that its capacity is increased. 
It is sometimes called " gastric ectasy," or " gastrectasis." 

Etiology. — While it is true that dilatation is the state which impresses 
itself most forcibly upon the clinician when a patient is examined who is 
suffering from this malady, it is also a fact that the dilatation is always the 
result of some primary difficulty in expelling the contents of the stomach 
into the duodenum. In some instances this is due to stenosis of the pylorus 
produced by a thickening, as in chronic gastric catarrh; in others it may be 
due to what is called hypertrophic stenosis of the pylorus, and in still others 
the obstruction may be offered by a tumor at this point or by a cicatrix or 
other form of stricture. Rarely the pylorus becomes so glued to nearby 
tissues that it is held abnormally high, and is so fixed that it is almost 
impossible for the stomach to force its contents past the orifice. 

A second cause of difficulty in emptying the stomach exists in a weakness, 
congenital or acquired, which so impairs the motor power of the viscus that 
it is too feeble to empty itself. Neither obstruction nor inherent weakness 



GASTRIC DILATATION 573 

of the muscle fibres in the gastric wall are necessarily associated with dila- 
tation, but it can be readily understood that these causes may so result. 
It is conceivable that in the obstructive cases the stomach may undergo 
some hypertrophy, and this takes place in a considerable number of cases 
as a primary result of the obstruction. The constant endeavor of the 
stomach to empty itself, however, ultimately causes fibroid changes in the 
muscle fibres from fatigue, and this condition is emphasized by impaired 
nutrition of the stomach, and perhaps by impaired nerve supply as well. 
Finally, it is undoubtedly true that, in some persons at least, the repeated 
distention of the stomach by large amounts of food and drink may cause 
permanent dilatation, particularly if these materials be of such a character 
that they produce chronic gastritis, and so impair the tone of the gastric 
walls. Workmen in breweries who partake of large amounts of beer, and 
diabetics who eat and drink to excess because of their disease, often suffer 
from gastr ectasia. 

Dilatation of the stomach is usually a disease of middle age or of adult 
life, but cases are not uncommon in children. The youngest case I ever saw 
was in a child of eighteen months. The dilatation due to obstruction is the 
type in which the greatest enlargement of the stomach develops. 

Pathology and Morbid Anatomy. — The size of the stomach may be greatly 
increased, so that the average capacity of a quart (1000 c.c.) increased to 
even four quarts. Under these circumstances, the lower border of the 
stomach extends far below the normal level. Its walls are decreased in 
thickness, there is atrophy of the lining mucous membrane, and the mus- 
cular fibres are even more wasted, so that many of them disappear and 
are replaced by connective tissue. When primary atrophy of the muscularis 
has been present, it not rarely happens that an excess of muscle fibres are 
found in the pyloric region, although advanced secondary wasting has oc- 
curred elsewhere. In some cases of dilatation the gastric walls do not become 
thin, but may appear thicker than normal, because of an overgrowth of 
connective tissue which supplants the muscular layer of the organ. 

Gastric dilatation does not always result in an equally well-developed 
increase in size. In some instances the cardiac orifice and the pylorus are 
near one another, so that the great curvature hangs like a plumber's trap; in 
other cases cicatrices distort it and even cause an hour-glass form, with a 
dilatation on either side. 

Symptoms. — The symptoms of gastric dilatation are usually considered 
by the patient to be those of "chronic dyspepsia." There is usually loss of 
appetite, a sense of gastric discomfort and weight, or a feeling of dragging 
down in the abdomen and a good deal of belching of gas, which is often 
accompanied by some particles of food mixed with fluid. The sense of dis- 
tention and distress gradually increases until it is almost insupportable, and 
then the viscus finding the burden too great, unloads itself by an attack 
of vomiting, in which the patient is surprised to find articles of food ingested, 
perhaps, several days before. Both the physician and the patient are, not 
rarely, amazed at the quantity expelled, for the volume shows that it repre- 
sents the ingested fluids and solids of several days. Such an attack of vomit- 
ing, in which the quantity expelled is far in excess of the amount recently 



574 DISEASES OF THE STOMACH 

swallowed, is a very important diagnostic point. These attacks of vomiting 
usually occur at night. When the dilatation is severe, so that the stomach 
cannot completely empty itself, the relief given by vomiting is only partial, 
and perhaps no relief follows. 

The bowels are constipated, and the stools when passed are scanty, because 
so much of the food ingested is not passed on into the duodenum. The 
urine is also scanty. Not rarely it is decreased to one-third the normal 
quantity. 

Many of the symptoms are due to stasis of the food in the stomach, fermen- 
tation, and the absorption of toxic materials from bacterial growth. 

In cases in which bile appears in the urine, the cause of the dilatation 
probably does not depend upon gastric dilatation alone, but upon some 
obstruction in the duodenum, which dams back the food in the pyloric orifice 
and so forces the stomach to undergo distention. 

The physical signs of gastric dilatation are as follows: On inspection in 
some of these cases, it may be possible to outline the stomach if it is dis- 
tended with food and gas. This determination of its area and limitation is, 
however, much better accomplished by percussion after the stomach has been 
emptied by the use of the stomach tube and then has been distended by gas. 
This distention may be produced either by giving the halves of a Seidlitz 
powder separately (or by the use of 30 grains of tartaric acid in one-half glass 
of water and 2 drachms of sodium bicarbonate in another half -glass of water), 
or by introducing a stomach tube, attaching a Davidson syringe to it and 
then pumping air into the stomach until it is distended. This latter plan is 
probably the safer of the two if ulcer is supposed to be present, but if the 
patient is not accustomed to the use of the tube its presence causes so much 
retching and gastric unrest that it is usually impossible to make a satisfactory 
examination of the true area of gastric tympany. 

The tympanitic note produced by the percussion of a stomach so dis- 
tended very clearly outlines it in many cases. If there is doubt as to the 
presence of gas in the colon, which may cause tympany, the large intestine 
should be filled with fluid, by the injection of a large clyster, when the 
areas of gastric tympany and intestinal flatness on percussion can be readily 
defined. In other cases the stomach may be filled with fluid, and, if need be, 
the bowel filled with air to develop the same outlines. 

It has been held by some clinicians that the use of carbonic acid for the 
purpose of dilating the stomach for diagnostic purposes is dangerous, but 
when we consider the hundreds of instances in which it has been used in 
every part of the world without evil effect, we must conclude that it rarely 
does harm. Behrend has recently reported 3 cases, however, in which 
death followed its use, the patient in one instance suffering from a profuse 
hemorrhage, another patient bringing up froth and blood, and the third, 
which did not die for five days, suffering from great distress and prostra- 
tion. Wharton and Musser have reported a perforation of the stomach after 
drinking a glass of carbonated water. All of these cases were complicated 
by gastric ulcer. 

Auscultation of the epigastrium may reveal splashing, or succussion, in 
many cases of gastric dilatation, but this sign should never be regarded of 



GASTRIC DILATATION 575 

very great import, for not rarely the same sound is produced by fluid in the 
bowel. 

Some years ago Einhorn invented the electric light method of diagnosticat- 
ing dilatation (gastrodiaphany) . This consists in filling the stomach with 
water and then passing a small electric light into the stomach, the patient 
and physician being in a dark room. If the abdominal wall be not too thick, 
the area of light can be readily outlined and the size of the stomach deter- 
mined. The efficiency of this method of determining the size of the stomach 
can be much increased by the use of fluorescent media. The best of these is 
developed by the use of two solutions. One solution consists of bicarbonate 
of sodium, 40 grains, dissolved in 1 pint of distilled water. The second is 
composed of the same ingredients plus 2 drachms of glycerin and J of a 
grain of fluorescin to the pint. Before the test is used the patient should 
take 2 grains of quinine three times in a day. He then swallows J pint of 
solution No. 1 and \ pint of solution No. 2, when, on the introduction of 
the gastrodiaphane, the illumination of the stomach becomes very marked. 

Another means of diagnosis is the use of the ar-rays after the patient has 
received a large dose of bismuth subnitrate (2 to 4 ounces). By this means 
the area of the stomach can be determined. The bismuth must always 
be washed out after the test to prevent poisoning. 

Another aid is Turck's gastric sound, the end of which can be felt through 
the abdominal wall, if it is thin, as it is moved about in the stomach. 

The use of drugs, which are dissolved only in -the intestine, to test the 
motor power of the stomach is of some diagnostic value. Salol, for example, 
is given in the dose of 15 or 20 grains, and the urine tested after five hours 
for salicyluric acid by means of the perchloride of iron test, which consists 
in adding tincture of iron chloride to the urine, when, if this acid is present, 
a purple color is obtained. When dilatation is present there may be no 
response for twenty-four hours. 

Finally, as a means of determining that the digestive power of the stomach 
is greatly impaired, a test meal should be used after the stomach has been 
cleaned by lavage. If dilatation is present, the digestive process will always 
be very slow and imperfect. 

Cases of gastric dilatation sometimes develop a state called gastric tetany, 
in which tetanic spasms develop in the extremities. This is preceded by a 
sensation of formication, or numbness, associated with drowsiness. It has 
ensued, as a rule, upon the employment of lavage. Following the sensory 
symptoms the patient is seized with violent vomiting, and after or during 
this attack of emesis the muscles of the thumb and fingers contract, so that 
the thumb is drawn into the palm of the hand and the fingers are flexed. 
The wrist is also strongly flexed, but it may be extended. The forearm is 
flexed on the arm, and the biceps is hard and tense. These positions may 
not be maintained, but be changed into extension. Both sides are involved, 
but one side usually suffers more than the other. When the legs are affected 
the toes are flexed and the knees bent. The facial muscles may be in spasm 
and the patient may have explosive speech, as if in a shouting delirium. If 
the affected arm be pressed upon over the course of its vessels or nerves, the 
attacks may be reproduced (Trousseau's sign); if the point of exit of the 



576 DISEASES OF THE STOMACH 

facial nerve be tapped, facial spasm develops (Chvostek's sign) ; if electricity 
is used it is found that the muscles are excessively irritable (Erb's sign). 
The cramp-like contractions are painful. In severe cases death may occur 
from exhaustion. Out of 101 cases reported by European clinicians, no less 
than 75 died. 

Although the employment of the stomach tube has induced attacks of 
gastric tetany in some cases, attacks not due to this cause are to be pre- 
vented by frequent and thorough lavage, and are to be combated, when 
present, by nerve sedatives such as morphine or hyoscine hypodermically. 
Their occurrence in a mild form urges upon the physician the need of 
operation for the gastric state. 

Gastric tetany occurs in cases of dilatation more frequently than in cases 
of ulcer. 

Diagnosis. — As a rule, the diagnosis of gastric dilatation, in its well- 
developed stage, is not difficult. Care must always be exercised, however, 
that dilatation and gastroptosis are not confused, for in both affections the 
lower border of the stomach may be found far below the normal level, par- 
ticularly if it is distended with liquid or gas. The use of any of the methods 
of percussion and palpation, or the other means of diagnosis just described, 
will speedily separate the one state from the other, and the relatively limited 
capacity of the stomach in ptosis and its large capacity in dilatation will 
be another factor in deciding upon the real state which is present. 

Treatment. — The treatment of gastric dilatation is not promising unless 
the patient is seen and his condition recognized in the early stages of the 
disease. At this time, and later on as well, his diet should be most carefully 
regulated. He should be instructed to avoid all fatty articles of food which 
may give rise to lactic and butyric acid fermentation, and should also avoid 
the use of sweet materials, which may also undergo fermentative changes. 
The food which he takes should be thoroughly masticated and insalivated, 
it being remembered that the saliva is an important digestive juice, and that 
much may be done in aiding the digestion by thoroughly moistening the 
food with this secretion. The patient must also be warned not to eat a large 
amount of food at any one time, but rather to subsist on four or five small 
meals a day. He should also be instructed not to take large quantities of 
liquids with his meals. 

As to the articles of diet, he may have beef, mutton, chicken, or other 
simple varieties of meats, broiled or roasted, but not fried. Potatoes 
should only be taken when baked, and then in moderation. Zweiback, 
or soda biscuits which have been once more cooked by pouring scald- 
ing water over them, may be taken in moderation. The digestion of the 
starches should always be aided by the simultaneous ingestion of a capsule 
containing 2 grains of taka-diastase and 2 grains of pancreatin. If the 
diet is largely a meat diet, digestion should be aided by the use of 
hydrochloric acid and pepsin, 5 to 20 drops of the dilute acid and 2 tea- 
spoonfuls of a good essence of pepsin being used. Often it is wise to add to 
this mixture 10 drops of the tincture of nux vomica, or -^ of a grain of 
strychnine, for its effect as a bitter tonic and for the purpose of improving, 
if possible, the activity of the stomach. 



GASTRIC DILATATION 577 

In no case should the patient be allowed to accumulate fluid and food 
in the stomach for more than twenty-four hours. In other words, we should 
not wait until nature relieves the stomach by an attack of vomiting. 

As in chronic gastric catarrh, lavage should be performed once in every 
twenty-four hours, preferably at night before going to bed, and in all cases 
it should be remembered that it is not only futile but harmful to introduce 
food into a stomach which is already partly filled with fermenting materials, 
and which is therefore incapable of dealing with new food, which if taken 
simply adds to the decomposing mass already present. 

In many of these cases it is advisable, after emptying the stomach of its 
contents, to wash it out with one of the solutions named in the article on 
the Treatment of Chronic Gastric Catarrh. 

Emptying the stomach by means of the stomach tube and forbidding the 
use of excessive quantities of food are not only advantageous in that they 
permit digestion, poor as it may be, to proceed, but also do good in that they 
prevent the stomach from being overloaded and distended, and so further 
dilated, by its contents. It seems hardly necessary to add that beer, sweet 
wines, and champagnes should be absolutely forbidden for such patients. 

The medicinal treatment of gastrectasy consists in the use of nux vomica 
or strychnine in full doses combined with physostigma, the object being to 
improve the tone of the muscular fibres of the stomach. A pill composed 
of \ grain of extract of nux vomica and \ grain of extract of physostigma 
may be given three or four times a day with advantage. Gastrointestinal anti- 
septics are usually not particularly useful. From 2 to 5 minims of creosote or 
guaiacol may be given in capsule one or two hours after eating, with the hope 
that they will stop fermentation. In other instances guaiacol carbonate may 
be given in the dose of 2 to 5 grains in capsule. In still other instances 
naphthol may be given in the dose of 2 to 5 grains in capsule three times 
a day, or benzonaphthol may be used in the dose of 10 grains, in the same 
manner. 

Many physicians of experience resort to the use of faradic electricity in 
these cases, introducing a stomach tube containing the positive electrode 
and applying the negative electrode to some point on the surface of the body. 

In cases in which the dilatation is so severe and the symptoms so distress- 
ing that none of the measures so far suggested give adequate relief, the 
question of operative interference must be considered. Under these circum- 
stances, the question as to the cause of the dilatation becomes an important 
factor. If it is dependent upon pyloric stenosis, a gastroenterostomy or 
pylorectomy is indicated. But if, on the other hand, it does not depend upon 
this cause, but upon inherent atony and failure of the gastric walls, pylorec- 
tomy is, of course, of little value, and a gastroenterostomy is indicated. 
Before proceeding to operation, however, it must be remembered that there 
is some difference between an operative recovery and benefit to the patient. 
Rarely in these cases the patient survives the operation and makes a sur- 
gical recovery, but abdominal discomfort persists, either because of the 
presence of adhesions, irritation of nerve fibres, or other causes which it is 
difficult to determine, and which may be dependent upon the altered course 
of food from the stomach to the bowel. 
37 



578 DISEASES OF THE STOMACH 

Acute Gastrectasis. — Under the names acute gastric dilatation, gastro- 
intestinal paralysis, atonic gastrectasis, toxic gastrectasis, and paralytic 
dilatation of the stomach, there occurs an acute, often rapidly fatal, dila- 
tation of the stomach alone or of the stomach and intestines. 

Etiology. — Some cases are apparently causeless, and even at autopsy no 
cause may be demonstrable. Others occur in the course of acute infectious 
processes, some of which are systemic, such as scarlet fever and typhoid 
fever; in others the lesion is some distance from the affected viscus, as in 
pneumonia and meningitis, while still others depend for their development 
upon infectious processes in the neighborhood of the stomach or intestine, 
conspicuous among which may be mentioned peritonitis. The condition 
occasionally follows surgical anaesthesia, and it has been suggested that 
swallowing of mucus saturated with the anaesthetic may be the cause in some 
cases. It has been attributed to acute pyloric obstruction, as by foreign bodies 
or spasm, but that this is not always the cause is shown by the reported 
instances in which dilatation extended through the pylorus and first and 
second parts of the duodenum or even into the ileum. It has been thought 
to depend upon obstruction of the duodenum by the superior mesenteric 
vessels. It sometimes follows operation involving the peritoneum, and may 
commence after labor. Reynier strongly urges the influence of the nervous 
system in the production of acute gastrointestinal paralyses. 

Morbid Anatomy. — At autopsy the stomach is large, thin, and flaccid; it 
may extend almost to the pubes. It contains gas and fluid; the latter may 
be thick and viscid, but it is usually thin, watery, greenish or occasionally 
brownish in color, and frequently contains flocculi. The gastric mucosa 
may weep blood and the vessels be widely distended. 

Symptoms. — These usually come on rapidly. In operative cases they may 
be delayed twenty-four to forty-eight hours. There is marked abdominal 
distention amounting to actual ballooning; the dilated organ occupies the 
middle and upper left areas of the abdomen, and may be outlined through 
the abdominal wall. Peristaltic waves are rarely recognizable. Vomiting 
is nearly always present. In the few reported cases in which vomiting has 
been absent, it has been suggested that the associated relaxation in the 
abdominal wall has rendered emesis impossible. The vomited fluid is thin, 
watery, greenish or brownish. Profound depression or symptoms border- 
ing on collapse quickly appear. The pulse is small, rapid, and weak; the 
respirations shallow and frequent; the temperature, in the absence of com- 
plications, is usually low and may be subnormal. Thirst is intense, and, 
on account of suppressed absorption and prompt vomiting, is unrelieved by 
drinks. The urine is scanty or even suppressed. 

Diagnosis. — The acuteness of the symptoms and rapidly progressing 
collapse differentiate the condition from chronic dilatation. The vomiting 
is more incessant and the pain less than in volvulus of the stomach, which 
in some respects it closely resembles. The gastrorrhcea that accompanies it 
and the character of the vomit is unlike acute indigestion, and, ordinarily 
there is no expulsion of fragments of the mucosa as in true toxic gastritis 
The relaxed abdominal wall is quite unlike the rigid wall of perito- 
nitis. 



GASTRIC ULCER 579 

Prognosis. — The mortality is high; in HerfT's series of 34 cases, 29 died. 
In the so-called reflex group — those unassociated with any intra-abdominal 
lesion — prompt treatment promises some relief. 

Treatment. — Its prevention after operation may be accomplished by 
lavage immediately at the end of anaesthesia, and if vomiting appear and 
persist, lavage should be repeated. As it is probable that the condition is 
of toxic origin, free lavage should repeatedly be practised, and the stomach 
kept empty by the frequent use of the stomach tube. Water and food had 
best be given by enema. Strychnine and atropine have been suggested. 
As early as possible saline purgatives should be administered in small, but 
often repeated, doses. As relapses are possible as late as the third day, 
feeding, and even the administration of fluids, must be begun most cau- 
tiously in cases fortunate enough to survive. 



GASTRIC ULCER. 

Definition. — Ulcer of the stomach, often called peptic ulcer, or ulcus 
ventriculi, is due to necrosis of a part of the mucous membrane of this organ, 
so that an exposure of the submucous tissue is present. 

Etiology. — Almost ever since the processes of gastric digestion have been 
known, animated discussions have arisen as to why the stomach is not 
digested by its own juices and a large number of explanations have been 
offered, many of which have been anything but satisfactory. At present 
the conditions which result in gastric ulcer are known to be closely con- 
nected with the inability of the gastric mucosa to resist the action of the gas- 
tric juice. If, by any cause, the vital resistance of the mucous membrane 
is impaired, at the point of greatest impairment an ulcer may be developed. 
In very rare instances an injury to the surface of the abdomen may extend, 
or be transmitted, deeply enough to cause a lesion in the gastric wall; but it 
is more common for injuries to occur by internal agents, as by the use of 
certain articles of food which may interfere with the circulation in the wall 
of the stomach, as, for example, boiled tea, taken very hot, which contains 
an excess of tannic acid. So, too, an embolus or thrombus in a branch of 
a gastric artery may deprive an area of its blood supply, and subsequent 
digestion remove the dead tissue and so form an ulcer. Another predis- 
posing cause of ulcer is the secretion of superacid juice or of an excess of 
ordinary juice, and finally, in some cases, a local necrosis of the tissues is 
produced by the entrance of infecting micro-organisms, which, however, 
cannot enter the mucosa if normal vital resistance is maintained. 

Frequency. — The frequency of gastric ulcer in some parts of the world 
is far greater than in others. Even between England and the United States 
the difference is extraordinary. Out of 59,762 medical cases in the London 
hospitals, there were 1649 cases of gastric ulcer; while out of 75,612 medical 
cases in hospitals in different cities in the United States, there were only 446 
cases. According to these figures the morbidity of gastric ulcer is more than 
four times as great in England as it is in the United States. Since these 
figures were compiled Howard has confirmed them by others. 



580 DISEASES OF THE STOMACH 

In regard to the relationship of age and ulcer statistics vary slightly, but 
those of Welch are still to be considered the most competent. He found that 
the largest number of cases of ulcer occurred between twenty and thirty 
years of age, and Lebert also found that seven-tenths of 252 cases were 
between twenty and forty years of age. A case of ulcer in an infant only 
thirty hours old has, however, been recorded by Goodhart. Cutler, in an 
exhaustive search in literature, found only 24 cases under ten years of 
age with autopsy and 2 without autopsy, and has added 3 more which { 
occurred in the Massachusetts General Hospital; 29 in all. 

Women suffer from ulcer far more frequently than men. This is shown 
by all statistics and is illustrated by the following figures: Of 1548 cases 
of gastric ulcer collected from the official reports of hospitals in the United 
States and England, 1273 occurred in women and 275 in men. Of 1699 
cases examined postmortem and studied by Welch, 1020 were in women 
and 679 in men. Cantlie states that out of 20,586 cases in Montreal there 
were 85 cases of gastric ulcer, and of these 82 were women. The average age 
was twenty-seven and a half years. 

Other etiological factors of interest are occupation and associated disease. 
Thus, seamstresses and servant girls are singularly prone to ulcer, as are also 
tailors and shoemakers. Such persons are usually chlorotic or ansemic. So, 
too, ulcer is sometimes a complication of tuberculosis, and it may be in 
itself tuberculous. 

Gastric ulcer may be divided into four classes: In the first the lesion is 
very mild, the mucous membrane being eroded in such a manner that its 
superficial epithelium is destroyed. All authors do not agree, however, that 
these erosions are a form of peptic ulcer. The second type is characterized 
by an ulcerative process which penetrates more deeply, so that the submucous 
tissues are affected. The third invades the submucous, muscular, and even 
the peritoneal coat, and may cause perforation. The fourth type is that in 
which as a result of cicatrization and contraction scars and deformities 
develop, which produce serious consequences. 

Pathology and Morbid Anatomy. — Gastric ulcer is usually single, but cases 
are not very rare in which the ulcers are numerous. When acute it forms 
rapidly and presents a peculiar punched-out appearance. In the usual 
chronic form the edges are more shelving, indurated, and not so sharply 
defined. The size of the ulcer varies from a small spot scarcely larger than 
a pinhead to an enormous excavation covering nearly two-thirds of the 
gastric surface. These large ulcers are, however, very rarely met with. 

The depth to which the ulcerative process extends is also variable. The 
mucous membrane nearly always suffers most, but the tissues beneath it are 
affected as well, and the destructive process may, as just stated, extend as 
far as the peritoneal coat. Undermined ulcers are extremely rare. Around 
the edge of the ulcer there is usually marked hyperemia, and the surround- 
ing tissues, especially in chronic ulcers, are often infiltrated by formative 
cells or by the development of connective tissue. Usually the rest of the 
stomach exhibits more or less marked chronic gastritis. 

Ulcer of the stomach is usually found on the posterior wall of the viscus 
near the pylorus and on the lesser curvature (75 per cent.), probably because 



GASTRIC ULCER 581 

this is the part of the stomach which carries out the grinding process and 
urges the food into the duodenum, and therefore is exposed to injury and 
abrasion. Armstrong has, however, analyzed 240 cases of gastric ulcer arid 
found the anterior wall affected in 125 cases, the posterior wall in only 32. 
If the healing process is not rapid enough to arrest the ulcerative process, 
the wall of the stomach may be perforated and so produce severe abdominal 
symptoms. More commonly, however, as the inflammatory process ap- 
proaches the surface of the stomach it causes this viscus to become glued 
to a neighboring organ, and so it happens that the floor of the ulcer may be 
formed by an adjacent viscus. In this way neighboring organs may be 
involved in the inflammatory and septic process, and not rarely subphrenic 
abscess is due to this cause. Sometimes a perforation takes place into the 
colon or duodenum, and cases have been recorded in which the pericardium 
and pleura have been involved in this manner. The liver is also sometimes 
infected. Fenwick, in an analysis of 127 cases, found the stomach adherent 
to the pancreas in 49, to the liver in 33, and to the liver and pancreas in 10. 

Fig. 79 




Diagram showing the situation of ulcers of the stomach on the lesser curvature and near 
the pylorus. (Modified from English.) 

Ulcers on the anterior surface of the stomach are less common, but 
more prone to perforation into the peritoneum than those situated poste- 
riorly. It is held that the anterior wall is more movable than the posterior, 
and hence time for adhesion to apposed tissue is less. 

In many cases, a tendency to healing asserts itself and gradually, the 
exposed tissues are healed by the formation of a cicatrix which may cause 
considerable puckering as it develops. 

If the ulcer has been near the pylorus this may cause pyloric stenosis, or 
if it be near the middle of the stomach and the ulcer has been extensive an 
hour-glass contraction may result. (See Hour-glass Stomach.) 

Symptoms. — Ulcer of the stomach, at least in its milder forms, may exist 
for years without its presence being suspected, the patient suffering from a 
train of moderate gastric symptoms, generally described as dyspeptic. In 
most cases, however, it makes its presence known by symptoms which sooner 
or later send the patient to her physician for relief. The symptoms now 



582 DISEASES OF THE STOMACH 

complained of are discomfort and pain after eating, with a constant gnawing 
between meals when the stomach is empty. Not infrequently this gastric dis- 
tress is relieved by taking some food, and then increases as an excess of gas- 
tric juice is poured out to digest the food. The pain, when characteristic, 
is peculiar in its distribution, for it radiates from the epigastrium back to 
the shoulder-blade, or to a spot between the shoulder blade and the spine. 
Head has also shown that in gastric ulcer there is an area of cutaneous hyper- 
esthesia in a small triangular spot in the left epigastrium. This is demon- 
strable by a light touch, and not on deep palpation. At times the pain is 
exceedingly severe, and it may require active medication because of its inten- 
sity. Oftentimes the patient attempts to find relief by lying on the stomach 
or placing a pillow against it, but as a rule the epigastrium is so tender that 
any pressure on the part of the physician makes the patient wince. Careful 
palpation may, however, reveal an area of thickening or induration, if the 
ulcer is a chronic one. Associated with these symptoms there is often 
vomiting of very acid fluid, and an examination of the gastric contents will 
show an excess of hydrochloric acid both as to percentage and actual quan- 
tity. Constipation is usually marked, and the urinary flow is scanty. 

It is important to remember that ulcer of the stomach does not by any 
means always cause the same train of symptoms. Attention has already 
been called to the fact that the symptoms may be latent. In other cases 
there may develop, with great suddenness, a profuse ha^matemesis or symp- 
toms of collapse from perforation, and one of these accidents may be the 
first symptom of any importance. In other instances there is a general failure 
of health, marked emaciation, and a development of profound anwmia. In 
still others violent neuralgic pains (gastralgia) are the chief manifestations. 
In some instances the disease lasts but a few weeks ; in others it is prolonged 
for years. 

The symptoms so far described are chiefly those of acute or subacute 
ulcer. Chronic ulcer, on the other hand, may produce none of these symp- 
toms when the patient presents herself for treatment. Beyond a history of 
gastric distress, which may have existed for many years, there may be no 
pain on pressure and no soreness, in the sense of tenderness. Indeed, the 
symptoms may be those of gastric dilatation, or of pyloric stenosis. The 
patient is emaciated by reason of voluntary starvation, to decrease discom- 
fort, and by the loss of food by vomiting. So, too, a cicatrix near the 
middle of the stomach may produce an hour-glass stomach. This may 
become evident on distending the stomach with gas or fluid, but it is to be 
recalled that there is danger that rupture may ensue from this practice. 
(See Pyloric Stenosis and Dilatation of the Stomach.) 

In no other disease, save pernicious anaemia, is there such a notable 
diminution of red blood cells as takes place in many cases of chronic gastric 
ulcer. This is due to the more or less constant loss of blood which escapes 
by the bowel, the loss of which is usually not recognized. When hemor- 
rhage does not occur great anaemia is rare, although the patient may appear 
pallid. 

When hemorrhage from the stomach takes place the blood may be 
vomited or be passed by the bowel. The hemorrhage may follow many 



GASTRIC ULCER 583 

weeks of suffering or it may be the first sign that the gastric mucous mem- 
brane is diseased. The quantity of blood lost may be very small or so 
large as to almost exsanguinate the patient, the variation depending upon 
the size of the bloodvessel which is eroded. If a large vessel is perforated 
by a small ulcer it is not difficult to understand why it is that hemorrhage 
may be the first symptom. In other words, the hemorrhage may be the first 
symptom of ulcer. On the other hand, not infrequently gastric hemor- 
rhage, particularly if it be from a chronic ulcer, may be so scanty as never 
to cause bloody vomiting, the small amount of blood escaping with the 
food into the bowel. Moynihan believes that all ulcers bleed at some time 
in their existence. (See Diagnosis.) 

In studying the question of perforation of gastric ulcer it is well to 
recall that this accident may or may not be preceded by symptoms which 
will serve as a warning to the physician if not to the patient. There is, in 
some cases, a progressive increase in discomfort and pain after eating, a 
greater degree of tenderness or pain over the epigastrium, and more fre- 
quent vomiting. When such signs are present the patient must be placed at 
absolute rest, and if the symptoms do not speedily become modified opera- 
tion must be considered. On the other hand, the literature on this subject 
contains cases in which the history of gastric disorder was entirely absent, 
and the patient was suddenly seized by symptoms of perforation. 

When perforation does develop, it is usually in the anterior gastric wall, 
and from what has been said of the various ways in which perforation of the 
stomach occurs, it must be evident that the symptoms may vary over a wide 
range of severity. When no inflammatory adhesions have been formed 
and the gastric contents escape suddenly into the general peritoneal cavity, 
the onset is, of course, startling in its acuteness and the fain is exceedingly 
severe, but the locality of the pain is frequently far removed from the area 
of the accident. Vomiting and collapse may soon develop, and general 
peritonitis begins if operative relief is not promptly given. 

If the perforation is more gradual the symptoms are less violent and the 
opening may at first be so small that only a little of the gastric contents 
escapes into the peritoneal cavity. In those cases in which adhesions have 
formed before perforation takes place a subphrenic abscess may result. 
In such instances the perforation is usually on the posterior wall of the 
stomach. 

Sometimes perforation of the stomach may take place without the sharp 
and decisive symptoms just described. 

While the pulse usually is rapid it may not be materially increased in 
rate. 

Again, it is important to remember that after perforation of the stomach 
there may be a " period of repose," or " fallacious calm," during which 
time the patient feels less pain and distress, and the pulse approximates 
its normal speed. 

At one time, it will be recalled, a decrease in the area of liver dulness 
was supposed to be indicative of gastric or intestinal perforation, but we 
now know that the absence of this sign does not negative perforation. Thus, 
Pearson found a decrease in the area of liver dulness in 33 per cent, of 140 



584 DISEASES OF THE STOMACH 

cases of gastric ulcer at some period during their stay in the hospital, yet 
perforation took place in none of them. 

Diagnosis. — Gastric ulcer in some instances is so manifestly present that 
there is little difficulty in determining the cause of the illness. Care must 
be taken that the pain of appendicitis, gallstone colic, renal colic, and intense 
menstrual colic is not taken for that due to perforation. Moynihan speaks 
of 3 cases operated upon for perforation in which menstruation was the 
cause of the pain, and states that of 49 cases of perforated duodenal ulcer 
appendicitis was thought to be the cause of illness in 18. In the gastralgic 
cases ulcer must be separated from ordinary gastric neuralgia by the recol- 
lection of the fact that true gastric neuralgia is very rare, by the additional 
fact that the pain of neuralgia is not induced by taking food and by the 
fact that in neuralgia evidences of gastric indigestion are not constantly 
present, as they are in most cases of ulcer. Severe pains in the stomach due 
to locomotor ataxia (gastric crises) can usually be excluded by the presence 
of Argyll-Robertson pupils, absence of knee-jerks, and swaying when the 
patient stands with the eyes shut. 

The irritation produced by gallstones may produce symptoms resembling 
gastric ulcer, but in these cases the history of gallstone colic will be given 
and the taking of food has no influence upon the pain. Then, too, the pain 
in the back due to ulcer is to the left of the middle line near the twelfth 
dorsal vertebra, whereas that due to gallstone is on the right of the median 
line and a little lower down. So, too, palpation of the neighborhood of the 
gall-bladder may reveal an enlargement of this viscus, and jaundice points 
to cholelithiasis rather than to ulcer. 

Cases of chronic ulcer of the stomach with much cicatricial tissue around 
the ulcer, or at the seat of an ulcer which has healed, may present symp- 
toms almost identical with those of gastric cancer. Pain and obstruction 
to the passage of food through the pylorus, gastric dilatation due to this 
latter cause, and emaciation from all these causes may combine to present 
a clinical picture of gastric cancer, particularly if the physician finds, on 
palpation, that he can feel a mass or masses in the gastric wall. The com- 
parative youth of the patient in cases of ulcer, the absence of cachexia even 
if ansemia is marked, and a remembrance that ulcer of the stomach is most 
common in the female sex helps to make the diagnosis possible. Again, in 
ulcer the gastric contents show an excess of hydrochloric acid after a test 
meal, whereas in cancer this acid is usually absent or less than normal. 
(For the tests of the stomach contents see article on Gastric Cancer.) 

Finally it must be recalled that duodenal ulcer may cause symptoms so 
closely resembling gastric ulcer that a differentiation may be impossible. 
If hemorrhage occurs, and blood is passed in the stools in considerable 
quantity, the lesion is probably duodenal. (See Duodenal Ulcer.) 

Boas considers the demonstration of minute quantities of blood in the 
feces to be of great value in the diagnosis of gastric ulcer, and especially in 
determining whether obscure cases of gastric disease are pure gastralgia 
or conditions in which the symptoms are produced by ulcerative lesions of 
the gastric mucosa. It has been proven experimentally that the ingestion 
of so small a quantity as 3 c.c. of blood gives a positive reaction for blood 



GASTRIC ULCER 585 

in the feces, and this fact shows that even minute hemorrhages may give 
rise to similar positive reactions. 

Before performing the test all other sources of hemorrhage, such as the 
swallowing of blood from wounds in the mouth or from lesions in the re- 
spiratory tract must be guarded against, and the absence of hematuria, and 
in women metrorrhagia and menstrual blood, must also be assured. No 
rare meat, fish, or sausages are allowed for two days before the test is made. 

Boas prefers the aloin test as recently recommended by Klunge and 
Schaer to the older guaiacum test. It is performed as follows: 5 to 10 
grams of feces, which, if hard, are to be softened by the addition of a 
small quantity of water, are mixed with 20 c.c. of ether, 3 to 5 c.c. of 
glacial acetic acid, and the mixture is well shaken in a reagent glass. Then 
more ether is added, and also 20 or 30 drops of an old oil of turpentine. If 
to this mixture there now be added 10 or 15 drops of a solution made by 
dissolving in 3 to 5 c.c. of 70 per cent, alcohol as much aloin as can be 
taken up on the tip of a small spatula, a light-red color is soon produced 
if blood is present. This light-red gradually assumes a cherry-red hue if 
the mixture is allowed to stand. If no blood is present the mixture remains 
of a yellow color for from one to two hours, when it changes to rose red. 

The possibility of parenchymatous gastric hemorrhage, and of hemor- 
rhage from varicose or atheromatous bloodvessels in the oesophagus or 
stomach, must of course be taken into consideration before a diagnosis of 
doubtful cases is made. 

In several cases Boas has found blood present in the feces shortly after 
patients had experienced an attack of pain in the epigastrium. After 
several days of mild diet it was often found that no blood could be detected 
in the feces. 

Prognosis. — The prognosis of cases of gastric ulcer must, of course, vary 
greatly with the severity of the lesion, and the time during which it has 
lasted. In those cases in which superficial erosions are present, the patient 
probably recovers in the great majority of instances. When actual ulcera- 
tion is present, the proposition is, of course, a different one. The most 
divergent views exist as to the prognosis in this type of case. Brinton, in 
his now somewhat ancient statistics, states that 50 per cent, recover under 
medical treatment. Tricomi places the percentage at 25, as do also De- 
bove and Ramond. Leube states that 25 per cent, die as a direct effect of 
the disease. Whatever may be the percentage as to recovery, it cannot be 
doubted that in many instances it is once an ulcer always an ulcer, in the 
sense that relapses take place soon after the ulcer seems well. In a collection 
of 500 cases at the London Hospital, made by Bulstrode, 211 had had ulcer 
before, 18 per cent, died, and 42 per cent, were not cured on discharge. 

Ulcers near the pylorus heal more slowly than those which occur else- 
where. Some gastric ulcers probably become cancerous in later life. 
Graham has found a history of ulcer in 60 per cent, of 125 cases of cancer 
of the stomach — a fact of some prognostic importance. 

The mortality in cases which suffer from hemorrhage is not high. 
The direct mortality from this cause is only 2.1 per cent., according to 
Russell. So far as recovery from the ulcer is concerned when it is severe 



586 DISEASES OF THE STOMACH 

enough to cause haemorrhage the outlook is not good — 44.7 per cent, con- 
tinued in ill health and 42.6 per cent, recovered (Russell). 

Treatment. — The treatment of gastric ulcer consists in restricting the 
diet, in the administration of medicines qualified to improve the state of 
the gastric mucous membrane, and in the institution of rest for the general 
system as well as for the stomach. Foods which are very hot or very cold, 
particularly those which are very hot, should be carefully avoided, and 
hyperacidity is to be counteracted by the use of calcined magnesia or bicar- 
bonate of soda. 

Hi . — Sodii bicarbonatis, 
Magnesise ponderosse, 

Calcii carbonat aa ^ j . 

01. menth. piperitse TT[x. 

Sig. — A heaping teaspoonful in half a glass of water when needed 

In most instances it is wise to insist that the patient remain in bed for 
a period of three or four weeks, during which time the rest cure may 
be instituted in a modified form, since with the improvement in general 
health and the cure of anaemia healing of the ulcer progresses more rapidly. 

The diet should consist of milk which is predigested by a peptonizing pow- 
der either before or immediately after it is taken into the stomach. Under 
certain circumstances it may be permissible to give the patient very soft 
milk-toast in small quantities, or to give scalded soda-biscuits digested by 
means of taka-diastase or pancreatin. When the ingestion of food increases 
gastric pain and distress it may be necessary to give the patient nothing by 
the stomach for a period varying from one or two days to two weeks, and 
to nourish him as far as possible during this period by nutritive enemata, 
which should consist of four ounces of peptonized milk and one egg, injected 
three times in the twenty-four hours, the bowels being carefully washed out 
with normal saline solution before each injection in order that the residue 
from the previous injection may be removed. 

For the purpose of relieving thirst, it is often advantageous, when the 
stomach is irritable, to give, daily, normal saline solution by hypodermoclysis. 
In other instances a pint to a quart of normal saline solution may be given 
high up into the colon. 

A number of years ago the late J. M. Da Costa strongly recommended 
ice-cream as a diet for these cases. Care should be taken that the ice-cream 
does not contain too much sugar, as this will cause fermentation and dis- 
tress. Frozen milk flavored with vanilla is better. 

The patient suffering from gastric ulcer should receive, in the way of 
medicine, i of a grain of nitrate of silver with \ of a grain of extract of 
hyoscyamus in pill three or four times a day and take them an hour before 
taking food, in order that these drugs may act upon the stomach, exercising 
a healing influence, and preventing an excessive secretion of gastric juice. 
If pain is severe, opium may be substituted for hyoscyamus, but there is 
some evidence that opium does not decrease, and may sometimes increase, 
the flow of gastric juice. In other instances chloretone in the dose of from 
3 to 5 grains may be given three or four times a day, and it is particularly 



GASTRIC ULCER 587 

useful if pain is present. In other cases hyperacidity and pain are best 
controlled by 10 to 20 grain doses of bromide of strontium or of sodium. 

The administration of massive doses of bismuth subnitrate has been 
strongly recommended, chiefly by Fleiner. He gives 150 to 300 grains, 
stirred in 5 or 6 ounces of warm water, after the stomach has been care- 
fully cleansed by lavage. Of course a heavy precipitation of bismuth occurs 
upon the gastric mucous membrane. This plan is more suitable for chronic 
cases than for acute ones. 

In all cases of gastric ulcer it is important that the bowels should be moved 
every day or two by means of one of the alkaline purgative waters, of which 
probably Carlsbad water has the greatest reputation. The Carlsbad and 
Hathorn spring-waters at Saratoga do almost, if not quite as well, as the 
imported water. The advantage of employing these waters is that they 
not only unload the bowels, but tend to correct acidity and relieve chronic 
gastric catarrh by their favorable influence upon the gastrointestinal mucous 
membrane. 

Should hemorrhage from the stomach occur, the patient should be put to 
bed, and if not too depressed by the bleeding, a small ice-bag may be placed 
over the epigastrium, and 2 teaspoonfuls of adrenalin chloride (1 : 1000) 
mixed with 2 or 3 ounces of water may be given by the mouth, with 
the hope that the adrenalin chloride will contract the bloodvessels and 
arrest the hemorrhage. Where adrenalin chloride cannot be obtained, 
from 5 to 30 drops of Monsel's solution may be given in 2 ounces of water. 
The use of ergot hypodermically, or by the mouth, in this condition can 
scarcely be of benefit, as it will raise arterial pressure in other parts of the 
body and may increase the hemorrhage. The general treatment in these 
cases is, of course, identical with that of profuse hemorrhage occurring 
from other parts of the body, and consists in the use of \ of a grain of 
morphine hypodermically to allay mental distress, and hypodermoclysis of 
normal salt solution. Should the hemorrhage be sharp and very profuse, 
the question of operative interference arises. 

The decision as to whether an operation should be performed in gastric 
ulcer with hemorrhage is a most difficult one to reach. We are rarely tempted 
to operate in such cases unless the hemorrhage is so severe as to be alarming, 
and yet its very severity renders the condition of the patient unfavorable 
to operation. 

In deciding whether an operation is needful in a case which has had an 
attack of gastric hemorrhage, consideration must be given to the character 
of the ulcer. Even those surgeons who are most radical in advising opera- 
tive measures in these cases state that in cases of hemorrhage from acute 
ulcer medicinal measures will usually control that particular bleeding, and 
as an immediate second hemorrhage is rare operation is not demanded. 
(See Prognosis.) When the hemorrhage does recur and particularly if it be 
profuse on recurrence, operation is to be considered carefully, whether the 
ulcer be acute or chronic. The operation of election is gastroenterostomy, 
for it has been found impossible to find the bleeding spot in most cases 
because the bleeding often comes from several spots, and indeed may ooze 
from a multitude of eroded spots. Needless to say that the gastroenterostomy 



588 DISEASES OF THE STOMACH 

is not designed to stop a bleeding already in active progress, but is to 
be performed as soon as possible to prevent further bleedings. 

When the ulcer is very chronic — that is, has lasted a long time — its edges 
may be so indurated and the bloodvessels in its cavity so eroded that 
little hope of cure by natural processes can be entertained, an operation is 
wise. It is not necessary to excise the ulcer. A gastroenterostomy gives 
the stomach rest and the circulation in its walls becomes modified. Not 
only does such an operation remove the danger of hemorrhage, but it may 
change the patient from a chronic dyspeptic to a well-nourished, healthy 
individual. If, however, the ulcer causes suffering or chronic gastric dis- 
tress, surgical interference should be carefully considered. This holds true 
with special force, if the existence of a chronic ulcer near the pylorus is 
causing obstruction. 

Operation for the removal of the ulcer, when as yet it has neither under- 
gone perforation nor produced hemorrhage, has been advised, but of course 
has not been very popular, as few patients care to submit to it, and few 
physicians have considered it advisable to strongly urge operative inter- 
ference. 

The surgical treatment of gastric ulcer with perforation is now a well- 
recognized procedure in modern medicine. When perforation occurs opera- 
tion should be resorted to at once, unless the patient is profoundly shocked, 
when some delay is advisable in order that she may rally. 

The best results are obtained in the cases which are operated on during 
the first twelve hours after the occurrence of perforation. An analysis of 
these statistics shows that the mortality under operation has been pro- 
gressively reduced: 

In July, 1899, Tinker added 57 cases to Keen's list of 156, and in 1900 
he collected 19 others, which made the total number 232, with a mortality 
of 48.81 per cent. Later, in the year 1900 Finney made an addition of 36 
cases to Tinker's last list, thus bringing the number up to 268, of which the 
mortality was 48 per cent. Of 163 cases collected since the publication of 
Finney's paper in 1900, 102 recovered and 61 died — a mortality percentage 
of 37.04. These figures bring the statistics up to June, 1904. 



CANCER OF THE STOMACH. 

Gastric carcinoma is one of the most common forms of malignant growth. 
Many years ago Welch showed that in 31,482 cases of cancer the disease 
affected the stomach in 21.4 per cent. Startling statistics as to the increasing 
frequency of cancer have been published within the last four years by several 
writers, of which one of the leaders has been Roswell Park, of Buffalo. In 
the United States census for 1890, the deaths from gastric cancer were placed 
at 2014 as against 304 for cancer of the rectum, and 876 from cancer of the 
liver; whereas, in the census for 1900, there were 4220 deaths from cancer 
of the stomach, 574 from cancer of the rectum, and 1784 from cancer of the 
liver. As a large proportion of cases of cancer of the liver are secondary to 
growths elsewhere, particularly in the stomach, these facts are of great 



CANCER OF THE STOMACH 589 

interest. In the city of Washington the deaths from cancer of the stomach 
in the decade from 1881 to 1890 were 191, and in the decade from 1891 
to 1900, 339, which shows an increase greater in proportion than the growth 
of the city population. So, too, Templeton, of Dundee, found that from 
1877 to 1902 the death rate from gastric and oesophageal cancer increased 
12.66 per 10,000. 

Etiology. — Gastric cancer is far more common in males than in females. 
Welch states the proportion to be 5 to 4, but in Osier's cases the proportion 
was 5 to 1. The fact that gastric ulcer may in some cases seem to be the site 
for the development of gastric cancer has little real bearing upon the etiology 
of this disease. While some patients state that they have been subject to 
gastric disorders for years before the final illness develops, it has been my 
experience that a very large proportion of patients state that hitherto they 
have had perfect digestion, and have never known what it was to have gastric 
distress in previous years. In other words, given a man who complains of 
grave gastric symptoms and loss of weight, who has not cirrhosis of the 
liver, or dilatation of the stomach, who has not used alcohol to excess, 
and who boasts of his good stomach during the first forty years of life, 
that man will often be found to have gastric cancer. We have no knowl- 
edge of the etiology of gastric cancer beyond the facts already named. 

Morbid Anatomy. — Gastric cancer is usually primary, but it may be second- 
ary. The most common form is the medullary carcinoma, a form of the 
spheroidal-cell cancer; the adenocarcinoma, the malignant adenoma of 
German writers, or cylindrical-cell cancer, is second in point of frequency. 
The scirrhus type is the third in frequency. Gelatiniform degeneration 
occurs in the first and second, and when present such tumors are called 
colloid cancers. 

The medullary, or spheroidal-cell type, is the most rapid in its growth, 
usually tends to ulcerate early, and is followed by metastasis and direct 
extension to contiguous organs sooner than the other types. 

The scirrhus is a denser growth, infiltrating and indurating the sub- 
mucosa often to some distance, or even all of the organ ; under such circum- 
stances, the thick, dense, gastric wall has led to the condition being called 
"India-rubber bottle stomach, " or "leathery stomach." 

The colloid growths form tumors of greater size, often extending by con- 
tiguity and matting adjacent organs into a solid mass. On section the clear 
or grayish gelatiniform trembling matrix is found to be enclosed in alveoli, 
often of macroscopic dimensions. 

The pylorus is the part of the stomach usually affected ; next to it in fre- 
quency is the lesser curvature, but out of Welch's 1300 cases the pylorus was 
affected 791 times and the lesser curvature but 148. 

Mr. Moynihan, of Leeds, has investigated the subject of how malignant 
growths spread in the gastric wall, and has concluded: 

1. That malignant disease of the stomach begins in the majority of instances 
near the pylorus, just below the lesser curvature. 

2. That from this point it spreads most rapidly and most widely in the 
submucosa. 

3. That the rate of growth toward the cardiac orifice is rapid, toward 



590 



DISEASES OF THE STOMACH 



the duodenal side extremely slow. The duodenal extremity of the viscus 
is rarely affected extensively. 

4. That the tendency of the growth is to drift toward the curvatures. 

He found that the lymphatic system of the stomach was comparatively 
simple. There are three chief lymphatic areas of the stomach (Fig. 80). 

1 . An area along the lesser curvature (a) from which the lymphatic vessels 
pass upward and to the left into the coronary glands. The coronary glands 
lie along the artery of the same name. At the cceliac axis they become con- 
tinuous with the glands along the upper border of the pancreas. 

2. An area (6) along the greater curvature from which the lymphatic vessels 
pass downward and to the right into the glands lying along the greater curva- 
ture. These glands are more numerous near the pylorus, and from here pass 
to the head of the pancreas and become continuous with the hepatic group 
of glands which lie along the hepatic artery, and in part along the pyloric 
artery. 

,Fig. 80 




The lymphatic vessels and glands of the stomach: a is the most frequently affected area, b is next, 
and c is the " isolated area." (Moynihan.) 



3. In addition to these two areas is a third (c), for which I (Moynihan) 
suggested the name "isolated area." This area comprises the greater 
tuberosity of the stomach, the lower end of the oesophagus, and an area 
along the greater curvature as far, approximately, as the limit of supply 
of the left gastroepiploic artery. Its lymphatic vessels pass downward to 
the hilum of the spleen. The term "isolated area" seems singularly 
appropriate for this region, for it is very rarely affected by growth spread- 
ing upward from the pylorus. 

If a cancer of the stomach arising independently of ulcer is examined in 
its early stages it will usually be found covered with mucous membrane, 
which later ulcerates. The entire wall of the viscus may soon be involved, 
but in the colloid form the mucous membrane may not be destroyed. 

The effects of cancer of the stomach upon the shape of this viscus depend 
largely upon the character of the growth, and chiefly upon its situation. The 
general tendency is for the stomach to be decreased in size, but if the growth 



CANCER OF THE STOMACH 



591 



obstructs the pylorus the stomach may be greatly dilated. When the tumor 
is widely diffused the gastric walls are much thickened, and if it be of large 
size it may displace the pylorus very greatly by its weight. 

Perforation of the stomach through the cancerous mass may occur, but 
this is not a frequent complication. 

Symptoms. — The symptoms of gastric cancer may not manifest themselves 
for a long period after the growth has begun, and even when the general 
nutrition is impaired the patient may not complain of gastric disorder. It is 
a mistake to suppose that gastric cancer is usually very painful. 



Fig. 81 




Stomach. Large, ulcerating, fungoid, cylindrical-cell carcinoma, situated on the posterior wall near 
the pylorus, which was slightly obstructed by the projecting growth. A glass rod is passed through a 
perforation near the centre of the floor of the ulcer. The cardiac end of the organ is moderately dilated 
There was secondary enlargement of the lymph nodes behind the stomach, and metastatic nodules in 
the liver. 

When symptoms are present they may be divided into the objective and 
the subjective. The objective symptoms are pallor, which becomes well 
marked ; a loss of weight, which is often extraordinary, amounting to a loss of 
from fifty to seventy pounds in a few months, and with this there is usually a 
rapid loss of strength. The ancemia is chiefly the result of a marked decrease 
of haemoglobin, although marked reduction and morphological alteration in 
the erythrocytes may yield a blood picture resembling pernicious anaemia. 
Sooner or later leukocytosis occurs. 



592 DISEASES OF THE STOMACH 

The symptoms presented by the patient, in the sense that they are com- 
plained of by him, are loss of strength, gastric distress and "dyspepsia," loss 
of appetite, nausea, and not rarely vomiting. Vomiting is a far more con- 
stant symptom when the pylorus is obstructed than when it is free, and the 
matters vomited may indicate a feeble digestive power and be colored like 
coffee grounds due to exuded and altered blood arising from the ulcerated 
growth. Sometimes a free hamatemesis develops. Care should be taken that 
the presence of altered bile in the vomit is not taken for altered blood. 

Not rarely the patient complains of constant gnawing pain in the stomach, 
which may or may not be increased by the taking of food. The pain is 
usually more severe when the disease is in the region of the pylorus. If the 
skin over the epigastrium is lightly touched, it may be very sensitive. 
There may be moderate fever, constipation, and oedema of the ankles. 

Robson states that pain is present in 86 per cent, of cases, vomiting in 
85.3 per cent., and a tumor is palpable in 76.6 per cent. These figures refer 
to the entire history of the cases recorded, and, as pointed out elsewhere, 
none of these symptoms may be present during the early stage of the dis- 
ease, when it is most amenable to surgical treatment. Such percentages 
are, therefore, of greater value from a statistical than from a diagnostic 
standpoint. 

Diagnosis. — The pallid, cachectic hue of the patient, combined with a his- 
tory of loss of weight, and with the fact that the patient is usually beyond 
the fortieth year, should make the physician suspect at least the presence 
of a malignant growth, and this suspicion becomes stronger as he is able 
to exclude other causes of ansemia and emaciation, such as, for example, 
diabetes, Bright's disease, and pernicious ansemia. The presence of cough 
will usually be a guide to the examination of the lungs for pulmonary tuber- 
culosis. It must not be forgotten that abdominal tuberculosis produces, as 
a rule, a dry, harsh skin, instead of the peculiar waxy or greasy skin of malig- 
nant growth and pernicious ansemia. 

In the diagnosis of malignant growth the blood may give considerable 
information and aid us in separating this condition from pernicious ansemia, 
which resembles it very closely in some of its objective symptoms. Malig- 
nant growth is characterized by a marked decrease in the amount of haemo- 
globin and in the hsemoglobin index, a condition the reverse of that in per- 
nicious ansemia. When the case is far advanced there is usually a dimi- 
nution in the number of red cells, but this diminution is only moderate in 
early cases. Leukocytosis is usually present in moderate degree, averaging, 
perhaps, 20,000 to 25,000, and it is much more marked if metastasis, 
hemorrhage, ulceration, or septic infection occur. The increase in white 
cells is chiefly in the polymorphonuclear neutrophiles. It is a noteworthy 
point that these cells may be relatively increased without a distinct leuko- 
cytosis being present. Normoblasts and myelocytes are sometimes found in 
limited numbers when the disease is far advanced. 

While it is true that in a few cases of pernicious ansemia there is a marked 
diminution in the quantity of hydrochloric acid, it is rarely if ever so per- 
sistently absent as it is in gastric carcinoma. 

Another condition which may give rise to much difficulty in diagnosis is 



CANCER OF THE STOMACH 593 

ulcer of the stomach, with thickening and induration around it. This condi- 
tion is particularly prone to appear in the neighborhood of the pylorus, and 
it may be impossible by palpation to differentiate ulcer and induration from 
scirrhous cancer. In other words, every case in which a mass can be felt in 
the stomach is not one of cancer. In such a case the excess of hydrochloric 
acid in ulcer and its absence in cancer are valuable factors in diagnosis. 
Then, too, ulcer is much more frequently present in persons under forty, 
but cancer is more common in persons over forty. 

Inspection of the epigastrium very often gives most valuable information, 
because it may reveal a bulging and undue pulsation due to impulse from the 
aorta transmitted by the growth, or the presence of a nodule. A deep breath 
taken during inspection may reveal distinct movements of the mass. If 
a Seidlitz powder is taken in two parts, so that the contents of one paper 
follow the other, the tumor can sometimes be seen to be projected against 
the abdominal wall by the distended viscus. Palpation may reveal a mass 
which usually presents an uneven surface, and this may be distinctly nodular. 

The position of the mass may be varied by the pressure of food in the 
stomach. If a mass cannot be felt, immersing the patient in a hot bath 
may relax the tense belly wall so that the tumor may be demonstrable. 
Percussion, if it is carefully and gently performed, over the mass may give 
an impaired note. 

Additional signs on palpation consist of a hardening of the gastric walls 
due to contraction of their muscular fibres, and if the patient is thin the mass 
may be so movable that it may be pushed high up under the ribs or far 
down toward the pelvis. The mobility is of great diagnostic value, for if 
the mass be due to induration about an ulcer the gastric wall will nearly 
always be glued to adjacent tissues, and therefore be made fast. As a rule, 
tumor at the pylorus is more readily palpated than one at the middle of the 
stomach, and a growth at the cardia is rarely to be felt. 

Auscultation may reveal constant, direct, or reversed peristalsis if the 
growth obstructs the pylorus, and all the symptoms of gastric dilatation may 
be present if the growth be so situated. (See Gastric Dilatation.) 

A very useful and reliable method for the purpose of determining the 
presence of gastric cancer is the determination of the character of the 
stomach contents. 

If the stomach contents are examined after a test meal, there will be an 
almost complete or total absence of hydrochloric acid and an abnormal 
amount of lactic acid present. To determine these facts, we resort to the 
use of a test meal and certain chemical tests, as follows: 

Boas' test meal consists in the use of an ordinary breakfast roll weighing 
about 1 ounce, with 10 ounces of water, or of weak tea, which should contain 
no milk or sugar. This is allowed to remain in the stomach for one hour, 
and then is removed by the stomach tube. The quantity of fluid obtained 
should equal from three-quarters of an ounce to an ounce and a half. It is 
best to examine this fluid microscopically, and then, after filtering it, to 
apply the tests for hydrochloric acid and the organic acids. The two common 
tests for free hydrochloric acid are Giinzburg's phloroglucin-vanillin and 
Boas' resorcin test. Gunzburg's reagent is composed of: 
38 



594 DISEASES OF THE STOMACH 

Phloroglucin gr. xxx (2 grams) 

Vanillin . . . . . .... gr. xv (1 gram) 

Alcohol (absolute) 3j(30c.c.) 

This solution should be carefully protected from the light by being kept 
in a dark bottle and should be frequently prepared, as stale solutions are 
uncertain. One or two drops of this reagent are placed in a porcelain dish or 
capsule, with an equal quantity of the filtrate obtained from the gastric con- 
tents. The dish is then gently heated over an alcohol lamp or Bunsen burner 
to such a degree that slow evaporation takes place. If free hydrochloric acid 
is present, a typical rose-red hue develops at the edge of the mixture where it 
is drying on the dish, or it may be less of a pink and more of a bright red. 
This test is exceedingly delicate and very certain. 

Boas' reagent depends upon the fact that resorcin produces a somewhat 
similar reaction with free hydrochloric acid. This reagent is composed of: 

Resublimed resorcin gr. lxxv (5 grams) 

Cane-sugar . . . . . . . . gr. xlv (3 grams) 

Alcohol (94 per cent.) ...... ^iijss (100 c.c.) 

A few drops of this reagent are placed in a porcelain dish and an equal 
quantity of the stomach filtrate added to them. Heat is applied as in the 
previous test, and if the acid is present a very perceptible red color appears 
at the edge of the evaporating mixture. 

Still another point of diagnostic importance is the examination of the 
stomach contents by the microscope, which may reveal blood cells and 
portions of malignant growth. While it is true that the presence of blood 
may be due to ulcer, the associated pieces of growth are, of course, diag- 
nostic. 

Rommelaere asserts that if a patient over forty years of age with chronic 
gastric disease eliminates less than 180 grains of urea a day, he has cancer. 
This is probably too dogmatic. A better way of putting it is to say that when 
a patient with these symptoms eliminates 450 grains a day he has not 
gastric cancer. 

It is important to note that a bacillus called the Oppler-Boas bacillus is 
present in the stomach contents of cases of gastric cancer with great con- 
stancy. Indeed, it is present ninety-nine times in a hundred. This bacillus 
is a very long, non-motile organism, which has the power of converting sugar 
into lactic acid, and lactic acid is present in large amount in this disease. 

Prognosis. — The prognosis is only hopeful in inverse ratio with the size of 
the growth, the ability of the surgeon to remove it, and the general state of 
the patient. Even surgery can offer only temporary relief, for in the majority 
of cases recidivity takes place. Fenwick asserts that if the potassium sulpho- 
cyanide disappears from the saliva, the patient dies within a month. 

Duration. — This varies greatly. In some instances death comes in a few 
weeks after the disease is recognized. In others it is deferred for months, 
particularly if the growth be scirrhous and involves the pylorus, when a 
gastroenterostomy, by relieving obstruction and permitting nourishment, 
may prolong life for a long period. My colleague, Dr. Keen, performed 
gastroenterostomy in a case under my care in which the growth was so great 



HYPERTROPHIC STENOSIS OF THE PYLORUS 595 

that excision was impossible. The patient was greatly emaciated and more 
than sixty years of age, yet he gained nearly thirty pounds in six months, and 
lived in comfort for two years and a half after the operation. 

Treatment. — The medicinal treatment of gastric cancer consists first in the 
administration of anodynes if there is much pain. These anodynes may consist 
of small doses of morphine or codeine or cannabis indica. Much of the dis- 
tress due to so-called dyspepsia can be relieved by the use of 5 to 10 drops 
of dilute hydrochloric acid, with 1 or 2 drachms of the fluid extract of con- 
durango, given immediately after or with each meal. If starchy foods are 
taken, taka-diastase may be used. 

The use of a stomach tube for washing out the stomach is usually 
inadvisable, as it may produce a perforation if the growth is soft or the 
ulceration deep. 

Should vomiting occur and blood be in the vomit, the directions for the 
treatment of hsematemesis in the article on Gastric Ulcer should be followed. 
Many patients with gastric cancer can be much improved and their lives 
prolonged by operation, but it is essential that the growth shall be limited 
to the stomach and that it does not involve neighboring parts. For this 
reason it is of vital importance that the diagnosis of the disease shall be 
made at the earliest possible moment. Indeed, it may be said that every 
patient who develops persistent gastric symptoms after the age of forty 
should be regarded as a possible case of gastric cancer until repeated studies 
of the gastric contents have excluded this disease. In the opinion of the 
writer, every case of gastric cancer in its early stages should at least be 
subjected to exploratory operation, since by this means it may be dis- 
covered that the diseased area may be excised. The danger of exploratory 
operation, as compared to the certainty of death if the growth is not 
interfered with, is not to be considered. 

Kronlein has shown that the average duration of life after patients come 
under observation is about nine months. If they submit to operation it is 
more than twelve months. The duration of life was greater in those treated 
by gastrectomy than in those treated by gastroenterostomy. 



HYPERTROPHIC STENOSIS OF THE PYLORUS. 

Definition. — This condition, as its name implies, is one in which there is 
thickening and overgrowth of the muscular fibres in the pyloric portion of 
the stomach, with spasm and consequent obstruction to the free passage of 
its contents into the bowel. 

Overgrowth of the tissues about the pylorus may be divided into three 
types. In one the gastric walls become thickened by an overgrowth of con- 
nective tissue, which not only results in an increased diameter of the part, but 
also in a diminution of the size of the entire stomach. A second form has 
been described by French authors, which is associated with sclerotic hyper- 
trophic changes in the other abdominal viscera, such as the liver, pancreas, 
and kidneys. The third form is that which is known as congenital hyper- 
trophic stenosis, which has no etiological relationship to the two forms just 



596 DISEASES OF THE STOMACH 

described. All three of these forms are quite rare, the last being most 
frequent. 

Etiology. — We have little knowledge of the causes of hypertrophic stenosis 
of the pylorus. In some instances it has been thought that the overgrowth 
is the result of some congenital defect, or, in other words, that it is a primary 
condition, but in others it has seemed to be certainly secondary. It is 
probable that in the hypertrophic stenosis of adults the underlying cause is 
chronic gastritis. When it occurs in adults hypertrophic stenosis is usually 
a disease of middle life. 

Morbid Anatomy. — In that form of this disease which arises in middle life 
and which develops as a result of chronic gastritis, notwithstanding the non- 
existence of the obstruction at the pyloric opening, dilatation of the stomach 
as a secondary condition seems to be rare, but this depends somewhat upon 
how diffuse the overgrowth of connective tissue happens to be. When it is 
limited strictly to the pyloric region, dilatation ensues because of the obstruc- 
tion. W r hen it is more diffuse, the stomach may be diminished in size. Very 
rarely does the overgrowth of connective tissue develop to such an extent as 
to make it possible to discover any mass by careful palpation. 

W T hen the condition is due to some congenital defect, the pathological con- 
dition is somewhat different. It is found that the organ is larger than normal 
and that its walls are thickened by overgrowth of its muscular fibres. At the 
pylorus these muscular fibres have undergone great hypertrophy, so that 
this part of the stomach feels like a solid mass between the fingers, and on 
section it is found to be dense and firm, the mucous membrane lining the 
part being thrown into folds which lie in the direction of the long axis of the 
organ. Sometimes one of these folds is so much larger than others that it 
aids in producing obstruction and seems to form a large part of the over- 
growth. Moynihan has well said that such a stomach may appear and feel 
much like the bladder and prostate when they have been removed by dissec- 
tion. If the duodenum is opened, the pyloric orifice may resemble that of 
the cervix uteri when it is seen through the vagina. The thickening of the 
muscular fibre is not always limited to the pyloric area, but sometimes 
extends into the duodenum. The longitudinal muscular layers are not 
greatly increased in size, and, although there is a general hypertrophy of the 
muscular element throughout the entire organ, it is often so slight at the 
cardiac end of the stomach that it is scarcely noticeable. 

Symptoms. — The symptoms of stenosis of the pylorus in adults consist in a 
sensation of fulness, pressure, and pain in the stomach. There are also evi- 
dences of motor insufficiency, and when the obstruction to the pylorus 
becomes marked, vomiting may come on to relieve the stomach of materials 
which cannot escape into the intestine. So, too, the patient may lose flesh 
as the result of interference with the digestion and with the retention of 
proper quantities of food. The hydrochloric acid of the gastric contents is 
usually diminished, probably because of the chronic gastritis which precedes 
the disease. 

Diagnosis. — It may be exceedingly difficult to differentiate hypertrophic 
stenosis of the pylorus in an adult from gastric cancer occurring in this por- 
tion of the stomach. In the article on Gastric Cancer it was pointed out that 



HYPERTROPHIC STENOSIS OF THE PYLORUS 597 

many of these patients give a history of perfect digestion and no gastric dis- 
tress until the cancer develops; but in hypertrophic stenosis there is usually a 
history of many years of discomfort, with a constant endeavor to find food 
which would not cause indigestion. The absence of cachexia, although the 
patient may be anaemic, also points toward hypertrophic stenosis. On the 
other hand, if the liver or gall-bladder seems to be affected, the condition is 
almost certainly carcinomatous. In some instances it is impossible to make 
a differential diagnosis without operation, and even then it may require a 
microscopic examination to determine that the thickening is not malignant. 
So far as probabilities are concerned, it may be stated that the presence of 
obstruction at the pylorus in a person at or past middle life is very much 
more likely to be carcinoma than hypertrophic stenosis, since the former 
condition is quite common and the latter condition is very rare. 

Difficulty may also be experienced in differentiating hypertrophic stenosis 
from cicatricial contraction due to the remains of an old gastric ulcer. The 
physical signs and symptoms present at the moment of examination "may 
give us no information, but the past history of the case may aid us materially. 
Thus, when gastric ulcer has been present, there may be a history of hemor- 
rhage and severe pain, which is absent in cases of stenosis. 

Congenital Pyloric Stenosis. — As already stated, the condition of 
pyloric stenosis, when not due to ulcer or cancer, is met with in the majority 
of cases in very young children, and in such is undoubtedly congenital. In 
such instances the child is born apparently healthy, and after two or three 
days, or several weeks, of life is seized with sudden and persistent vomiting, 
for which no errors in diet can be held responsible. The vomiting is often 
forcible and gives the child relief for the time being until more food is taken, 
when it recurs. The time during which the food is retained varies from a 
few minutes to several hours, and in some instances the mere act of swal- 
lowing seems to reflexly produce the motions of vomiting. In some 
instances the vomiting is sufficiently prolonged to empty the stomach thor- 
oughly; in others a considerable quantity of food may be retained. It is a 
noteworthy fact that even if the vomiting is severe, bile is never present in 
the ejected material, because the closed pylorus prevents it from being drawn 
from the duodenum. The result of the ejection of the food almost as soon 
as it is swallowed, combined with the deficient digestive function of the 
stomach which is nearly always present, is rapid emaciation, exhaustion, and 
death. Sometimes a period of semi-consciousness ensues, and occasionally 
the child is seized with a convulsive attack. 

The duration of life varies from four to five weeks to six months. 

As the disease progresses and emaciation becomes marked, it may be 
possible to see the outline of the stomach in its forcible contractions if the 
abdomen is carefully examined in a good light. If deep palpation can be 
practised, the thickened pyloric portion of the stomach can be felt forming 
a distinct contrast to the empty and collapsed intestines, which are pre- 
vented from containing their usual food and liquid by the obstruction at the 
pylorus. (See Fig. 82.) 

The points which are strongly in favor of hypertrophic stenosis of the 
pylorus in infancy are the causeless and persistent vomiting, the absence of 



598 



DISEASES OF THE STOMACH 



bile from the vomit, the constipation, the presence of a tumor in the pyloric 
area, the collapsed intestines and distended stomach, and the fact that gas- 
tric digestion is almost completely arrested, and, finally, that these symp- 
toms are present in a young child. 

Prognosis. — The prognosis in hypertrophic stenosis is unfavorable as to 
recovery, and it may be unfavorable as to life if the obstruction is very great. 
A very few cases are on record in which recovery without operation has 
occurred. 

Treatment. — The treatment consists in the use of lavage and in feeding 
through a rubber tube, so that the movements of swallowing are not neces- 
sary. In some cases it may be possible to prevent the vomiting by gently 
washing out the stomach before each feeding. When this measure fails, 
or if the symptoms are exceedingly severe, operative procedure must be 

Fig. 82 




Showing the gastric peristalsis. Note constriction of stomach by passing wave. 

(Ibrahim.) 

resorted to before the child is sufficiently exhausted to contraindicate the 
operation. The operation should either be pyloroplasty or gastroenteros- 
tomy. Moynihan states that anterior gastroenterostomy has been performed 
9 times, with 5 recoveries and 4 deaths, but 1 of these deaths was due 
to acute obstruction caused by a Murphy button. Loreta's operation of 
pylorodiosis has been performed 9 times, with 7 recoveries. 



HOUR-GLASS STOMACH. 



Definition. — Hour-glass stomach, sometimes called "bilocular stomach/' 
or " Sanduhrmagen," is a condition in which the stomach is divided into two 
parts by a contraction which may exist anywhere between the cardiac and 
pyloric orifices. Very rarely, indeed, a trilocular condition may be present, 
and, still more rarely, a quadrilocular state may exist. 



HOUR-GLASS STOMACH 599 

Etiology. — Hour-glass stomach may be congenital or acquired. There is 
some difference of opinion as to the relative frequency of these two forms, of 
the condition. Some authors have maintained that all cases are acquired, 
while others assert that the congenital cases are more common. Fenwick 
says that about 45 per cent, of the cases which have been so far recorded 
showed no sign of either ulcer or scar in the stomach, or if an ulcer or scar 
were present it was manifest that it was more recent than the stricture itself; 
and again he states that only 1 case of the acquired type has been found in 
the London Hospital in forty years, whereas several instances of the con- 
genital type were met with during the same period of time. To those who 
believe in the congenital origin of these cases, Moynihan is strongly opposed. 
He states that he has examined a number of specimens and searched the 
literature carefully, and can find no instance in which there is good ground 
for considering the contraction as congenital. He therefore contradicts 
those who think that the ulcer is secondary to the contraction. 

According to Moynihan, there are three causes of hour-glass contraction : 
first, perigastric adhesion; second, chronic ulcer; and third, malignant dis- 
ease. The perigastric adhesions are most commonly due to ulcer of the 
stomach or to a nearby inflammatory process set up by the presence of gall- 
stone. Chronic ulcer not only produces perigastric adhesions, but it may, 
in healing, cause much contraction and thickening of the stomach, so that its 
wall becomes puckered and its calibre decreased. Associated with this 
contraction, due to the formation of scar tissue, there is also a certain amount 
of muscular spasm, the circular muscular fibres contracting in such a way as 
to resemble a sphincter muscle. This spasmodic contraction accounts for the 
paroxysms of discomfort from which the patient occasionally suffers. 

Pathology and Morbid Anatomy. — On examining a stomach for the seat of 
hour-glass contraction, two sets of thickened muscular fibres, which cross one 
another, may sometimes be seen. These bundles are usually one-half inch 
or more in width, and cross one another at the point of contraction, and it is 
the shortening of these muscular fibres which produces the deformity. That 
this is not the cause in most instances, however, is shown by the fact that 
these muscular fibres are frequently absent, or, at least, are not abnormally 
developed. When the constriction is due to the formation of a cicatrix 
the narrowed band forming the dividing septum between the two pouches 
is composed of fibrous tissue; this may be puckered, indicating that it has 
followed an ulcer. 

Symptoms. — The symptoms of hour-glass contractions of the stomach are 
by no means definite. There are, however, certain physical signs which can 
be elicited in some cases which are of great importance. These methods are 
well described by Moynihan in the following words: 

"1. If the stomach tube be passed and the stomach washed out with a 
known quantity of fluid, the loss of a certain quantity will be observed when 
the return fluid is measured. Thus, if 30 ounces be used, only 24 ounces can 
be made to return. Woelfler, who called attention to this sign, said that some 
fluid seemed to disappear ' as though it had flowed through a large hole ' — as, 
indeed, it has, in passing from the cardiac to the pyloric pouch (Woelfler's 
' first sign'). 



GOO DISEASES OF THE STOMACH 

"2. If the stomach be washed out until the fluid returns clear, a sudden rush 
of foul, evil-smelling fluid may occur; or if the stomach be washed clean, the 
tube withdrawn and passed again in a few minutes, several ounces of dirty, 
offensive fluid may escape. The fluid has regurgitated through the connect- 
ing channel between the pyloric and cardiac pouches (Woelfler's ' second 

sign'). m ■ 

"3. Paradoxical dilatation. If the stomach be palpated and a succussion 
splash obtained, the stomach tube passed, and the stomach apparently 
emptied, palpation will still elicit a distinct splashing sound. This is due to 
the fact that only the cardiac pouch is drained; the contents of the pyloric 
pouch remain undisturbed and cause the splashing sound on palpation. For 
this phenomenon Jaworskihas suggested the appropriate name of ' paradoxical 
dilatation/ Jaboulay has pointed out that if the cardiac loculus be filled with 
water, a splashing sound can still be obtained by palpation over the pyloric 
pouch. The sign of paradoxical dilatation is best elicited after washing out 
the stomach in the ordinary manner. When the abdomen is examined at the 
completion of the washing, and when the stomach has been apparently 
drained quite dry, a splashing sound is readily obtained, for some of the 
fluid used has escaped into the pyloric pouch through the connecting channel. 

"4. Von Eiselsberg observed in one of his cases that on distending the 
stomach a bulging of the left side of the epigastrium was produced; after a 
few moments this gradually subsided, and concomitantly there was a gradual 
filling up and bulging of the right side. 

"5. Von Eiselsberg also called attention to the bubbling, forcing, ' sizzling' 
sound which can be heard when the stethoscope is applied over the stomach 
after distention with C0 2 . If the two halves of a Seidlitz powder are sepa- 
rately given and the stomach be normal or dilated, no loud sound is heard 
anywhere except at the pylorus; if a constriction is present in the stomach, 
a loud, forcible, gushing sound can be easily distinguished at a point two 
inches or three inches to the left of the middle line. 

"6. I (Moynihan) first called attention, two years ago, to a sign which I 
have since found of great service in establishing a diagnosis of hour-glass 
stomach. The abdomen is carefully examined and the stomach resonance is 
percussed. A Seidlitz powder, in two halves, is then administered. On 
percussing, after about twenty or thirty seconds, an enormous increase in the 
resonance of the upper part of the stomach can be found, while the lower 
part remains unaltered. If the pyloric pouch can be felt, or is seen to be 
clearly demarcated, the diagnosis is inevitable, for the increase in resonance 
must be in a distended cardiac segment. If the abdomen be watched for a 
few minutes the pyloric pouch may sometimes be seen gradually to fill and 
become prominent. 

"7. Schmidt-Monard and Eichhorst have both seen a distinct sulcus 
between the two pouches inflated with C0 2 . In one case the two 
pouches, with a hard — as I thought malignant — mass between them, could 
readily be seen. When both pouches were distended with C0 2 , alternate 
pressure upon them showed unmistakably that they communicated through 
a very narrow orifice, for the one could be emptied slowly into the other, and 
the fluid could be felt to ripple gently through. The diagnosis in such a case 



GASTRIC NEUROSES 601 

is simplicity itself. In another case a distinct notch was seen at the lower 
border of the inflated stomach. 

"8. Ewald has called attention to two signs which he considers of value in 
establishing a diagnosis. When the stomach is filled with water and exam- 
ined by gastrodiaphany, the transillumination is seen only in the cardiac 
pouch; the pyloric pouch remains dark. 

" 9. The deglutable India-rubber bag of Tiirck and Hemmeter is passed 
and distended. The bulging caused thereby is limited to the cardiac pouch, 
which lies to the left of the middle line. 

4 'The two aids to diagnosis of greatest value are, it will be seen, the wash- 
ing out of the stomach and its inflation with gas by the administration of a 
Seidlitz powder in two portions. The fluid used for the washing must be 
carefully measured before being used; the tube is then passed and the 
stomach emptied, the contents set aside in a separate dish, and the wash- 
ing commenced. All the fluid now returning is collected in a separate 
vessel and carefully measured. The two signs of Ewald are of little 
importance; a correct diagnosis can always be made without them." 

Treatment. — The only treatment for hour-glass contraction which can 
afford any relief is operative. Thus, a gastroenterostomy may be done 
from both pouches, or gastroplasty or pyloroplasty may be necessary. For 
these operations the reader is referred to books on surgery. 



GASTRIC NEUROSES. 

At the present time several states of the stomach are known to exist which 
depend upon an altered or perverted nerve supply, and are not connected 
with any pathological lesion which our methods of examination can detect. 
Gastric neuroses are not commonly met with as conditions independent of 
true lesions, and the physician must not rest satisfied with a diagnosis of 
gastric neurosis until he has exhausted every possible means of discovering 
an actual morbid change. In some instances the nervous affection of the 
stomach is a manifestation of disease of the central nervous system; in others 
it is a sign of perverted nervous function due to neurasthenia or nervous ex- 
haustion, and in still other cases it may be dependent upon growths which, 
being situated in adjacent tissues, press upon the gastric nerves and so cause 
pain or spasm. Finally, it is to be remembered that even if the physician can 
discover no sign of gastric lesion, this does not justify a diagnosis of gastric 
neurosis, because it not rarely happens that disease elsewhere causes pain 
which is incorrectly referred by the patient to the region of the stomach. 
Thus, a child with pericarditis or appendicitis may complain bitterly of 
epigastric pain. 

True gastric neuroses may be divided for study into three classes, viz., 
disorders of mobility, disorders of sensation, and disorders of secretion, and 
these in turn are divisible into states of excitation and depression. 

Cardiospasm, or cramp of the muscular fibres in the cardiac end of the 
stomach, is a result, as a rule, of irritation of the gastric mucous mem- 
brane by superacid secretion. Occasionally it may develop as the result 



602 DISEASES OF THE STOMACH 

of distention of the stomach by gas, and in some instances no direct cause 
for its existence can be discovered save that a state of nervous unrest and 
instability is present. Cramp of the cardia appears in an acute and fleeting 
form, and as a chronic condition which causes great distress and may be 
serious, in that it exhausts the patient. In the former cases pain and spasm 
seize the patient and then pass away. In the latter it often happens that the 
patient has difficulty in swallowing and expresses the feeling that the food 
cannot enter the stomach, but remains in the oesophagus. If the taking of 
food is persisted in, it speedily accumulates in the oesophagus, and when 
this tube is distended the patient regurgitates the food undigested and 
devoid of gastric juice, for it has never entered the stomach. The emaciation 
which follows this inability to take food may lead to the belief that a gastric 
carcinoma is present, particularly if the patient is advanced in years. When 
chronic cardiospasm lasts for a long time, dilatation of the oesophagus may 
develop, and even a diverticulum may be formed. 

Treatment. — The treatment consists in the use of remedies designed to 
prevent and counteract excessive gastric acidity, the avoidance of all irritat- 
ing or stimulating forms of food and drink, the use of lavage if there is any 
evidence of chronic gastric catarrh or of fermentation in the stomach, and in 
feeding through a stomach tube if there is any difficulty in giving the patient 
a proper amount of nourishment. Boas states that in some cases solids are 
taken more readily than liquids. Sedatives, such as chloretone, the bromides 
and chloral, may be used. Sometimes galvanic electricity gives relief, using 
for its application an intragastric electrode. In some instances the daily 
passage of a large-sized gastric or oesophageal bougie produces a cure. 

Pylorospasm. — Pylorospasm is nearly always secondary to lesions else- 
where, although a primary spasm may occur. In pylorospasm a contraction 
wave may be seen in a thin patient endeavoring to urge the gastric contents 
through the closed pyloric orifice, and if the spasm is persistent the stomach 
contents will not only be retained, as in gastric dilatation, but they may 
undergo fermentative changes as well, so that symptoms of chronic gastric 
catarrh or dilatation may be present. In other cases a reversed peristalsis 
is set up and vomiting comes on, so that symptoms like those of hypertrophic 
pyloric stenosis ensue. The treatment is identical with that of cardiospasm. 

Gastric Hyperperistalsis, called by Kussmaul "peristaltic unrest," is a 
condition in which the stomach almost incessantly continues to maintain 
peristaltic movement. As a rule, it is most active after meals, but it may be 
present when the stomach is empty, and even persist at night during absolute 
rest. Although marked pain is usually not present, the incessant movement of 
the stomach causes restlessness and gastric discomfort. Often the wave-like 
movements of the stomach can be felt through the abdominal wall, and their 
progress is from left to right. These undulatory movements are not demon- 
strable, as a rule, unless some gastric dilatation is present and the belly wall 
fairly thin. Three causes are recognized, viz., excessive acidity producing 
irritation, great reflex excitability, and, most important of all, stenosis of the 
pylorus, which obstructs the flow from the stomach. 

Treatment. — The treatment consists in the use of sedatives, such as the 
bromides, chloral, codeine, and hyoscyamus, and in the use of counter- 



GASTRIC NEUROSES 603 

irritation over the epigastrium. Not rarely an absolute rest cure, with rectal 
feeding for a week, may be needful to cause gastric quiet. Causes which 
produce nervous exhaustion and undigestible foods are to be forbidden and 
hydrotherapeutic measures should be instituted. 

Merycismus. — Merycismus is a neurotic condition in which the patient 
has the ability at will to regurgitate the food from the stomach into the mouth 
for the purpose of rechewing it, as is done by ruminants. It is usually met 
with in neurotic degenerates. 

Nervous Eructation. — Nervous eructation is not a very rare affection. The 
patient is usually very nervous and will often sit for hours " rifting up" gas, 
which, in many cases, is really swallowed air. In other cases the movements 
of eructation are performed without any gas being brought up. This condi- 
tion is commonly seen in hysteria. It is best treated by the rest-cure and 
the administration of tonics or nervous sedatives, such as the bromides, 
spirit of chloroform, asafoetida, or chloretone. 

Closely related to nervous eructation is nervous vomiting. 

Hyperesthesia. — Among the sensory disorders of the stomach is hyper- 
esthesia, in which the taking of food causes great gastric distress, so that the 
patient refuses to eat enough to maintain nutrition. In hysterical cases the 
patient may be able to eat what she wishes, yet has pain when other 
articles of food are given to her. 

This condition is to be separated from the hyperesthesia due to gastric 
ulcer, since it sometimes develops when this lesion is not present. Some- 
times it seems to arise from the abuse of alcohol, coffee, ice, or certain drugs, 
such as quinine and the salicylates, or tobacco. In other instances it arises 
from nervous exhaustion due to sexual excess, great mental strain, pro- 
longed lactation, or menorrhagia. So, too, it may develop in the course of 
chlorosis, and while in the majority of instances this condition in chlorosis 
points to ulcer, the possibility of no ulcer being present must be considered, 
in view of our knowledge of the existence of this state. 

Symptoms. — The symptoms consist in a sense of fulness and distention of 
the stomach, particularly in the neighborhood of the cardia, with some aching 
or burning, which extends upward under the ribs. Constipation is usually 
present. As the condition advances the disagreeable sensations in the 
stomach become so severe as to amount to pain, and the taking of food usually 
greatly increases the suffering. When fully developed the patient often 
suffers from vomiting, which may occur after every meal. In ulcer, vomit- 
ing usually gives temporary relief, but in hyperesthesia of the stomach it 
does not. If the disease persists, there is emaciation due to the pain and 
constant vomiting. The skin over the epigastrium is usually hypersesthetic, 
and the tenderness on deep palpation is diffuse and not localized as in ulcer. 
An examination of the gastric contents usually reveals a normal acidity, but 
in some cases the acidity may be above or below the normal. 

Gastralgia. — Gastralgia, gastrodynia, or gastric neuralgia, may be a cause 
of much severe suffering, for the patient may be seized by a paroxysm of 
pain which seems as violent as a renal or hepatic colic. This pain is felt not 
only in the epigastrium, but along the edges of the floating ribs to the spine, 
and it often recurs with a peculiar periodicity. It is not rare in hysteria and 



G04 DISEASES OF THE STOMACH 

neurasthenia. The gastric crises of locomotor ataxia, the pain of ulcer, 
and that caused by gas must be carefully excluded before a diagnosis of 
gastralgia is reached; indeed, a diagnosis of simple gastralgia should always 
be looked upon with suspicion, because gastric pain is so commonly due to 
some organic cause. Unlike the pain of ulcer, this form is usually relieved 
by taking food. 

Bulimia. — A neurosis of the stomach characterized by excessive hunger 
and the ingestion of great quantities of food to alleviate the discomfort is 
called "Bulimia." It is usually met with in cases of hysteria, in cases of 
exophthalmic goitre, and in cerebral tumor, and epilepsy. 

Anorexia Nervosa is a form of neurosis with persistent lack of appetite. 

Nervous Disorders of Secretion. — A form of nervous disorder of secre- 
tion consists in hypersecretion of gastric juice, producing the ordinary 
symptoms due to acid stomach. It is often met with in chlorotic girls, and 
is usually associated with constipation. The excessive secretion may occur 
in paroxysms or be continuous. 

The antithesis of this state is that in which there is an absence of secretion, 
sometimes called achylia-gastrica nervosa. This state of absence of HC1 is, 
of course, common in gastric cancer, and it arises also from atrophy of the 
gastric tubules, but there are instances in which, apparently because of dis- 
ordered nerve supply, there is absence of secretion for weeks, months, or even 
years, yet finally it is perfectly re-established. 

Treatment. — The treatment of these disorders of sensation consists in the 
institution of a rest cure for the rehabilitation of the patient's nervous tone; 
in the use of hydrotherapeutic measures and electricity designed to bring 
about the same result, and in the prescription of a mode of life which will 
avoid nervous worry and strain, provide a sufficient number of hours of sleep 
and out-door exercise, and prevent the ingestion of articles of food which are 
difficult to digest or irritating to the stomach. For the prevention or relief 
of painful or disagreeable sensations, a number of remedies may be employed. 
Not infrequently a dose of a drachm of spirit of chloroform and a drachm of 
compound spirit of lavender in a little water will dispel gas and distention 
and act as a sedative to the stomach. In other instances J to 1 grain of 
menthol may be given in capsule or pill. In still others one of the coal-tar 
products, as antipyrin, acetanilid, or phenacetin, may be used, and in some 
instances much relief will be obtained by the use of chloretone in capsule or 
tablet in 3 to 5 grain doses. Where there is a distinct hysterical element 
and it is considered desirable to exercise a mental influence, the stomach tube 
may be passed once or twice a day. If an excessive secretion of hydrochloric 
acid is present, associated with much nervousness, the bromides may be 
employed, or nitrate of silver and hyoscyamus may be used. 



HEMORRHAGE FROM THE STOMACH. 

Hemorrhage into the stomach is called gastrorrhagia, and when the blood 
is vomited the condition is one of hcematemesis. It may result from rupture 
of dilated gastric and oesophageal veins, from ulcer of the stomach, from 



HEMORRHAGE FROM THE STOMACH 605 

cancer of the stomach, and from dilatation of the gastric veins in chronic 
gastric catarrh. It has also been known to follow severe injuries over the 
epigastrium. Occasionally the vomiting of blood has been due to an aneurysm 
which has perforated the oesophagus and then drained into the stomach. 
The physician must also remember that malingerers sometimes swallow 
blood for the purpose of deceiving their attendants. Sometimes " coffee- 
ground vomit," due to the presence of altered blood, is met with in cases of 
gastric cancer, in certain forms of purpura, in haemophilia, and in persons 
suffering from such poisons as phosphorus and carbolic acid. Occasionally, 
too, in cases of exceedingly severe infectious disease, such as yellow fever 
and smallpox, vomiting of coffee-ground material occurs. By far the most 
frequent causes of bloody vomiting, however, are cirrhosis of the liver, ulcer, 
and cancer of the stomach. When due to cirrhosis it is usually met with in 
males, and when due to ulcer it most commonly occurs in females. 

Preble has made a most complete statistical study of gastrointestinal 
hemorrhage in hepatic cirrhosis, and finds that the great majority of cases 
occur in the atrophic form, although occasionally hemorrhage takes place 
in hypertrophic cirrhosis. In one-third of the cases the first hemorrhage 
is fatal; while in the other two-thirds the hemorrhage occurs at intervals 
varying from a few years to several years, the longest duration being over a 
period of eleven years. 

In some instances it is possible to make the diagnosis of hepatic cirrhosis, 
but in other instances the change in the size of the liver is so slow that not 
for months after the hemorrhage occurs is this organ found to be smaller than 
normal. In 80 per cent, of the cases, according to Preble, there are varices in 
the oesophagus, and in more than one-half of these there are evidences of 
their rupture (Fig. 83). It has also been found that fatal hemor- 
rhages may occur in cases which do not suffer from oesophageal varices. 
These cases are probably due to the rupture of a large number of capillaries 
in the alimentary mucous membrane. It is interesting to note that in only 
6 per cent, of the cases which showed oesophageal varices was the cirrhosis 
typical in the sense that the ordinary symptoms of this condition were 
present. Very profound hemorrhages may come from a very small open- 
ing in a bloodvessel, so that at autopsy it may be almost impossible to 
discover the source of the bleeding. 

Aside from the actual vomiting of blood, the symptoms of gastric hemor- 
rhage are those of ordinary hemorrhage, namely, 'pallor, faintness, or 
actual syncope, and sometimes death. The vomited blood, if it has been 
poured out in large quantities, is somewhat venous in color and filled with 
clots, and if it remains in the stomach any length of time it may become 
brown or granular in appearance, through the action upon it of the digestive 
juices. It must always be remembered that the quantity of blood vomited 
does not necessarily indicate the quantity of blood which has escaped from 
a bloodvessel, as a very large amount may leak into the stomach before 
vomiting occurs, and the stomach in vomiting may not completely empty 
itself. Care must be taken in determining that the blood comes from the 
stomach, and that the red color is really due to blood. Sometimes a bloody 
color of the vomit may be due to claret or the juice of various berries, A 



606 



DISEASES OF THE STOMACH 

Fig. 83 




Dilated venules in lower part of oesophagus due to hepatic cirrhosis. (Kast a nd Rumpler.) 



CYCLIC VOMITING 607 

distinction can be made by a microscopic examination, by the history of the 
ingestion of certain articles of food, and, if need be, by the use of the spectro- 
scope and the various tests which are employed to determine the presence 
of blood. It must also be borne in mind that persons who suffer from nose- 
bleed, in which the leaking vessel is far back in the nose, may swallow con- 
siderable quantities of blood and then vomit it. 

Hemorrhage from the lungs, or haemoptysis, is to be separated from haema- 
temesis by the fact that in hemorrhage from the lungs the blood comes up 
with coughing, and in hemorrhage from the stomach by vomiting, although 
at times both of these symptoms may be present in each class of cases. The 
characteristic appearance of a patient well advanced in tuberculosis will be 
of great diagnostic aid in such cases, and an examination of the chest in the 
case of haemoptysis will usually reveal some lesion; whereas, the lungs will 
be clear in haematemesis. In a case of haematemesis an examination of the 
abdomen may reveal an atrophied liver and an enlarged spleen, or some 
other abdominal state, such as the caput medusae, which will indicate that 
there is venous stasis in the abdomen. (See Hepatic Cirrhosis.) In haemop- 
tysis the blood is pink and frothy. In hemorrhage from the stomach it is 
dark, has little air mixed with it, and is often acid in reaction; whereas, that 
in haemoptysis is usually alkaline. In haemoptysis no dark, tarry stools are 
present, but they are frequently seen after an attack of haematemesis. A 
day after an attack of haemoptysis the patient may cough up some thick- 
ened, bloody mucus, but there is no difficulty in separating this from the 
more fluid, dark blood from the stomach. An additional aid in the diagnosis 
of haematemesis is Boas' test given in the article on Gastric Ulcer. 

Notwithstanding the profound mental shock and vital depression which 
often follows a profuse hemorrhage from the stomach, it is worthy of note 
that death very rarely occurs as the immediate result of this loss of blood, 
unless the patient is already devitalized by advanced disease or repeated 
hemorrhages. 

For the treatment of bloody vomiting see Treatment of Gastric Ulcer. 



CYCLIC VOMITING. 

Under the name of cyclic, periodical, or recurrent vomiting, a condition 
has been rarely met with in which, at certain periods, a child is seized by an 
attack of persistent vomiting, which not only continues while the stomach is 
being emptied of its normal contents, but persists for many hours afterward, 
and in some instances ends fatally. The condition in all probability depends 
upon a form of autointoxication. This autointoxication consists, appar- 
ently, in a condition of acidiosis. Marfan believed that it was due to an 
acetonaemia. Edsall, on the other hand, who has studied the disease most 
carefully, and who has done much work upon the subject of acid intoxication, 
reports 5 cases in which, at the time of the attacks, this condition existed. 
The urine between the paroxysms was normal, but immediately before the 
attack contained diacetic acid and acetone. He found that the immediate 
administration of large doses of bicarbonate of soda, as much as 2 drachms, 



608 DISEASES OF THE INTESTINES 

prevented attacks which seemed impending. He contradicts the theory of 
Marfan as to the cause of acetonemia, and does not think that acetone, as 
such, ever appears in the blood. 



DISEASES OF THE INTESTINES. 

DIARRHOEA. 

Diarrhoea is not a disease, but a symptom, just as headache and dropsy 
are symptoms. It occurs, however, from so many different causes and is so 
often present without the presence of any organic change in the intestinal 
walls that it is best considered as a malady, at least in several of its forms. 
Diarrhoea is the symptom or condition, above all others, in some cases, but 
in others it is of little significance as compared to the organic lesion which 
produces it. 

Serous Diarrhoea. — Serous or watery diarrhoea may arise from the inges- 
tion of irritating foodstuffs, which cause the intestinal mucosa to become 
hypersemic and to pour into the calibre of the bowel the serum of the blood, 
to dilute the poison, and to wash it out of the intestine. In many instances 
the attack is very brief, and even if by an accident an autopsy is possible, no 
lesion may be found. 

In still other cases the same result may follow sudden exposure to cold and 
dampness, in which case, if the visceral congestion is severe, a secondary 
catarrh of the intestinal mucosa may develop as a later condition. 

In some instances a serous diarrhoea seizes persons who are, or who are 
about to be, subjected to a severe nervous strain, as actors at their first 
appearance, or medical students about to go before a severe examiner, upon 
whose verdict much depends. Such a nervous diarrhoea is not rarely met 
with in hysterical persons. 

Finally, in chronic renal disease, patients sometimes are seized by a pro- 
fuse watery purging designed, apparently, to eliminate from the body certain 
poisonous materials that the diseased kidneys permit to accumulate. 

All of these forms of serous diarrhoea occur without being accompanied 
by much pain and without the passage of much flatus. 

Treatment. — The treatment depends largely upon the cause of the dis- 
order. If it is due to the ingestion of bad food, the patient should receive a 
moderate dose of castor oil (£ to 1 ounce), and with it a dessertspoonful of 
paregoric to prevent griping. By this means the offending matter is swept 
out and a secondary constipating influence follows, or can be produced by 
the measures about to be referred to. 

Aside from this condition, all cases of serous diarrhoea are to be treated by 
rest, counterirritation in the form of a capsicum or mustard plaster over the 
abdomen, the application of external heat if the temperature falls, and the 



ILEOCOLITIS OF CHILDHOOD 609 

internal use of a grain of camphor every two hours for three doses, or of a 
mixture of aromatic sulphuric acid and fluid extract of hsematoxylon in syrup 
of ginger every two hours. All foods should be forbidden until the diarrhoea 
is to some extent controlled, when predigested milk, arrowroot, and broths 
may be allowed. 

When the purging is an effort at elimination in Bright's disease, care must 
be taken not to check the diarrhoea suddenly, lest toxsemia develop. 



CATARRHAL ENTERITIS. 

Acute and chronic catarrh of the small intestine are of frequent occur- 
rence, and the symptoms produced in the acute form may be very like those 
described under serous diarrhoea, save that, as a rule, there is more pain and 
griping in the bowels. In both conditions there is present at first an acute 
hyperemia of the intestinal mucosa, followed by a true catarrhal process, in 
which the glandular epithelium becomes swollen and the submucous tissues 
infiltrated with exudate. A careful examination of the mucous membrane 
reveals slight, if any distinct reddening, except at the edges of the valvulse 
conniventes. If the process has been subacute or chronic the intestinal 
mucosa is boggy and swollen, but not reddened, and the lymph follicles, as 
well as the mucous glands, are enlarged. After some days, rarely earlier, 
and not in all cases, the swollen solitary follicles may be the seat of superficial 
necroses, shown by yellowish, grayish, or grayish-yellow erosions surmount- 
ing each follicular eminence; such ulcers are rarely of any size. When the 
process has lasted many days the mucosa may be thickened. It is to be 
remembered that in all of these cases the changes are not confined to the 
small bowel, but are also present in the large intestine as well. 

Symptoms. — Aside from the diarrhoea and griping pain already referred to, 
the patient suffers from rumbling in the bowels due to hyperperistalsis, from 
loss of appetite, and weakness due to the abdominal discomfort and the 
serous purging. The stools may be light yellow and very fluid, and in the 
water which is discharged will be found particles of undigested food, cast-off 
epithelium, flakes of bile-stained mucus, and myriads of micro-organisms. 
The pulse is usually quick, and there may be fever of moderate degree. 

Treatment. — The treatment is rest in bed, counterirritation to the abdomen, 
and full doses of bismuth after the bowel has been swept out by castor oil. 

ILEOCOLITIS OF CHILDHOOD. 

Definition. — The ileocolitis of childhood is a state in which symptoms of 
gastrointestinal disorder develops, as manifested by purging, vomiting, and 
abdominal distress. It cannot be distinctly separated from the catarrhal 
enteritis of adults, either from the standpoint of pathology or symptom- 
atology, yet clinicians have universally recognized the fact that such a 
division at the bedside is advisable. 

Etiology. — The ileocolitis of infancy depends chiefly for its existence upon 
the action of micro-organisms and their poisons on the intestinal mucosa. 
39 



610 DISEASES OF THE INTESTINES 

This infection may be produced by a large number of organisms, some of 
which are not pathogenic when the child is in perfect health, and which only 
become competent to cause disorder or disease when, by some additional 
cause, the general or local vitality of the patient is reduced. Thus, it not 
rarely happens that the stools contain myriads of streptococci, staphylococci, 
the Bacterium lactis aerogenes, or the Bacillus pyocyaneus, the pathogenic 
micro-organism which causes green stools, and other bacteria. More impor- 
tant than all, the bacillus of dysentery of Shiga and Flexner is now known 
to be a cause in a large proportion of cases. (See Cholera Infantum and 
Dysentery.) 

The relationship of specific micro-organisms to the summer diarrhoea of 
children is well summed up by Pease and Shaw in the following sentences: 

"We think it can be fairly concluded that there exists a group of bacilli 
having, in general, similar characteristics which differentiate them from the 
typhoid bacillus on the one hand, and the colon bacillus group on the other, 
which can be said to have an etiological relation to most cases of endemic 
and epidemic dysentery, whether the same occur in adults or children. That 
there probably are rare epidemics of this disease in which the clinical course 
may not conform exactly to the usual type, in which bacteria other than the 
group of dysentery bacilli are the etiological factors. An example of this kind 
is the epidemic of dysentery due to the Bacillus pyocyaneus infection reported 
by Lartigau. 

"Whether the cases of summer diarrhoea in children not showing symp- 
toms of true dysentery, and not having been more or less closely associated 
with true cases of the disease, can be considered as uniformly caused by 
either of these two types of dysentery bacillus is still open to question." 

The causes that usually permit these organisms to develop are exposure 
to cold or excessive heat, so that the bowel is congested and its circulation 
impaired, and the use of foods which are unsuitable in kind or have become 
so by infection or chemical change. Winds carrying dust, flies carrying 
infection, and air carrying gases may all aid in impairing the quality of food. 
At times the condition develops as a result of an attack of an infectious 
disease, such as measles. Heat and humidity not only reduce the resistance 
of the child, but greatly increase the number of micro-organisms in raw foods, 
especially milk, in which they sometimes number as many as 100,000,000 per 
cubic centimetre. (Park and Holt. 1 ) 

Pathology and Morbid Anatomy. — The ileocolitis of childhood affects par- 
ticularly the lower part of the ileum and the colon, the extent depending 
upon the vital resistance of the child and the virulence of the infection. Even 
in those cases due to the bacillus of Shiga, the most varied lesions are found. 
The degree of pathological change varies wdthin wide limits. In some 
instances there is only a superficial catarrh, with some infiltration of the 
mucous membrane, while in others the submucous tissues are affected, and 
in still others areas of mucous membrane may slough. In these severe 
cases the mucous membrane of the entire alimentary canal may show more 
or less catarrh. 

1 Those interested in the effect of temperature, season, and milk supply upon infant mortality should 
read a statistical paper by Park and Holt in the Medical News, December 5, 1903. 



ILEOCOLITIS OF CHILDHOOD 611 

If the mucous membrane of the small intestine is examined at autopsy, its 
villi are found to be soft and swollen, so that the surface of the bowel presents 
a velvety aspect. In mild cases the hyperemia is not intense. A universal 
congestion is present in severe cases, and even punctate extravasations of 
blood may be seen. The solitary follicles are swollen and protrude above 
the surface in both the small and large bowel and at the summits of follicles 
beginning ulceration, which rarely is extensive, is noticeable. Peyer's 
patches may also be infiltrated, but they are rarely ulcerated. In 
severe or long-continued cases the solitary glands may ulcerate, but the 
agminated glands very rarely. An appearance which at first glance may 
be thought to be an ulcerated Peyer's patch will be found to be due to the 
running together of several ulcers of solitary follicles. 

In severe cases a condition of acute membranous enteritis develops, the 
lower ileum and colon being covered by a thin false membrane, which can 
be seen in some cases only with difficulty. This membrane may be of a 
yellowish-green hue and it lies over a part of the bowel which is greatly 
thickened by an inflammatory process which involves its deeper coats. 
Curiously enough, ulceration of the mucous membrane in such an area is 
unusual. 

Symptoms. — The symptoms of acute ileocolitis in childhood vary greatly 
in their severity and duration. In the mild catarrhal form there is a slight 
rise of temperature of from 1° to 2°, with several loose movements of the 
bowel each day. These stools have a little mucus in each of them and perhaps 
a few small flecks of undigested food. 

If the condition is more severe there is pain in the bowels, with vomiting, 
high fever, and the frequent passage of yellow or greenish stools containing 
mucus and considerable amounts of undigested food, and if the condition 
persists the mucus may become streaked with blood, and tenesmus may be 
severe. There is little flatus and little odor to the passages. The tongue is 
coated and anorexia is marked. 

Because of the fever, vomiting, and diarrhoea, the patient is rapidly pros- 
trated and loses flesh with remarkable speed. 

If the course of the colon is palpated through the tumid abdominal wall, 
some tenderness is usually found. As recovery begins the stools become 
less frequent, have a more normal color, the quantity of mucus decreases, 
and the fever falls. If, on the other hand, at the end of a week or two there 
is no change for the better, the more severe state, in which ulceration of the 
intestinal lining takes place, is probably present, and death may ensue from 
exhaustion and depression, with signs of toxaemia. 

If recovery takes place it is very slow, a tendency to looseness of the 
bowels persisting for weeks, mucus being seen in almost every stool, and a 
relapse being threatened at each change in weather or in the food. 

In the well-developed ulcerated form the systemic disturbance is profound 
and often sudden in onset, and its very severity may serve to prevent a sharp 
febrile reaction. The stools are often much fewer per day than in the catarrhal 
form, but they contain more mucus and less blood. Unlike the stools in the 
milder type, these passages smell badly. The belly is distended and the general 
loss of flesh is very severe. The mouth and tongue are dry and foul. 



612 DISEASES OF THE INTESTINES 

In the membranous form the stools contain mucus and blood and par- 
ticles of false membrane, which are easily discerned if the stools are first 
mixed with water and then strained through a sieve. The degree of pros- 
tration and evidence of toxaemia in these cases is very severe, and upon the 
prolapsed rectal mucous membrane the false membrane may be sometimes 
seen. At times such cases present at onset, or late in the disease, severe 
cerebral symptoms which may mask the intestinal state. 

Diagnosis. — Ileocolitis must be separated from the typhoid fever of infancy. 
In most cases this is not difficult, because in the typhoid fever of children 
constipation is often present, and the rose spots may be found. The chief 
diagnostic points which separate the two affections are that enteric fever is 
rare and ileocolitis common, that in enteric fever the onset is usually gradual; 
in ileocolitis it is acute. In one there is an enlarged spleen and the Widal 
reaction; in the other neither one of these signs is present. If the illness 
is due to the Bacillus dysenteric, the agglutination test may reveal that fact. 
(See Dysentery.) 

Prognosis. — The prognosis depends upon several facts. Young children 
fare worse than children after the fourth year. City-bred children succumb 
more rapidly than children in the country, particularly if the weather is hot. 
Children who are strong and hearty at the onset have a better prospect than 
poorly nourished weaklings. High fever, many stools, much vomiting, much 
mucus, marked nervous symptoms and signs of toxaemia are of evil omen. 

Treatment. — The treatment of ileocolitis consists in the application of 
mild, continuous, counterirritation over the abdomen by means of a spice 
poultice, which consists of equal parts of powdered nutmeg, allspice, cloves, 
and cinnamon, moistened with warm brandy or vinegar. If this cannot be 
had a mustard plaster, composed of one-quarter to one-half mustard flour 
and wheat flour, may be applied, the idea being to produce continuous, but 
not severe, counterirritation. 

The child's diet should be carefully regulated. If it is passing undigested 
food in its stools, those articles which are not being properly dealt with 
by the digestive apparatus should be withheld. If undigested curds of 
milk are present, milk should be stopped, or diluted sufficiently to make its 
digestion easy, and pepsin and hydrochloric acid, or pancreatin with bicar- 
bonate of soda, should be used to aid digestion. Beef-juice, or beef-broth, 
and chicken-broth may be administered, and if the child is not a very young 
infant their nutritional value may be greatly increased by adding to them 
strained barley or wheat gruel. The digestion of these vegetable broths 
should be aided by the use of liquid pancreatin or liquid taka-diastase. If 
there are any evidences of inactivity of the liver, minute doses of calomel 
every third or fourth day are advantageous. 

If mucus is present in considerable quantity in the stools a moderate dose 
of castor oil, varying from a drachm to a tablespoonful, may be used once 
or twice. Griping may be prevented by the addition of a few drops of 
paregoric. 

In some instances small doses, such as 1 or 2 grains of chloride of ammo- 
nium dissolved in fluid extract of licorice and water, may be given twice or 
thrice a day. 






CHOLERA INFANTUM 613 

If the illness occurs in hot weather, it may be impossible to produce a 
cure without the aid of a change in climate. If the child's home is in the 
city, removal to the seashore may be absolutely necessary; whereas, if the 
condition develop while at the seashore, removal to a moderate altitude of 
1000 or 2000 feet is advisable. 

Antidysenteric serum may be given if an examination of the stools reveals 
the presence of the Bacillus dysenteric. 



CHOLERA INFANTUM. 

Definition. — Cholera infantum is an acute affection of infancy charac- 
terized by profuse watery purging, rapid emaciation, and profound depres- 
sion. It is so closely related to that form of diarrhoea due to catarrhal 
enteritis in adults and to that met with in the ileocolitis of infancy that it 
scarcely deserves a separate consideration from the standpoint of etiology 
and pathology, yet its symptom-complex aids us to some extent in making 
it a distinct entity at the bedside. The malady is almost always met with 
in the hot months of the year. 

Etiology. — The causes of cholera infantum are practically identical with 
those of enterocolitis, and in a considerable number of cases the bacillus of 
dysentery (Shiga's bacillus) is the cause. Thus, in a series of cases of typical 
summer diarrhoea occurring in Baltimore, Duval and Bassett isolated this 
bacillus from no less than 42 patients. It was found in large numbers in the 
stools of acute cases and in the mucous membrane of the bowel. They 
could not find this bacillus in the stools of 25 healthy children, nor in those 
of patients with ordinary diarrhoea. 

Pathology and Morbid Anatomy. — When a case of cholera infantum comes to 
autopsy the mucous membrane lining the bowel presents a peculiar pallor, 
which is most marked in the ileum. The colon may show areas of conges- 
tion. The tissues of the body are shrunken because of the profuse purging, 
the body is wasted, the skin wrinkled, and the eyes sunken. The belly may 
be distended or collapsed. If enterocolitis has been present before the 
severe choleraic character of the purging is developed, the lesions described 
under the discussion of that disease may be found. 

Symptoms. — Cholera infantum receives its name because its chief symp- 
toms are like those of Asiatic cholera, in that profuse watery purging, inces- 
sant vomiting, and collapse soon develop. The pulse rapidly becomes weak 
and feeble, the extremities cold and the face pinched, so that the expression 
of the child may be shrunken like that of a very aged person. This anxious, 
pinched look, with a peculiar drawing down of the mouth, as if the child 
were about to cry, is very characteristic. The fontanelles are depressed. 

i\.t first the child may be exceedingly restless and peevish, but if the attack 
is severe it speedily becomes apathetic, listless, and finally comatose. 
Although the peripheral temperature is low, the rectal temperature is often 
very high, even to 105° or 106°. There is often a mottling of the skin, due 
to the poor capillary circulation. Thirst is excessive, and cannot be relieved 
because of constant vomiting. The urine is scanty or suppressed. As the end 



614 DISEASES OF THE INTESTINES 

approaches, the patient develops irregular respirations, the head is retracted, 
the temperature is subnormal, and the life ends. When the cerebral symp- 
toms are marked, the condition is called one of "spurious hydrocephalus," 
a most unfortunate and inaccurate name. 

The symptoms are not only those of exhaustion, but of profound toxaemia 
as well. 

Prognosis. — Given a case of well-advanced cholera infantum, the prog- 
nosis is very grave. It depends upon the vitality of the child, the severity 
of the purging and vomiting, the degree of response to treatment, and the 
age of the patient, for very young infants seldom recover if the disease is once 
well developed. 

Treatment. — The treatment of cholera infantum consists first of all in the 
absolute prohibition of milk for twelve or twenty-four hours after the patient 
is first seen. It matters not whether the milk be from the breast or from the 
bottle, it must nevertheless be withheld from the child. Indeed, it may be 
said that there is little use in treating these cases medicinally if milk is given. 
This is particularly so when undigested particles of milk are passed in the 
stools. 

During the period in which milk is forbidden, the child should receive 
5 to 10 drops of Valentine's beef-juice in 1 or 2 tablespoonfuls of cool 
water every hour or two, according to its thirst and its age. In other 
instances a rump steak may be heated sufficiently to start its juices, 
then squeezed in a meat-press or lemon-squeezer, and this juice, pure or 
diluted with cool water, may be given to the child. When these juices cannot 
be obtained, or where for some reason they cannot be taken, barley-water, 
rice-water, or a water made by boiling and straining wheaten grits may be 
used. 

Over the abdomen of the child should be applied a spice plaster, com- 
posed of a tablespoonful each of powdered allspice, cloves, nutmeg, and 
cinnamon. This should be moistened with warm brandy or vinegar, and 
renewed as frequently as it becomes hard or dry. 

The child should receive internally -^ of a grain of podophyllin dissolved 
in a few drops of brandy, and mixed with a little water just before it is taken, 
every hour until three or four doses have been used; or, instead, ^-J-g- of a 
grain of bichloride of mercury may be given in the same manner. If the 
vomiting is incessant, it may be necessary to get the solution of bichloride or 
podophyllin into the stomach by dropping the medicine into the mouth of the 
child with a medicine-dropper, and only introducing a few drops at a time. 
It is of the greatest importance that the liver shall secrete and expel bile into 
the intestine. The appearance of a little bile upon the diaper of the child in 
place of the colorless liquid which has previously been expelled is a most 
encouraging sign, and its absence is correspondingly discouraging. 

If there is much distention of the abdomen, some relief to the tympany 
may be given by introducing a rectal tube through which the gas may escape, 
and if the stools are exceedingly fetid and musty it is often advantageous to 
irrigate the lower bowel with normal salt solution once or twice a day, insert- 
ing into the rectum alongside the nozzle of the fountain syringe a soft-rubber 
catheter, through which the injected material may readily return. The tube 



VPP i:\dicitis 615 

attached to the syringe should, however, pass up into the bowel for 
eight inches or a foot; while the tube of exit should be just within the 
sphincter. 

If much tenesmus is present, with a tendency to eversion of the bowel, 1 
or 2 tablespoonfuls of olive oil containing 2 grains of iodoform may be 
injected once or twice a day, or even oftener, for its local anaesthetic effect 
upon the intestine, and after this injection the anus should be supported by 
the nurse's hand, the ball of her thumb, covered by a napkin, being placed 
between the buttocks to aid in the retention of the fluid. In children, older 
than six or eight months, good results sometimes follow the use of weak sul- 
phuric acid solutions. Thus, 1 minim of aromatic sulphuric acid may be 
given in 4 tablespoonfuls of cool water every two hours. The acid not 
only acts as an astringent, but it probably also aids in destroying infecting 
micro-organisms. 

When symptoms of collapse ensue the patient should be surrounded by 
hot bottles, but care should be taken that a peripheral low temperature is 
not considered as representing the temperature of the central portions of 
the body, which are often highly febrile. When the peripheral temperature 
is low, the central temperature high, and the circulation in the peripheral 
capillaries is impaired, so that the child is somewhat livid and its skin mot- 
tled, excellent results will often be obtained by immersing it several times, 
for a fraction of a minute, in quite hot water for the purpose of producing 
a certain amount of reaction, relieving internal congestion, and bringing the 
blood to the surface. If marked fever is present and the extremities are hot, 
equally good results may come from the use of a cold bath or cold sponging 
with friction. 

Some practitioners have been in the habit of employing minute doses of 
morphine, hypodermically, or by the mouth. In some instances this method 
of treatment may be advantageous, but too often it seems to increase the 
toxaemia from which the patient is suffering. 

A very valuable method, which should always be recollected in desperate 
cases, is the use of normal salt solution by hypodermoclysis. 



APPENDICITIS. 

Definition. — Appendicitis is an inflammation involving the appendix vermi- 
formis. 

History. — Although inflammation of the appendix vermiformis had been 
described by a number of physicians many years before Reginald Fitz, of 
Boston, prepared his classical paper on this subject in 1886, the importance 
and frequency of this condition was not appreciated until he called attention 
to it. 

Etiology. — The causes of appendicitis may be divided into two classes, 
namely, those that depend upon the anatomical structure and position of the 
appendix and those that arise as the result of changes in its walls. 

The appendix vermiformis is a vestige of what was a large and important 
portion of the alimentary canal in our early evolutionary ancestry, and, like 



616 DISEASES OF THE INTESTINES 

most vestiges of this character, its tissues are possessed of less vital resist- 
ance than are those of active organs. This is the first reason why severe in- 
flammatory processes so often arise in it. Again, it is a sac the neck of which 
is usually narrower than the rest of its cavity, and as a consequence it happens 
that infecting micro-organisms find their way into it, and when imprisoned 
there by swelling of the mucous membrane rapidly attack and destroy the 
epithelial lining of the appendix and migrate into its walls. As is well known, 
nothing is more favorable for the growth of micro-organisms than the pres- 
ence of warmth, moisture, and a condition in which drainage is impossible. 
Nothing is less favorable to the vital resistance of a part than swelling, 
with pressure upon the bloodvessels and lymphatic channels. Still another 
anatomical cause of disease in the appendix is the fact that the mesoappen- 
dix is very short, and this results in the appendix being curved or drawn on 
one side. The mesoappendix carries the chief bloodvessel which nourishes 
the appendix, and if from swelling, or other cause, the appendix is distorted 
or twisted, the circulation of blood in the nutrient vessels may be so impaired 
that the vitality of the part is greatly decreased. Again, in those cases in 
which the appendix is very long (for it varies in length from one to six inches) 
the free end may become attached to other parts and become greatly dis- 
placed, the appendix itself being twisted. Finally, the fact that the appendix 
lies near, or on, the ileopsoas muscle may aid in provoking appendicular 
irritation, and this is probably one of the reasons why appendicitis so often 
follows violent rowing, golfing, and bicycling. 

Among the causes which exist in the appendix itself, in the sense that they 
are present in its cavity, is the presence of fecal concretions (20 per cent.), 
and rarely foreign bodies, of which a multitude have been recovered, such 
as pins, tacks, seeds, and other objects accidentally swallowed. Occasionally 
intestinal worms, amcebpe, and other parasites have been found. Foreign 
bodies, however, are comparatively rarely found in this viscus (less than 4 
per cent.). Primary tumor of the appendix, of which a number, mainly 
carcinoma, have been reported, appears to be at least a predisposing cause 
in some instances. 

In a very large proportion of cases, nearly 85 per cent., the micro-organism 
which is directly responsible for the inflammation is the Bacillus coli com- 
munis, which is always present in the bowel, and is benign unless the condi- 
tions are such as to make it malignant, as when it is confined in a swollen 
and closed appendix. In some instances the streptococcus or the staphylo- 
coccus is the cause. Any micro-organism capable of exciting inflammation 
upon gaining access to the appendix may be the cause. Thus, the pneumo- 
coccus, the pyogenic staphylococcus and streptococcus, the typhoid bacillus, 
and even the ray fungus may act in this way. 

Errors in diet may be a productive factor, for in a certain number of cases 
of appendicitis there is a history that the patient has, a few hours before the 
attack or immediately before it, eaten heartily of ordinary or indigestible food. 

The age of the patient is undoubtedly an important factor in the develop- 
ment of the malady. Although it is met with in young children and in old 
persons — that is, after sixty years of age — appendicitis is certainly very much 
more rare at these periods of life than in the interval. For this there is no 



APPENDICITIS 617 

adequate explanation. The period of greatest frequency is from the fifteenth 
to the thirtieth year, and Fitz states that more than half the cases occur 
before the twentieth year. 

Another predisposing factor is sex. About six times as many men as 
women have appendicitis. This is in part due not only to greater physical 
activity, but to the more frequent causes of intestinal catarrh in males. It 
also depends in part upon the fact that women have a second blood supply 
to the appendix, at least in many cases, namely, an artery which passes from 
the right ovary to the appendix by means of a fold of peritoneum, which has 
been called the appendiculo-ovarian ligament. By this means a greater 
blood supply enables the part to combat infection when the mesenteric vessel 
is twisted. Appendicitis is more frequent in the well-to-do than in the 
poorer classes, although it might be supposed that the greater muscular 
exertion in the latter class would predispose its members to the malady. 

Pathology and Morbid Anatomy. — A knowledge of the pathology of appendi- 
citis makes it possible to understand the symptoms which will be described 
farther on, for these depend, to a large extent, upon the severity of the 
changes in the appendix, and upon the extent to which adjacent tissues are 
diseased. 

Appendicitis may be divided for pathological study into the catarrhal, 
obliterative, ulcerative, gangrenous, and perforative types. 

In the catarrhal type hyperemia and congestion of the deeper layers of the 
appendix may be present, but the chief lesion is in the mucous membrane 
lining the organ. This results in a free secretion of mucus and in distention 
of the appendix, the cervix of which is occluded by the swelling of its lining 
membrane. By this means pain is produced and colic ensues, partly as a 
result of the endeavor of the appendix to expel its contents into the colon 
and partly as a result of colic in the large bowel produced by reflex irritation. 
It can be readily seen that this state may from this point proceed to recovery 
by a decrease in the constriction of the neck of the appendix and the escape 
of its contents, or to a far more grave condition dependent upon a continu- 
ance of the stoppage, a local and general impairment of resistance, and the 
presence of a virulent micro-organism. If the attack has been preceded 
by others, so that the vitality of the part is already greatly impaired and 
altered, the case is even more grave. 

Even in the mild catarrhal form just described there is usually left 
behind distinct traces of the presence of the acute attack, and this predis- 
poses the patient to another seizure. In those cases in which the catarrhal 
process is severe and in which the submucous tissues are much affected, it 
not infrequently happens that after the acute process passes away a subacute 
or low-grade inflammatory condition ensues, which results in round-cell 
infiltration and in thickening of the mucous membrane and submucous 
tissues. The epithelium lining the appendix is desquamated and slight 
ulceration may occur, with the result that the calibre of the appendix may 
be greatly decreased in several places, or even entirely closed by the adhesion 
of its opposing surfaces. In this manner appendicitis obliterans is developed. 

If considerable quantities of pus, or mucus, are imprisoned back of 
the constriction, pain, tenderness, and attacks of appendicular colic, or 



618 DISEASES OF THE INTESTINES 

true appendicitis, are prone to recur. When the inflammatory process is 
severe enough to affect the external surface of the appendix the free end or 
side of it may become adherent to the bowel or other parts, and by this means 
the appendix may not only be distorted and held fast, but the infecting germs 
may pass through its walls and affect nearby structures. 

When the ulcerative type is present, it is a condition but one degree 
removed in severity from that just spoken of, and it can be readily seen that 
no sharp dividing line can be drawn except that there is greater likelihood of 
the adjacent tissues being infected, owing to the fact that the unprotected 
submucosa, with its lymphvessels and bloodvessels, is a fair field for infec- 
tion and for its further spread. Ulceration is particularly prone to occur if 
a fecal concretion or other foreign body is present which may damage the 
mucosa. Tuberculosis or typhoid fever may cause it. Sometimes a foreign 
body may be the cause of such deep ulceration that perforation occurs, or in 
other cases the floor of the ulcer is unable to stand the stress of accumulated 
pus or mucus, and the same accident happens. 

The gangrenous type of appendicitis is the most important of all lesions 
of the appendix, not because it is the most frequent, but because it not rarely 
changes the apparently healthy man of one hour into a corpse within a few 
hours, and this without, it may be, any history of previous attacks which would 
lead to the belief that the appendix was gravely diseased and unable to resist 
infection. When this state is present in its most severe type, the appendix 
undergoes rapid necrosis, its tissues become gangrenous, and it may slough 
away completely in so short a time as forty hours, so that it may be impos- 
sible to find it in the pus which is set free by the surgeon's knife, only shreds 
of tissue being present. In other cases, however, the process is not so 
destructive, but nevertheless the organ is utterly necrotic and decomposed. 
In many instances the gangrenous process may not involve the entire 
appendix, but occur in one spot, speedily causing perforation and so 
endangering the life of the patient. 

Gangrene of the appendix arises from the invasion of its walls by virulent 
infecting germs when its vitality is impaired by some unknown cause, or it 
follows from thrombosis or capillary stasis in its nutrient bloodvessels, 
whereby the same destruction ensues. Gangrenous appendicitis may be 
rapid, widespread, and fatal, or the vital forces of the patient may be suffi- 
ciently vigorous in the work of resistance to wall off the infected area by 
lymph, and so confine the morbid process to the immediate neighborhood of 
the part affected. 

The secondary effects of the pathological processes just described are 
dependent entirely upon their severity and the ability of the patient to pro- 
tect himself from general infection. The acute catarrhal form rarely leaves 
behind it anything more than some thickening of the walls of the appendix, 
with an associated susceptibility to another attack. If all the coats have been 
involved, the tissues about the appendix become filled with lymph, and the 
consequent induration may be extreme, the appendix becoming buried in 
an adherent mass, which may not only hide it from view, and form with 
the adjacent tissues a matrix, but prevent the surgeon from finding the 
appendix if operation is attempted. 



APPENDICITIS 619 

When the inflammation is severe enough to result in the escape of infection 
into the adjacent tissues, we not only have pus in the appendix, but in the 
surrounding parts as well, a perityphlitic r periappendicular abscess, and 
in those instances in which the appendix is perforated either an abscess 
is formed and walled off from the general peritoneum by adhesions or a 
general peritonitis ensues. 

The situation of the abscess varies with the direction in which the infec- 
tion escapes from the appendix. If the infection escapes anteriorly the 
site of the abscess is often between the navel and the anterior superior 
spine of the ilium. When it escapes on the surface of the iliac fascia or 
in the pelvis behind the caecum, it, of course, lies behind the peritoneum, 
not in the serous cavity, and retroperitoneal suppuration develops. From 
here the pus may burrow in as many ways as only pus can burrow, upward 
to the region of the kidney, downward along the psoas muscle into the 
thigh, or it may discharge into the bladder, the rectum, or even into the 
scrotum. 

On the other hand, it must not be forgotten that appendicular abscess 
may develop with very little systemic disturbance and exist for a long time 
entirely unsuspected, being found by accident, it may be, when seeking for 
some cause of distress and discomfort with impaired health. At other 
times such an abscess, after having developed insidiously, produces signs of 
septic infection the source of which at first cannot be traced. 

Finally, attention must be called to the possibility and frequency with 
which infection of the retroperitoneal lymphatics and of the portal vessels 
may occur from disease of the appendix. Attention has been called to this 
by several writers, notably by A. O. J. Kelly, and by Munro in the Thera- 
peutic Gazette. Not only may retroperitoneal abscess be due to perforation 
of the appendix behind the peritoneum, but organisms passing along the 
mesoappendix produce pus when they reach the connective tissues in the 
retroperitoneum. Infection of the portal vessels and consequent hepatic 
abscess is not common, but several cases of this character have been 
reported. 

Symptoms. — It must be manifest from the description just given of the 
pathological changes that appendicitis is a malady capable of producing 
very different symptoms in degree and kind. It is not possible, for this 
reason, to enumerate a set of symptoms present in all cases. There are, 
however, certain symptoms which are fairly constantly present. The most 
constant symptom is pain in the abdomen. This may be diffuse, or at least 
the patient may not be able to localize it. Not rarely, if the physician 
repeatedly asks that it be localized, it is described as being in the "pit" of 
the stomach or in the epigastrium. If the epigastrium is pressed upon the 
pain may be increased. This fictitious localization of the pain in the early 
stages of appendicitis may be most misleading. As a matter of fact, how- 
ever, it should be most indicative, and every person seized with pain of this 
character should be suspected of suffering from appendicitis. In some 
cases the pain is referred to the left iliac region, and it is only when the 
physician applies pressure to the right iliac area that the patient appreciates 
that that is the real centre of his suffering, and by manifestations of an 



C20 DISEASES OF THE INTESTINES 

unquestionable character shows that the source of pain has been discovered. 
There is one spot called " McBurney's point," situated two inches from 
the anterior superior spinous process of the ilium, on a line drawn from 
this point to the navel, in which pain on pressure can nearly always be 
elicited. It corresponds rather with the origin than with the tip of the 
appendix. 

The pain of appendicitis is usually severe and sharp, and in some cases 
agonizing. It is usually sudden in onset, and for this, and the other reasons 
just given, it may be confused at first with renal or gallstone colic. I have 
seen more than one case in which the diagnosis of acute pleurisy had been 
made. Occasionally cases are met with in which the pain is less spasmodic 
and more dull in character, but they are the exception. 

Perhaps the most important fact that can be impressed upon the mind of 
the student in connection with the symptom of pain in appendicitis is this, 
viz., that the sudden cessation of pain in a case of appendicitis is not a good 
sign, but an exceedingly bad one in most instances, for it indicates that 
the distention of the inflamed appendix has been relieved by perforation or 
gangrene. 

When the pain occurs in paroxysms, it is thought to be due to contractions 
of the appendix — appendicular colic. 

Next to pain, the most important symptom in appendicitis is rigidity or 
fixation of the right rectus muscle. Barring voluntary rigidity of this muscle, 
which can usually be prevented by diverting the patient's mind from his 
abdomen, it is a sign of great reliability, and its degree often measures the 
severity of the inflammatory process. 

Vomiting is very commonly present in these cases. In some of them it 
occurs so early as to seem to usher in the attack. This is particularly apt 
to be the case if the stomach has been overloaded with food just before the 
attack. If the stomach is empty at the time of onset, vomiting is often 
absent. 

The febrile movement in a case of appendicitis is rarely very great. The 
temperature varies from 99° to 101°, and occasionally reaches 102° in 
adults. In children it may be higher. 

The pulse is quick, but not very rapid, unless serious abdominal disturb- 
ance has already developed. It ranges from 90 to 110 per minute. If it 
goes higher than this, general peritonitis is probably present. Distention of 
the belly with gas is usually a late symptom, and if well marked may be indic- 
ative of general peritonitis, when it is, of course, a very grave symptom. 

After the malady has been present for some days a swelling in the right 
iliac region may appear and be due to pus or to a large protective exudation 
of lymph. The latter formation is, however, usually met with in relapsing 
cases rather than in primary cases. 

Finally, we meet with cases, usually in women, but sometimes in men, in 
which there is present a true mucous colitis with, it may be, a chronic catarrh 
of the appendix. In these persons a tiny discharge of mucopus may daily 
infect the colon. They are to be considered as cases of chronic catarrhal 
appendicitis and operated upon, not because the appendix is so gravely dis- 
eased as because it causes disorder in the colon. 



APPENDICITIS 621 

Diagnosis. — When the question arises as to the cause of severe abdominal 
pain, an examination of the blood should be made. If a distinct leukocytosis 
is present, the white cells of the polymorphonuclear group being particularly 
increased, it is indicative of an acute inflammatory process somewhere in the 
body, and probably in the appendix, if the symptoms are appendicular. It 
is, however, a great mistake to allow the determination to do an operation 
to rest upon this sign, for it has at times proved a " hollow reed." At best 
it is to be regarded as collateral and not direct evidence of appendicitis. 

One of the most important differentiations for the physician and surgeon 
is that between appendicitis and early typhoid fever. At first glance this 
would seem to be easy, but those of experience know that it is often 
difficult, not that typhoid fever often develops suddenly, but that appendi- 
citis may develop slowly during a mild influenzal infection, or during an 
attack of gastrointestinal catarrh that has been obscure in its nature. Further 
than this, the lymphoid tissues of the appendix and nearby parts are usually 
involved in typhoid fever, and may cause appendicular symptoms. (See 
Plate I.) These localized typhoid lesions may cause pain and tenderness 
in the right iliac area. The absence of very severe pain, the failure to 
find the leukocytosis of acute inflammation, the peculiarly coated tongue, 
the presence of tympany, and the later development of rose spots and 
the Widal test will prove the case to be one of typhoid fever. 

Care should be taken that pain and swelling in this area occurring in one 
who has tuberculosis is not taken for appendicitis. It is not rare to find these 
signs in consumptives who are by no means far advanced in their disease. 
The condition is often one of local tuberculous infection of a chronic type. 

Hepatic colic is separated from appendicitis by the presence of a history of 
previous attacks, by the absence of jaundice, the absence of tenderness over 
the gall-bladder, and by the fact that in gallstone colic the pain is referred to 
the chest between the right shoulder-blade and the spine; whereas, in appen- 
dicitis it is not so referred. 

Renal colic is differentiated from appendicitis by the pain being referred 
to the testicle, pelvis, or the inside of the thigh; by the fact that the urine 
contains blood, if not macroscopically, at least microscopically; there is no 
excess of pain on pressure over " McBurney's point," and there may be a 
previous history of renal stone. Irritability of the bladder is of no value as a 
differential symptom, as it is often present in both renal colic and appen- 
dicitis. In neither form of colic is leukocytosis marked. 

Ovarian or tubal inflammation may simulate appendicitis, but a pelvic 
examination will usually reveal these states. 

In some cases of intestinal obstruction the pain may resemble that of 
appendicitis, but the presence of obstinate constipation, the development of 
fecal vomiting, and the discovery of a mass in the belly elsewhere than at the 
appendix may enable the physician to make a differential diagnosis. 

The possibility of acute hemorrhagic pancreatitis being present is to a large 
extent excluded by the fact that it is a very rare condition, by the site of 
the pain and the onset of early collapse in this disease. 

Osier has pointed out that in persons subject to the erythematous erup- 
tions, severe attacks of abdominal pain may develop which give rise to a 



622 DISEASES OF THE INTESTINES 

diagnosis of appendicitis, which may be excluded only after a careful study 
of the case with reference to this state and urticaria. 

Prognosis. — The prognosis of appendicitis depends largely upon the 
severity of the condition. Statistics which show that a certain percent- 
age of all cases get well are of interest, but they do not help the physician 
in an individual case, because definite statements as to the character of the 
statistics are not given. A series of mild catarrhal cases will give a recovery 
percentage of 100; whereas, a series of severe gangrenous cases will give a 
mortality of 100 per cent. That recovery frequently takes place is shown by 
the fact that about one-third of all postmortems show signs of the existence 
of appendicular disease at some time in life, yet there may be no history of 
such an illness. 

The substance of our present knowledge is that the prognosis in an ordinary 
attack of appendicitis is good for recovery from that attack, but that recur- 
rences are likely. In the perforative or gangrenous type the prognosis is 
always grave and often fatal. Much depends upon prompt surgical inter- 
ference. If this is delayed, death is the result in the majority of cases of 
this type. 

If, however, all cases of appendicitis of whatever type are considered 
statistically, it is found that the percentage of mortality is only about 15 
per cent, under medical treatment. (See Treatment.) 

Treatment. — There is perhaps no more difficult point for decision in med- 
ical practice than that as to the treatment for appendicitis. It is impossible 
to discuss the vast array of arguments for and against early operative inter- 
ference in this brief space. 

Given a case of appendicitis of the acute type, the first thing for the 
physician to do is to call in a surgeon as a consultant, not as an operator, 
provided a surgeon qualified to do good abdominal surgery, if it is required, 
is obtainable. If none such can be had, the patient is far better off without 
than with operation. If by medical treatment the case can be controlled and 
carried through the acute attack, the surgeon should not interfere, for the 
mortality of operation in the acute stage is far greater than it is when the 
operation is performed in the interval between the attacks. 

Fourteen years ago Fitz showed that 40 per cent, die after surgical meas- 
ures, and 11 after medical treatment; but this does not prove that the 
latter is better than the former, but rather that the surgical cases did not 
get to the surgeon unless desperately ill. At present the percentage 
of deaths in surgical cases is far less, chiefly because they are seen 
early enough or operation is performed at the time of election; but 
even at a much later date than that of Fitz's paper we find Caley (1899) 
recording 98 medical cases with 3 deaths, and 102 surgical cases with 22 
deaths. When we consider Sprengel's statistics of 516 cases, 232 of which 
were operated on in the interval with 2 deaths, and 284 during the attack 
with 57 deaths and Sahli's 7000 cases treated medically with 90 per cent, 
recoveries, the value of delay, in mild cases, is evident. 

The plan of treatment in mild cases is as follows : The patient is required 
to take absolute rest in bed. An ice-bag is placed over the appendix. No 
purgatives are given nor pain-relieving drugs are to be used unless the pain 



INTESTINAL OBSTRUCTION 623 

is excessive, when enough morphine may be used hypodermieally to take 
the edge off of the agony, but never enough to make the patient comfortable 
or to make him sleep, for such an effect masks the symptoms. Xo food is to 
be given by the mouth and no drink is to be taken. If need be, liquid can be 
given by hypodermoclvsis or by rectal injection. If the bowels move, a bed- 
pan must be used. If the pulse is excitable it may be quieted with a little 
aconite. Under this treatment the acute inflammatory process may be 
arrested, and the operation can be performed, if need be, after it has sub- 
sided. If by the end of twelve or twenty-four hours the symptoms are not 
rapidly subsiding, it is necessary to operate at once. Fowler has shown 
that when operation is done within forty-eight hours 83 per cent, recover. 
When the cases are left to the fourth day 60 per cent, recover; to the fifth 
and sixth days, 58 per cent.; to the seventh and eighth days, 50 per cent.; 
and to the ninth and tenth days, only 33 per cent. 

The signs, however, which will force the surgeon to immediate operation 
when the patient is first seen, or if he does not improve under treatment, are: 
great rigidity of the rectus muscle, persistent vomiting, a rapid pulse (above 
110), an anxious facies, and, perhaps, as an indication of some importance, 
a very high leukocytosis. In such cases the only salvation of the patient lies 
in immediate surgical interference, and each hour of delay diminishes the 
chance of recovery. The whole question is one of severity of infection. If 
there is reason to believe that the tissues are becoming infected and that the 
local tissues cannot resist the spread of the inflammation, then we must 
operate. 

This question of deferring operation to the interval between the attacks is 
still under debate. There are some radicals who insist that operation should 
be resorted to without waiting, and, indeed, before the appendicitis is severe. 
There are others who are content to wait till the storm is past, and still others 
who believe that, given a patient who has had but one attack of moderate 
severity, he may go free until another, or a third attack, makes it evident that 
a recurrence is likely to take place at any time, when he should be operated 
upon in the interval. As Dennis well says: "The plan of allowing the simple 
catarrhal cases which are doing well after thirty-six hours to recover without 
immediate operation, and relegating them subsequently to the group known 
as interval cases, and the prompt operation after thirty-six hours when the 
cases are not doing well, seems to hold out the best prospects of recovery. 
The pendulum has swung too far toward indiscriminate operation. But 
now the introduction of the interval operation has brought the pendulum 
back to swing within the proper limits." (See Peritonitis.) 

It must not be thought that patients who have had recurrent appendicitis 
can be promised perfect comfort by operation, for not rarely, while they 
recover from the operation, they continue to have tenderness and pain in 
the right groin for years. 

INTESTINAL OBSTRUCTION. 

Definition. — Intestinal obstruction is a term applied to a condition of the 
bowel in which, by reason of some mechanical impediment or intestinal 



624 DISEASES OF THE INTESTINES 

paralysis, the normal movement of its walls and contents cannot take place. 
In its acute form it occurs as the result of no less than six causes : first, con- 
genital malformation; second, invagination, or telescoping of one portion of 
the bowel within the other, or so-called intussusception; third, strangulation 
by bands, diverticula, membranous adhesions, or by attachment to other 
organs, and by the slipping of a coil of intestine through an aperture; fourth, 
as a result of twisting of the bowel, called volvulus; fifth, from lodgement of 
foreign bodies, as gallstones, etc.; and sixth, from intestinal paralysis and 
distention. 

Chronic intestinal obstruction arises from stricture, from tumors in the 
bowel, from tumors external to the bowel, and from the impaction of fecal 
masses. 

Congenital Malformation. — Congenital malformations usually consist in 
closure of the intestinal tube by reason of improper development. Such a 
closure may exist at any part of the alimentary canal from the oesophagus 
to the anus. Rarely the bowel becomes strangulated or incarcerated or 
twisted because of some congenital defect. A common congenital defect is 
imperforate anus and rectum. Less frequently there is atresia at the pylorus. 
Not rarely children born with this condition have other congenital defects 
in the alimentary canal. In the statistics collected by Martin and myself, 
28 per cent, of such cases showed more than one point of obliteration. In 
cases in which the atresia does not exist in the anus or rectum, it is most 
commonly found near the ileocecal valve, in the duodenum, or in the 
sigmoid flexure. 

Symptoms. — The symptoms of intestinal obstruction due to congenital 
causes usually appear after food is first taken. There is no passage of 
meconium from the anus, and the vomited materials are often fecal in odor 
and in appearance. Not rarely violent peristaltic waves can be seen through 
the abdominal wall. There is also pain and efforts at defecation. 

Diagnosis. — An examination of the anus or rectum will usually reveal the 
cause of the trouble. If the finger cannot reach the obstruction, a bougie 
may discover it. In other cases, water from a fountain syringe, hung, not 
over two feet, above the patient's buttocks, may be allowed to flow into the 
bowel to determine its capacity. 

Prognosis and Treatment. — The prognosis is, of course, exceedingly 
unfavorable, but if the closure is near the anus a surgical operation may give 
relief, and, as all die without operation, the knife should always be resorted to. 
Death ensues from inanition or exhaustion. 

Intussusception. — The invagination in this condition is composed of three 
layers of bowel. The intussusceptum is composed of the entering and 
returning layers, while the receiving sheath constitutes the intussuscipiens. 
To the point where the entering layer is turned sharply upon itself to form 
the returning layer, the name "apex" is applied. The word "neck" is 
applied to the ring which results from the flexure formed by the returning 
layer as it merges into the sheath. 

Intussusception may be separated into divisions, according to the 
severity of the condition, or according to the part of the intestine which 
is involved. Rafinesque makes three divisions, namely, those which 



INTESTINAL OBSTRUCTION 625 

are ultra-acute, death taking place within the first twenty-four hours; 
those which are acute, death occurring in the first week ; those which are 
subacute, lasting a month and upward. From an anatomical stand- 
point, intussusception may be divided into the enteric, in which the small 
intestine is alone involved; the ileocecal, in which the ileum and caecum, 
together with the ileocecal valve, are turned into the colon; and the ileo- 
colic, in which the ileum is prolapsed through the ileocecal valve, the latter 
retaining its proper position, at least for a time. When the condition is 
called "colic," it involves the colon only. In still other cases, the rectum is 
solely affected, forming the rectal type of the malady. In the great majority 
of cases the upper segment of the gut is received into the lower, but occa- 
sionally the reverse condition occurs, and when this happens the term 
'" retrograde intussusception" is applied. Double and triple intussusception 
has occasionally been noted. 

Etiology. — The causes of intussusception are not clearly understood, but 
probably depend upon irregular innervation of the intestine, whereby a 
sudden, spasmodic contraction of one portion of the bowel occurs, the 
adjacent portion being relaxed. Intussusceptions of this character are not 
infrequently met with at the postmortem table, having occurred at the 
time of dissolution. Polyps of the intestine may be forced along the lumen 
of the canal, thereby dragging the wall at the point of attachment and 
causing intussusception. 

Frequency. — In 1652 cases of intestinal obstruction, excluding hernia, col- 
lected by Leichtenstern and Bryant, 657 cases, or, approximately, 40 per 
cent., were due to intussusception. It is evident, therefore, that this form of 
obstruction is not rare. Intussusception occurs most frequently during 
the first twelve months of life. After the fifth year it becomes compara- 
tively rare until the fortieth or fiftieth year, when it again increases in fre- 
quency. The ileocecal region is the favorite site of invagination at all ages, 
but ileum invagination is exceedingly rare. If the colic form occur, it is 
usually at the sigmoid flexure. 

Pathology. — The pathological changes resulting from intussusception con- 
sist in an extravasation of the blood into the mucous membrane and mesen- 
tery of the part affected, and in an acute inflammatory process in the walls 
of the intestine, which particularly affects the serous surfaces of the entering 
and returning layers, so that they become glued to one another. Not infre- 
quently, however, this condition does not arise, and adhesions do not form. 
As a result of the strangulation of the invaginated bowel, it sometimes hap- 
pens that this portion of the intestine sloughs away, and if sufficiently 
strong adhesions have formed between the neck and the upper portion of 
the intussusceptum, the coming away of this slough may result in the 
recovery of the patient. Very large portions of bowel have been known to 
be passed in this manner. Pampier has recorded one instance in which 
124 cm., Bottcher another in which 112 cm. were passed. In other 
instances, however, if gangrene of the bowel develops, perforation and 
general peritonitis ensue. 

Symptoms. — These depend upon the degree of constriction at the neck of 
the intussusceptum. Usually the first symptom is sudden and violent pain. 
40 



626 DISEASES OF THE INTESTINES 

This pain sometimes ceases as suddenly as it begins, the patient being in 
comparative comfort. After an interval the pain returns, and the paroxysms 
become violent and prolonged, with shorter intervals of ease. Pressure does 
not always elicit tenderness; indeed, at times it seems to relieve the pain. 
Vomiting is an even more constant symptom than pain, and usually begins 
early in the attack, but in adults it may be absent. Of all forms of intussus- 
ception the ileum invagination is the one which is most frequently accom- 
panied by early vomiting, chiefly because it produces the most complete 
obstruction. In children a very constant symptom is the passage of bloody 
mucus. Out of 108 cases, analyzed by Martin and myself, occurring in the 
first year of life, this symptom was absent in only 4. 

Tenesmus and bearing down is also commonly met with. In about one- 
half the cases the tumor can be felt through the abdominal wall, and under 
the pliable abdominal wall of children it should always be most carefully 
sought for. Such a tumor is most commonly found when the ileocecal type 
is present. Occasionally in the colic type the invaginated bowel can be felt 
in the rectum. The movement of the bowel may distinctly change the 
position of the tumor. 

Prognosis. — The prognosis in intussusception is not very good. Treated 
by the expectant method, the mortality is 70 per cent., according to Leichten- 
stern. The statistics of Martin and myself give a mortality of 90 per cent. 
The mortality is greater in infants than it is in older persons. The sloughing 
and discharge of the intussusceptum is always to be considered distinctly 
favorable, and Martin and myself found that in 408 children in whom slough- 
ing had not taken place 85 per cent, died, while of 149 who passed a portion 
of the intestine 41 per cent, recovered. Sloughing rarely occurs before the 
second or third week of the disease. 

Treatment. — The treatment consists in the use of a fountain syringe filled 
with normal salt solution, at the temperature of 105°, and this fluid is to be 
injected slowly at the rate of 4 ounces to the minute. The pressure in the 
hydrostatic syringe should not be over two pounds. This method is available 
only when the intussusception occurs in the lower portion of the bowel. If 
it is in the ileum it is valueless. If, after pressure has been continued for the 
period of a half-hour, the tumor does not disappear under gentle manipula- 
tion, abdominal section must be resorted to at once. The older statistics in 
regard to this operation were not very favorable, most of them being gathered 
in preantiseptic days. At the present time operation gives much more 
favorable results. 

Internal Strangulation. — Internal strangulation by bands is the next 
most frequent form of intestinal obstruction, forming about 36 per cent, of 
the classified cases. The condition occurs most frequently in males between 
the twentieth and fortieth years, and seems to arise in the majority of cases 
from a former peritonitis; although occasionally the bowel is strangulated by 
slipping through the foramen of Winslow or through a slit in the diaphragm. 
Numerous cases of obstruction due to a Meckel's diverticulum have been 
reported. The diverticulum may become twisted or by adhesions to neigh- 
boring structures form a constricting band. 

Out of 151 reported cases the small intestine was involved in 133. 



INTESTINAL OBSTRUCTION 627 

Symptoms. — The symptoms consist in sudden agonizing pain which is con- 
stant, although it has paroxysmal increments. The pulse becomes rapid and 
weak; the temperature is abnormal; the vomiting is persistent, and becomes 
fecal, but this condition of the vomit rarely develops before the beginning 
of the third day. Constipation is present, but fecal matter may be passed 
from the lower part of the bowel once or twice. If a large coil of gut is 
involved, a distinct area of distended intestine may perhaps be found. 
While the presence of this train of symptoms in a young child would be 
indicative of intussusception, in an adult it is indicative of strangulation by 
a band, for intussusception is rare in adults. 

The only method of treatment which is satisfactory is operative. 

Volvulus. — According to Brinton, this condition occurs in 8 per cent, of 
fatal cases of intestinal obstruction; according to Treves, in 2.5 per cent., 
and according to Martin and the writer's statistics, in 4 per cent. Some- 
times the intestine is twisted for three or four complete turns. The condition 
occurs most frequently after middle life, and occurs more frequently in men 
than in women. In 18 cases collected by Haven, 16 were men. In Martin's 
and my own table of 100 cases, 64 were men. The twist is usually about the 
mesentery as an axis and involves the small intestine. Occasionally it may 
appear in the colon; rarely the stomach may be affected. The twisting 
of the intestine interferes with its circulation, and this, combined with the 
decomposition of the intestinal contents and the resulting distention, soon 
produces peritonitis, and even perforation. The abdomen is prone to 
become immensely distended. 

Symptoms. — The symptoms consist in absolute constipation, vomiting, and 
abdominal distention. Meteorism is constant. The points in favor of a 
diagnosis of volvulus are the advanced age of the patient, the fact that the 
disease usually occurs in a male, that the pain is not as agonizing as in 
other forms of obstruction, and that the obstructed bowel is greatly dis- 
tended. 

Prognosis. — The prognosis is much more favorable than in other forms of 
intestinal obstruction. When intestinal obstruction is due to paralysis, the 
cause is most frequently some injury or an operation upon the abdominal 
contents. The bowel is simply dilated or kinked, and the failure in peri- 
stalsis is due to paralysis of its muscular fibres. This is the type of obstruc- 
tion which all abdominal surgeons greatly fear as a sequence of operation 
upon the peritoneal contents. 

Treatment. — When the volvulus is due to paralysis after operation it is to 
be treated by the administration of concentrated salines repeated until the 
bowels are moved. When distention has reached a very great degree and 
vomiting is present, salines are no longer useful. The rectal tube should be 
passed in the hope of exciting peristalsis and drawing off gas. The patient 
should be freely stimulated and the rapidly interrupted faradic current 
should be applied to the abdominal wall, or one pole may be placed in the 
rectum and the other passed to and fro over the abdomen. 

If the condition is not due to paralysis after operation purgatives are 
absolutely contraindicated, and enemata can be of no value. Such cases 
should be subjected to operation. 



G28 DISEASES OF THE INTESTINES 

Obstruction from Foreign Bodies arises from such articles as coins, 
pebbles, knives, and scissors, gallstones and enteroliths. While gallstones are 
usually small, they at times may be very large, and are often greatly added 
to by concretions. Thus, Leichtenstern states that one such stone was five 
inches in circumference, and he describes an enterolith nine inches in circum- 
ference. Such a stone is usually formed by concretions about a foreign body, 
as a cherry-stone. Cases of intestinal obstruction of this character are, how- 
ever, very rare, about 0.2 of 1 per cent, of all cases. The obstruction is 
usually found in the small intestine, sometimes at the ileocecal valve, and 
occurs more frequently in females than in males. 



DUODENAL ULCER. 

Ulcer of the duodenum is probably a more frequent condition than is gen- 
erally supposed, and in some cases is associated with ulcer of the stomach. 
The proportion given by Burwinkel of gastric and duodenal ulcer is 12 
to 1. On the other hand, von Wyl found only 3 duodenal ulcers in nearly 
13,000 postmortem examinations, and Kinnicutt, in an analysis of 30,000 
postmortems, places its frequency at 0.4 of 1 per cent. The condition may 
arise at any period of life, but is most frequent between the tenth and fortieth 
years. Hahn has recorded a case in a child only a day and a half old. Such 
an ulcer must have been antenatal. 

Unlike gastric ulcer, the great majority of duodenal ulcers are found in 
men. Murphy, of Chicago, quotes Laspeyres as stating that men are 
affected two or three times oftener than women. Thus, Krauss, in 64 
cases, found the ratio to be 10 to 1; Lebert, in 39 cases, 4 to 1; Trier, in 
54 cases, 5 to 1; and out of 176 cases collected by Weir, 144 were in men. 

Etiology. — Among the causes of duodenal ulcer may be mentioned 
burns, which in some unknown way produce ulceration in this portion of 
the bowel. Renal disease, which occasionally results in the ulceration of 
the large bowel, may also cause this lesion in the duodenum. Pulmonary 
tuberculosis, which produces its lesion by infection of a solitary follicle, 
and diseases of the heart and liver, which result in impairment of vitality 
in the intestinal wall, so that localized infections may occur, are also 
causes. 

As with gastric ulcer, so with duodenal ulcer, a large number of theories 
have been advanced as to its direct causation. Most authorities at the 
present time believe that it is due to erosion produced by the gastric juice, 
the vital resistance of the part having been diminished by inflammation or 
circulatory changes. That acidity of the gastric contents may so result seems 
likely, from the fact that ulcer most frequently occurs in the duodenum near 
the pylorus, at a point where the acidity of the gastric juice may be but little 
modified by the alkaline secretion which it would meet a few inches farther 
on in the bowel. 

It would seem probable, however, that a number of factors may produce 
this form of ulcer, acting in some cases together and in other cases singly. 
These factors are well summed up by Murphy and made into four divisions : 



DUODENAL ULCER 629 

hyperchlorhydria, local infection, embolism with thrombosis, and foreign 
bodies. To these four divisions Murphy would add a fifth, namely, disorders 
of the organs of elimination, as in burns of the skin or other serious 
lesions in this part of the body, as pemphigus and erysipelas, and in other 
cases renal disease. 

Pathology and Morbid Anatomy. — Duodenal ulcers are usually single, but 
they may be multiple. Out of 233 cases collected by Collins, 195 were single. 

Ulcer usually occurs in the first part of the duodenum. Out of 149 cases 
collected by Perry and Shaw, the first portion of the duodenum was involved 
123 times, the second portion 16 times, and the third and fourth portions 
twice. These statistics agree with those which have been collected concerning 
the area and greatest frequency of perforation complicating ulcer of the 
duodenum. 

When perforation occurs, it takes place nearly twice as often in the 
anterior as in the posterior wall, still more rarely in the superior wall, and 
almost never in the inferior wall. Perforation occurs much more frequently 
in ulcer of the duodenum than in ulcer of the stomach, if we can rely upon 
the statistics which have so far been collected. Thus, in 404 cases mentioned 
by Chvostek, Collins, and Oppenheimer, perforation took place in 246. On 
the other hand, it must be remembered that a very large number of cases of 
duodenal ulcer are not recognized unless perforation does occur, and it is 
highly probable that this accident is far less frequent in duodenal ulceration 
than these statistics would indicate, because it is a well-known fact that 
duodenal ulcer is a condition most difficult to recognize unless it is found in 
the course of an abdominal section, and, further, it is well known that these 
ulcers frequently heal. Thus, Perry and Shaw found evidence of repair in 
half of their cases, and Krug, in 1220 autopsies, met with 30 cases of healing 
of duodenal ulcer. 

As in perforations of the stomach, so in perforation of the duodenum, 
a general peritonitis ensues, or a localized peritonitis may develop, 
the extravasated materials being walled off from the rest of the peri- 
toneal cavity by an inflammatory exudate. As with gastric ulcer, so 
again with duodenal ulceration, adhesions may take place in neighboring 
organs, and perforation may take place into them. Thus, it has occurred 
that the duodenum has been perforated, and so permitted its contents to 
enter the gall-bladder, the abdominal aorta, the vena cava, the portal vein, 
the superior mesenteric vein, and the hepatic artery; but Murphy asserts that 
a gastroduodenal fistula has never been found as a result of perforation of a 
duodenal ulcer. In some instances perforation of the duodenum has resulted 
in subphrenic abscess. 

Symptoms. — The symptoms of duodenal ulcer, unless the ulceration pro- 
ceeds to hemorrhage or perforation, are too indefinite to make a positive 
diagnosis possible in most cases. Indeed, in fully half the cases in which 
duodenal ulcers are found at autopsy, there have been no symptoms during 
life which have raised suspicion of its existence. 

When the symptoms do occur, they so closely resemble those of gastric 
ulcer that a differentiation may be impossible. There is pain and vomiting, 
and if a bloodvessel is ulcerated there may be hcematemesis or bloody stools. 



630 DISEASES OF THE INTESTINES 

The pain is usually much less severe than in ulcer of the stomach, but at 
times it may be agonizing. There seems to be a general consensus of 
opinion that it rarely radiates toward the back, as does the pain of gastric 
ulcer, but cases have been reported in which pain in the neighborhood 
of the shoulder-blade has been a pronounced symptom. It differs from 
gastric ulcer in that the taking of food is not immediately followed by 
pain, the pain being delayed for several hours after a meal, then develop- 
ing when the food enters the duodenum from the stomach. Moynihan 
says that the nearer the ulcer is to the stomach, the sooner is the pain 
developed. 

The hemorrhage, when it takes place, may be sufficiently profuse to 
cause death, or it may be small in amount and be frequently repeated, in 
which case death may ultimately occur from exhaustion. Vomiting rarely 
occurs except when the stomach is overloaded, or when blood enters it from 
the duodenum. 

Perforation of a duodenal ulcer may be the first manifestation of any 
lesion in this portion of the bowel. According to Schwartz, patients suffer- 
ing from perforation of the duodenum were healthy in 20 out of 25 instances 
prior to the accident, and in Weir's 51 cases they were without gastric or 
duodenal symptoms in 25 out of 34. So, too, in Perry and Shaw's 151 
cases, 91 per cent, presented no evidences of disease until perforation or 
hemorrhage developed. 

While cases of ulcer may recover, the tendency is to a progression of 
the disease. On the other hand, progress does not necessarily mean early 
death, for Chvostek has reported a case in which there had been present 
symptoms of duodenal ulcer occasionally for thirty-nine years. 

Symptoms of perforation of duodenal ulcer are severe epigastric or right 
hypochondriac pain, followed it may be by collapse; the symptoms resemble, 
perhaps, acute hemorrhagic pancreatitis, and death occurs sometimes as 
early as twenty-one hours after the accident. The symptoms of general 
peritonitis soon develop, or, if the lesion is localized by adhesions, localized 
peritonitis is found, as already stated. Leukocytosis is usually marked. 

Diagnosis. — The tests for minute traces of blood in the stools, which are 
described in the article on gastric ulcer, may be used in these cases. 

Duodenal ulcer must be separated from gastric ulcer, if possible. In 
the majority of instances this, perhaps, cannot be done unless there are 
bloody stools, the character of the blood being dark and tarry, owing to 
its alteration by the intestinal juices. If it is bright in character, it probably 
comes from ulceration of a lower portion of the bowel. Another important 
point in the diagnosis is the period at which pain develops after food is taken, 
for, as already pointed out, the development of pain is delayed in cases of 
ulceration of the duodenum, and is immediate, as a rule, in gastric ulcer. 
While von Wyl admits that it is impossible to make a differential diagnosis 
in 90 per cent, of the cases, he gives us the following points which are of value 
in differentiation: 



DUODENAL ULCER 631 

Gastric Ulcer. Duodenal Ulcer. 

1. Usually in women twenty to thirty-five 1. Most frequent in men. 

years of age. 

2. Pain comes on soon after eating. 2. Pain two to four hours after eating, 

and located in right hypochondrium. 

3. Pain lessened by vomiting. 3. Vomiting does not relieve pain. 

4. Vomitus contains mucus, food rem- 4. Vomiting more rare than in gastric ulcer, 

nants, and often blood. and does not often contain blood. 

5. Severe dyspeptic symptoms usually 5. Dyspeptic symptoms slight. 

present. 

6. Melaena rare. 6. Melsena comparatively frequent. 

Gallstone colic is to be separated from duodenal ulcer by the fact that 
hemorrhage does not occur in gallstone colic, and by a previous history of 
gallstones; but it is to be remembered that the absence of a history of jaundice 
is of little value, for jaundice is not a constant symptom in cholelithiasis. As 
Murphy well points out, jaundice was present only 16 times in 400 cases 
of cholelithiasis operated on by him. 

Acute fat-necrosis often can not be differentiated from duodenal ulcer with 
perforation. As a rule, the vomiting in fat-necrosis is more persistent, and 
the depression or collapse is more prompt and severe. A high-pitched per- 
cussion note is found in the right hypochondrium in fat-necrosis, but this 
area is usually flat in perforation of the duodenum, unless peritonitis has 
already progressed to the stage of general tympanitic distention. In fat- 
necrosis there is an absence of leukocytosis; in perforation there is a marked 
leukocytosis. In fat-necrosis there is usually no rise in temperature; in per- 
foration there is not infrequently a primary rise. 

Intestinal obstruction may closely resemble perforated duodenal ulcer. 
The pain in ulcer is constant; in obstruction colicky; there is hyperperistalsis 
in obstruction ; there is an absence of peristalsis in perforation ; there is absence 
of leukocytosis in obstruction; there is marked leukocytosis in perforation. 
In both there is usually a history of constipation. 

As illustrative of how difficult it is to make a correct diagnosis, even when 
perforation occurs, Moynihan tells us that in only 12 out of 51 cases of 
duodenal ulcer was a correct diagnosis made before operation, and that in 
49 cases of perforated duodenal ulcer 18 were operated upon for appendicitis. 

Prognosis. — The prognosis, like that of gastric ulcer, is not good for recov- 
ery. In perforative cases, if operation is not performed, the outlook depends 
entirely upon whether the infective material is walled off by adhesions. If 
this is the case, and a subphrenic abscess is formed, much depends upon 
the point at which this abscess ruptures. If the extravasated material is not 
confined by adhesions, death occurs from general peritonitis. 

When the condition is recognized and operation is performed, the prog- 
nosis is much more favorable. The difficulty is that in many cases the 
diagnosis is so obscure that operation is not performed until so many hours 
have passed that recovery is impossible. Thus, out of 51 cases operated 
upon in Moynihan's collection there were only 8 recoveries, and in 20 cases 
collected by Darras only 3 recovered. In 79 cases collected by Weir and 
Foote the mortality after operation was 71 per cent. 



632 DISEASES OF THE INTESTINES 

Treatment. — The treatment of these cases consists in absolute rest in 
bed. Aside from these measures it is purely surgical. If perforation has 
taken place and surgery cannot be resorted to, then there is nothing left 
for the physician but to relieve pain by the use of opium and to hope that 
the inflammatory process may be localized. 1 



ENTEROPTOSIS. 

Definition. — Enteroptosis is a condition in which the intestines fall to a 
lower level than that which they normally occupy. Not only the intestines, 
but the stomach, liver, spleen, and kidneys may be displaced downward, the 
displacement being due to stretching or relaxation of the mesenteric and 
peritoneal ligaments and to laxity of the abdominal wall, so that it fails to 
support the contents of the belly cavity. Of the various names which have 
been applied to this state, other than enteroptosis, may be mentioned splanch- 
noptosis, visceroptosis, and "Glenard's disease. " When the stomach is chiefly 
affected it is called gastroptosis. Enteroptosis is a condition, not a disease. 

Etiology. — Glenard thinks that overloading the transverse colon with feces 
may cause so great a strain upon that portion of the mesocolon which sup- 
ports the large transverse bowel, particularly at its right flexure, that this 
part may sag and so predispose the rest of the colon to drop downward, 
drawing with it other parts. The objection to this argument is that the right 
flexure of the colon is practically never loaded heavily with feces, or, at least, 
the instances in which it is so loaded are far more rare than is enteroptosis. 
Further than this, the ligaments concerned in the support of the abdominal 
contents are not the chief source of support. Schwerdt states that they do not 
bear more than one-eighth of the weight. The upper organs are buoyed up 
by the lower ones, provided these are retained in a normal position. Although 
constipation may be a minor factor in producing this state, the chief factors 
are relaxation of the abdominal wall and the loss of fat produced by an acute 
illness or some chronic disease, and occasionally by old age. This affection 
is not uncommon in the insane, particularly when chronic constipation, 
inactivity, and wasting are associated. The relaxation of the abdominal 
wall may also be due to loss of fat and to repeated pregnancies, particularly 
if the woman has, by wearing corsets, weakened her abdominal muscles and 
then had them subjected to prolonged distention in pregnancy. Occasionally 
the rectus muscles not only atrophy, but separate. I have in my ward as I 
write a woman who has this very condition. (Figs. 84 and 85.) Cases 
occasionally arise in which enteroptosis follows the removal of a large 
ovarian cyst or of ascites. 

To appreciate the failure on the part of the abdominal muscles in a 
well-developed case of enteroptosis, it is only necessary to stand behind the 
patient and place the palms of the hands upon the lower zone of the abdomen, 
pressing upward and inward, when the entire weight of the abdominal con- 

1 The literature of this subject, which is of increasing importance, can best be obtained by consult- 
ing the valuable papers of Weir in the Transactions of the American Surgical Association, and of 
Murphy in the American Journal of Obstetrics for December, 1902. From these contributions much of 
the information in this article was obtained. 



ENTEROPTOSIS 
Fig. 84 



633 



ifehjfc ^ 


■•■ Jfrw 




^L >? 


> - 


' 


• 


Es^B ^H 




';, ._ - 



Fig. 85 




Enteroptosis due to relaxation of the abdominal wall. Hornets'-nest belly. 



634 DISEASES OF THE INTESTINES 

tents may be felt resting upon the hands. The complete inability of the 
abdominal wall to give support is then appreciated. 

Enteroptosis is far more frequent in women than in men. Glenard found 
it in women in 306 out of 404 cases. 

Symptoms. — The symptoms in many cases are by no means definite. The 
patient is often regarded as a chronic dyspeptic, as, indeed, she is. There is 
more or less constant discomfort in the abdomen, and the intestines may be in 
a state of peristaltic unrest, so that borborygmi and rumbling are annoying. 
At times the bowels seem hypersesthetic, and the patient complains, not of 
pain, but of a sense of movements which in health are never felt. Some 
patients describe the sensation as if their abdominal contents were " falling 
out" of them. Some have a distaste for food; others crave it, with the hope 
that it will relieve the sense of emptiness, and then regret taking it because 
its presence in the displaced stomach increases the distress. Constipation is 
usually persistent, and the use of purgatives may serve to cause a great 
increase in rumbling without causing a satisfactory evacuation. The reason 
for this is evident, for the fallen bowel presents sacculations or depressions 
that act like a plumber's trap and prevent free progress of the contents of 
the intestinal tube. 

Associated with these symptoms there is often a good deal of nervous 
unrest and mental depression, and not rarely some vertigo on changing the 
posture of the body. There may also be cardiac palpitation and breath- 
lessness. 

An examination of such a patient will reveal on inspection, provided 
a certain degree of leanness or emaciation is present, that the abdominal 
wall is thinner than normal, that it is relaxed, and that when the patient 
stands erect its muscles are soft and without tone. In health palpation of 
the abdominal wall reveals some resistance, whereas in this state it yields 
readily to pressure like the side of a partly filled water-bag. Inspection not 
rarely reveals the fact that the zone of the abdomen between the ensiform 
cartilage and the navel is empty, and that below the navel the abdomen 
is unduly prominent and sags. 

The appearance of such a patient is often noteworthy, for emaciation may 
be so marked as to raise the suspicion of malignant disease, a suspicion which 
is increased by the ansemia which is present. Rarely the patient suffering 
from enteroptosis may develop jaundice because adhesions constrict the 
bile-ducts. 

If the patient with enteroptosis be placed upon the back in a good light, 
and the abdominal wall observed at a distance, peristaltic waves may often 
be seen traversing it. Tapping the knuckles of intestine through the 
abdominal wall with the finger-tip will increase or arrest these movements 
for a moment. 

Deep palpation may reveal the liver much lower than normal. That this 
is not due to an enlargement of this organ may be proved by the discovery 
that as its lower border passes down into the abdomen its upper border 
also becomes lower, the actual area of liver dulness on percussion being 
the same as in health. The liver is, however, rarely out of place, except in 
extreme cases. 



ENTEROPTOSIS 635 

Distention of the stomach with gas from a Seidlitz powder, or by 
pumping air into it with an atomizer bulb attached to a tube, will reveal 
its abnormal position, and if it is carefully outlined it may be found that 
this viscus occupies a more vertical position than in health, the pylorus 
being greatly displaced, while the cardiac portion is in a relatively normal 
posture because it is more firmly suspended. The cardia is very rarely greatly 
displaced, but Steele has reported five such cases in a comparatively short 
time of observation. The gastrodiaphane of Einhorn may be used for the 
purpose of defining the site of the stomach. Ptosis of the stomach is not 
rarely associated with dilatation and with motor insufficiency, (For the 
measures by which the presence of gastroptosis can be determined see 
article on Gastric Dilatation.) 

The spleen is very commonly displaced. It may be well forward in the 
median line, or it may fall more directly downward and be found as low as 
the pelvic organs 

Nephroptosis is described in the section devoted to Diseases of the 
Kidneys. 

During the performance of deep palpation there can sometimes be felt a 
moderately firm mass lying transversely in the abdomen in the epigastric area. 
This is said by Glenard to be the colon, but if this be the case the colon is 
not much displaced, and is certainly contracted rather than dilated — a condi- 
tion opposed to that stated by Glenard to be usually present. Ewaldi believes 
that this mass is the pancreas which has been uncovered by the enteroptosis. 

Auscultation of the belly in these cases often reveals a large number of 
liquid sounds, and if the patient is shaken there may be heard succussion 
notes and sounds which may be called "slopping." 

While some patients with moderate enteroptosis present many of the 
symptoms just described, it is a fact worthy of note that others with very 
marked falling of the abdominal contents often have no complaint to make 
of the abdominal state, and if they are told of it at once become mentally 
"centred" on their alimentary tract, and, if already neurasthenic, speedily 
drive themselves and their medical attendant almost demented by their 
constant discovery of new symptoms. 

Treatment. — The treatment of enteroptosis is manifestly to be directed to 
the support of the displaced organs and their replacement. Not rarely, if 
the physician stands behind the patient and presses upon and lifts the 
abdominal contents by pressing the hands in front of the abdomen, relief 
from the sense of abdominal relaxation is at once noticed. 

The adjustment of a properly filled abdominal belt or binder is, therefore, 
a valuable aid in this condition. It should be applied every morning before 
rising and not until after the patient, by gentle strokings with his hands, 
has placed the abdominal contents at about the proper level. Its greatest 
pressure must be exercised inward and upward in the zone below the 
navel. Sometimes the use of a broad flannel binder about the lower zone 
may be sufficient, but the support must be upward as well as inward. 

Great care should be taken as to diet. Starches and milk, both of which 
are prone to produce flatulence, should be avoided. If starch is used in an 
easily digested form, as rice and cornstarch, some taka-diastase should be 



636 DISEASES OF THE INTESTINES 

given with it. Cheese and beans are absolutely forbidden, and fats are also 
harmful. Small quantities of green vegetables may be taken, and roast or 
broiled beef and mutton allowed at each meal. Eggs are also permissible. 
The patient should be warned against eating heavily at any one time, since 
an overweighted stomach or colon will make the ptosis much worse. If 
gastric dilatation exists, lavage may be useful. 

In the way of drugs, there are only three which produce much benefit, 
namely: nux vomica in full dose — say, J grain four times a day; extract of 
physostigma in the dose of J grain four times a day, and capsicum, 1 grain 

three or four times a dav. Sometimes it is well to combine all of these in 

«/ 

one pill or capsule. 

In the way of digestants, hydrochloric acid and pepsin, soda and pan- 
creatin, and taka-diastase are to be employed. As laxatives, cascara sagrada 
and aloes may be used, 1 grain of the extract of the former and -^ grain of 
aloin being given once, twice, or thrice a day, according to the obstinacy of 
the bowels. The bitter fluid extract given in capsules is the best preparation 
to employ. 

In cases in which the symptoms are so severe as seriously to impair health 
and comfort and even the chances of life, operative interference is indicated; 
the displaced organs being fixed by suturing. Up to the present time quite 
a number of such cases have been operated on by different methods. Duret, 
in a case in which the stomach came within four inches of the pubis, placed 
stitches through the lesser curvature of the stomach, then through its anterior 
wall, and made it fast to the peritoneum of the anterior abdominal wall. 
Recovery followed. In other cases the intestines have been raised by taking 
a reef in the mesentery. Rovsing has fastened the stomach by three stout 
sutures passed through the abdominal wall and through the outer coats of 
the stomach, with the result that the patient gained forty pounds in weight. 
Beyea has taken tucks in the gastrophrenic and gastrohepatic ligaments, with 
good results, and Webster has treated a large number of cases by excising 
the tissues between the recti muscles and then stitching the edges of these 
muscles together, thereby affording support for the abdominal contents. 



COLITIS. 

Acute Colitis. — This is a very common condition and follows exposure to 
cold, particularly if the abdominal contents have been the parts chiefly 
deprived of warmth. The inflammatory process chiefly affects the lower 
part of the colon and extends to the rectum as well, so that proctitis is 
developed. The primary hyperemia of inflammation is followed by an 
increasing secretion of mucus, with the throwing off of dead epithelial cells 
mixed with white and red blood corpuscles which have escaped from the 
engorged vessels. If the process is very severe, a suppurative state may be 
developed. In most cases the tendency is to rapid recovery, but if the 
inflammatory process persists, one of two conditions may be developed, 
either small areas of necrosis or ulceration occur, or there is deposited in the 
submucous tissues a considerable amount of connective tissue, which may 



COLITIS 637 

by its contraction impair the function of the glands and perhaps narrow the 
calibre of the bowel. 

Symptoms. — The symptoms consist in severe abdominal pain, with tender- 
ness in the region of the sigmoid flexure, and in frequent movements of 
the bowels, which movements soon become very small, so that they finally 
consist in nothing but a little mucus, which is passed with great tenesmus. 

Treatment. — The treatment consists in the use of absolute rest in bed. 
The application of a mustard plaster over the sigmoid flexure and the injec- 
tion into the bowel of 4 ounces of starch-water, with 40 grains of potassium 
chlorate and 30 drops of deodorized laudanum, every three or four hours. 

Acute infectious colitis has already been considered in the article on 
Dysentery. 

Mucous Colitis. Definition. — Under the name of mucous colitis physi- 
cians meet with a condition which is, next to dysentery, the most common 
affection of the colon, and in temperate zones is more frequent. It affects 
persons suffering from neurasthenia, in the great majority of cases, and is 
met with in the overworked or overwrought of both sexes, but most fre- 
quently in women of from twenty to forty years of age. 

The affection is a chronic one, often lasting for several years, and during 
its continuance causing a great impairment of nutrition and much general 
ill-health. Not rarely the irritable state of the colon causes constant abdom- 
inal distress. Severe colicky pain is also present, and a state of hyper- 
peristalsis of the small bowel exists, so that food is often hurried on into the 
large bowel before it can be digested and absorbed, the patient suffering from 
lienteric diarrhoea, not because the digestive power is impaired, but because 
the food does not remain in one part of the small bowel long enough to be 
digested. The stools are not as frequent as those of other kinds of chronic 
diarrhoea. 

Mucus in considerable amount is often passed, and this mucus may 
be so thick that it resembles a false membrane, whence the term "muco- 
membranous enteritis. " Not rarely the patient has excessive peristalsis 
every time food is taken. 

Blood is almost never passed unless there are hemorrhoids which bleed. 
There is no fever, but profound mental depression. Areas of marked 
tenderness can be found in the abdomen on palpation, and the cutaneous 
sensibility is often increased. 

Treatment. — The treatment of mucous colitis, while it is not capable of 
producing, in the majority of cases, very marked improvement within a 
short time, is nevertheless successful in a large proportion of patients, pro- 
vided that it is carefully and persistently carried out, and if the patient's 
mode of life and her diet is arranged in such a way as to be favorable in 
their effects. As the majority of these patients have been subjected to 
nervous stress and are neurasthenic, it is essential that they shall be sub- 
jected to the rest cure, in order that by re-establishing nervous tone and 
equilibrium a normal intestinal peristalsis and normal digestive functions 
may be established. Without rest in cases of this character other treatment 
is commonly useless. 

In order that the greater part of digestion and assimilation may be 



638 DISEASES OF THE INTESTINES 

carried out in the stomach and duodenum, foods easy of digestion and 
readily assimilated should be given, and should consist chiefly in pro- 
teids, that is, broiled or roasted meats. Green vegetables and fatty foods 
should not be allowed. Easily digested starches, such as rice and corn- 
starch, may be given, provided that pancreatin or taka-diastase is given with 
them to hurry their digestion. All vegetable foods which leave a bulky resi- 
due should be forbidden, as, for example, oatmeal and wheaten grits. The 
patient should take liquids in small quantities frequently, rather than in 
large quantities at long intervals, and should avoid taking liquids with her 
food. She should also avoid taking liquids before going to bed at night, 
as not infrequently liquids taken at this time seem to lie in the bowel unab- 
sorbed, and on the assumption of the erect posture by the patient in the 
morning a morning diarrhoea is developed. All fatty articles of diet should 
be avoided. 

Continuous counterirritation, produced by frequently repeated appli- 
cations of tincture of iodine over the whole abdominal surface, should be 
maintained, and if there is much tenesmus a suppository containing 5 to 
10 grains of iodoform may be inserted into the rectum in the morning after 
a movement of the bowels, not only for its local counterirritant effect, but 
for the beneficial influence of the iodine, when absorbed, upon the catarrhal 
condition of the bowel. In some cases where the colon is chiefly at fault, 
clysters of 1 or 2 quarts of hot normal saline solution, or of pure water con- 
taining 20 grains of sulphocarbolate of zinc to the pint, should be gently 
given, care being taken that the fluid does not run in so rapidly as to irritate 
the bowel. The patient should lie on the left side until the sigmoid flexure 
is filled, then turn on the back while the transverse colon is filled, and 
perhaps after this turn on the right side with the hope that the fluid will 
enter the ascending colon. 

In those cases in which there is a history of repeated mild attacks of 
appendicitis, or of pain in the right iliac region, appendectomy sometimes 
produces excellent results, the chronic colitis being due to the infection of 
the colon by small quantities of pus which escape from the appendix. Prob- 
ably the enforced rest which follows an operation for the removal of the 
appendix also is advantageous in producing a cure in these cases. 

Follicular and Croupous Colitis. — Follicular colitis, sometimes called 
nodular colitis, is a form of inflammation of the colon characterized by 
marked swelling of its solitary glands, or lymph nodes, rendering these 
structures unusually protuberant. After this primary stage of enlargement 
necrosis and sloughing ensue, leaving round ulcers, which are frequently 
numerous. By the failure of these to heal the more chronic state of ordinary 
ulcerative colitis is developed. 

Ulceration of the colon is, of course, also due, in many cases, to the typhoid 
bacillus, the tubercle bacillus, the Amoeba dysenteria?, and sometimes to infec- 
tion by Shiga's bacillus. It also develops as a terminal infection in some 
cases of chronic renal disease. Ulcerative processes in the intestines are 
very common in the insane, and they have been associated with locomotor 
ataxia. 

Under the name of croupous colitis, a condition exists in which the mucous 



DILATATION OF THE COLON 630 

membrane of the colon becomes engorged and coated with a false membrane, 
and the underlying tissues becoming filled with dead leukocytes and fibrin. 
As in the small bowel, so here, this false membrane may be widely diffused 
or occur in patches. After the formation of the membrane the disease either 
disappears by the exfoliation of necrotic material or the deeper coats of 
the bowel are affected, so that areas of submucous tissue become necrotic 
and are passed in the stools as sloughs. At the site of these sloughs 
healing by cicatrization develops, or the process extends still more deeply 
to the peritoneum and causes serious secondary lesions. In this way is 
formed a necrotic colitis, the ulcerated areas being gangrenous in appearance 
and of great size. A large number of pathogenic organisms have been found 
in the bowel in such cases. 

Treatment. — This consists in following a plan identical with that advised 
for mucous colitis, and in addition in giving an injection of nitrate of silver 
in the strength of 40 grains to the quart each evening in place of the normal 
saline already spoken of. 

Pseudomembranous Colitis. — This is a condition in which not only the 
large intestine, but the small bowel as well is affected by a superficial necrosis, 
which may be diffuse, but is more commonly distributed in patches. The 
process closely resembles croupous colitis, and by some writers the two con- 
ditions are held to be identical. The false membrane consists of dead 
epithelium, mucus, fibrin, and white blood cells which have passed out 
of the bloodvessels. In some cases the false membrane is almost purely 
mucin-bearing and quite fibrin free; the latter element is only exceptionally 
abundant. Not rarely the submucous tissues may be infiltrated by serum 
and leukocytes. 

Pseudomembranous enteritis develops in the course of a number of the 
acute infectious diseases, in pyaemia and septicaemia, in persons who suffer 
from chronic Bright's disease, and occasionally after the taking of poisons 
which cause gastrointestinal irritation. It is important to recall the fact 
that this pseudomembranous condition is not diphtheritic in the sense that 
it is due to the Klebs-LoefHer bacillus, and that the proportion of fibrinous 
exudate is far less than in the membrane of that specific disease called diph- 
theria. Perhaps the most common cause of this lesion is the ingestion of 
poisonous quantities of arsenic, for this drug is eliminated by the mucous 
membrane of the alimentary canal and in the process a necrosis of the lining 
epithelium takes place. 

DILATATION OF THE COLON. 

Hale White places dilatation of the colon in four divisions. The first of 
these is that type of dilatation which is due to acute distention from the 
accumulation of gas. This is not rarely met with in severe infectious dis- 
eases, as in the pneumonia of drunkards and in severe cases of typhoid fever 
with toxaemia. The distention of the colon under these circumstances often 
interferes with the action of the lungs and heart by mechanical pressure 
against the diaphragm. The zone of the abdomen between the umbilicus 
and the ensiform cartilage, and between the right and left hypochondrium 



040 DISEASES OF THE INTESTINES 

is distinctly bulging and tympanitic on percussion. Tympanites of this 
kind possesses a double significance: first, it is an evil in itself by reason 
of the pressure which it produces, and, second, its presence is evil in that it 
indicates a lowered vitality and an inability of the intestine to expel gas which 
otherwise would not be allowed to accumulate, and which in health would 
not form. 

The treatment of this form of tympanites consists in the application of a 
hot turpentine stupe over the abdomen and the injection into the rectum 
of 6 ounces of milk of asafcetida containing 1 drachm of oil of turpentine, 
the two fluids being thoroughly mixed in order to prevent the turpentine 
from damaging the bowel. In other cases, where it is considered advisable to 
stimulate the circulation at the same time that the gas is expelled, and when 
it is feared that the turpentine may be absorbed and irritate the kidneys, 
excellent results will follow the use of this quantity of milk of asafcetida 
with the addition of J to 1 ounce of Hoffmann's anodyne. When obstinate 
constipation is present, and the sigmoid flexure is filled with feces, an ordi- 
nary soapsuds enema, followed by 1 ounce of sulphate of magnesium in 
4 ounces of water and 2 ounces of glycerin, may be injected. A few years 
ago it was suggested by Ogle, and others, that puncture of the bowel through 
the abdominal wall should be performed in those cases in which the gas 
could not be dislodged and when it was causing dangerous pressure. While 
this advice is theoretically good, practically it is of little value. I have tried 
it in a number of instances, and it has either failed entirely or has permitted 
but a small quantity of gas to escape from a single knuckle of intestine, 
the bowel contracting in such a manner as to prevent most of the gas from 
finding its way to the aspirating needle. If a fine needle is used but little 
gas can escape, while if a coarse needle is employed a sufficiently large 
puncture may be made in the bowel to permit of the escape of gas or liquid 
into the peritoneal cavity after the needle is withdrawn. 

The second group of cases depends upon the accumulation of foreign 
bodies. These are so rare in human beings as to be scarcely worthy of con- 
sideration. Occasionally, however, the dilatation may be due to the presence 
of enormous gallstones which have been still further increased in size by 
fecal additions. Such cases are to be treated by operation. 

The third form is that due to obstruction of the lower part of the colon, so 
that fecal accumulation and secondary ulceration may occur. The obstruc- 
tion may be due to volvulus, to a band or to a coil of adherent small intestine. 
It is also due to stricture or to syphilitic, cicatricial, or neoplastic growths, par- 
ticularly cancer. These cases are very rare, and the treatment is operative. 

Finally, in the fourth type we find cases of so-called idiopathic dilatation 
of the colon, which are also exceedingly rare. Many years ago Formad 
reported an extraordinary case of this character, and Hale White has collected 
several from literature. In most of these instances the enormously dilated 
colon is loaded with accumulated fecal matter. 

Treatment can be of little value in the last type of cases, for a congenital 
defect in the muscular and other tissues forming the wall of the intestine is 
responsible for the condition. Relief may, perhaps, be given by making 
an artificial anus at the sigmoid flexure. 



ACUTE PERITONITIS 641 

DISEASES OF THE PEKITONEUM. 

ACUTE PERITONITIS. 

Definition. — Peritonitis is a term applied to inflammation of the serous 
membrane, the peritoneum, lining the abdominal cavity and covering in 
its reflections the organs which this cavity contains. 

Etiology. — Within comparatively recent years it was generally considered 
that acute peritonitis was usually idiopathic, but with an increasing knowl- 
edge of the methods by which infection occurs, we have come to learn that 
most, if not all, cases of peritonitis are due to an infection which has come 
to the peritoneum through primary disease or the presence of infecting 
organisms in other organs. While we are not in a position to deny the exist- 
ence of idiopathic peritonitis, we should, nevertheless, always doubt it, and 
use every effort to discover the source of the infection which is present, even 
if it is not readily found. Nearly half a century ago Habershon found, in 
an analysis of 501 autopsies after death from peritonitis, that over 50 per 
cent, resulted from some primary disease not involving the peritoneum, and 
more recently Kelynack, in studying 124 cases of acute peritonitis, found 
that every one of them developed the disease as a secondary lesion. 

It may be true that exposure to cold and severe strain are productive of 
peritonitis, but if this is the case it is only because these influences diminish 
the vital resistance of the peritoneum. 

The two great causes of peritonitis are appendicitis and disease of the 
Fallopian tubes. In both of these instances it is due to the extension of 
an inflammatory process, which in turn arises chiefly from the spread of 
infecting micro-organisms. 

The method by which pathogenic micro-organisms are enabled to pass 
through the walls of an inflamed appendix has already been spoken of in 
the article on Appendicitis, and it is worthy of note that any cause which 
seriously interferes with the health of even a small part of the intestinal 
wall may permit the escape of micro-organisms into the general peritoneal 
cavity. Of the micro-organisms which commonly produce peritonitis under 
these circumstances, the Bacillus coli communis is, perhaps, the most fre- 
quent, but a large number of other micro-organisms are often present, and 
there is every reason to believe that, they are active in the production of the 
inflammatory process. Next to the Bacillus coli communis stands the Strep- 
tococcus and the Pneumococcus, the Staphylococcus albus, and the Bacillus 
pyocyaneus. The Bacillus aerogenes capsulatus is also not infrequently 
present. Occasionally the Bacillus typhosus seems to be responsible for 
the process. 

When infection takes place by means of the Fallopian tubes, the peri- 
tonitis may be due to the gonococcus; but in the majority of instances 
the inflammatory process is not due to this organism, but to the strepto- 
cocci or staphylococci which are associated with it; the presence of which, 
perhaps, enables the gonococcus to become pathogenic in this serous mem- 
41 



642 DISEASES OF THE PERITONEUM 

brane. Buram, however, believes that the escape of the gonococcus into 
the peritoneum is not usually followed by evil results. On the other hand, 
pure cultures of the gonococcus have been obtained from the abdominal 
cavity in two cases of acute general peritonitis by Young and Cushing. 

Subacute or chronic peritonitis is often due to the Bacillus tuberculosis 
and acute miliary tuberculosis of the peritoneum, which is usually looked 
upon as a form of acute peritonitis, is necessarily the result of the infection 
by the tubercle bacillus. In the acute peritonitis following labor, the 
so-called septic peritonitis, the streptococcus is the chief factor. Cases of 
peritonitis due to the pneumococcus have been frequently recorded. 

While we know, therefore, that peritonitis in its acute forms is a sec- 
ondary infection, it must not be forgotten that in a very large number of 
cases the peritoneum is capable of resisting infection and of destroying 
micro-organisms which may gain access to it. Indeed, the vital resistance 
of this membrane when in health is very remarkable, and a number of inves- 
tigators have shown that it is possible to place in the peritoneal cavity con- 
siderable quantities of septic material without serious result, provided this 
serous membrane is not subjected at the same time to insult whereby its 
vitality is decreased. 

Certain diseases which greatly decrease vital resistance greatly increase 
the susceptibility to peritonitis, as, for example, typhoid fever, Bright's 
disease, and advanced arteriosclerosis. 

Peritonitis in children, of course, develops as a result of the causes already 
enumerated. It also is sometimes seen in young infants suffering from con- 
genital syphilis, and in those who have intestinal obstruction. In still other 
cases it follows infection of the umbilicus after birth. In still others it is 
due to an extension of infection in empyema, and a few cases are on record 
in which sewer-gas poisoning has seemed to produce an epidemic of this 
character among children exposed to its influence. 

Striimpell states that a form of localized peritonitis in the left groin is 
occasionally met with in children, that it is prone to be purulent, and that 
the pus usually escapes through the rectum. 

Pathology and Morbid Anatomy. — The characteristic appearance of the 
peritoneum in primary acute peritonitis is hyperemia, with a diminution in 
the normal glossiness of the membrane involved. This is followed by a more 
or less copious fibrinous exudate, which may be well distributed, or appear 
chiefly in patches, upon the parietal and visceral peritoneum. In many cases 
there is little fluid exudate, the small quantities present being found in 
pockets formed by the coils of intestine which become agglutinated. In 
other instances the fluid portion of the exudation is very much more copious, 
and the quantity of fibrin thrown out is also of considerable amount, so that 
it is not only found well distributed over the surface of the membrane, but 
free flakes may be found floating in the serous exudate as well. 

When the infection is due to pyogenic micro-organisms, and particu- 
larly in those cases in which the vital resistance of the patient is very 
low, a septic peritonitis speedily develops. It is usually very diffuse in 
such cases, the entire peritoneum being involved. The quantity of exudate 
is moderately large, and is often offensive in character, forming what has 



ACUTE PERITONITIS 643 

been called "putrid peritonitis." In other cases when the vital resistance 
is not so depressed, the presence cf pyogenic micro-organisms produces a 
peritonitis in which pus alone is present. This form of peritonitis may be 
widespread, but is often localized — the so-called loculated or circumscribed 
peritonitis or peritoneal abscess — nature being able to wall off the area of 
acute infection by a plastic exudate, which prevents the infection from 
becoming well distributed throughout the peritoneum. In those cases of 
septic peritonitis in which death occurs early, the physician may be surprised 
on opening the abdomen at autopsy to find that but little change has taken , 
place in the appearance of the peritoneum and its contents. Save for some 
duskiness of the peritoneum and the presence of sanious fluid, the abdominal 
contents may seem to the naked eye to be but little altered. 

Occasionally we meet with what is known as hemorrhagic peritonitis, 
which may follow severe septic infection, and in cancerous and tuberculous 
cases, with ulceration, the fluid in the abdominal cavity may be blood- 
stained. 

Localized peritonitis, such as has already been referred to, is most fre- 
quently found in connection with diseases of the pelvic organs in women 
and with cases of appendicitis. It may be considered the rule rather than 
the exception, for the disease to be limited by an inflammatory exudate in 
such cases. Other forms of localized peritonitis which are not so frequently 
met with depend upon an extension of infection from the gall-bladder, from 
perforation or infection through a gastric ulcer, and occasionally we find a 
suppurative peritonitis in the lesser peritoneum as the result of disease of the 
pancreas or fat-necrosis. In other instances this condition arises as the result 
of renal calculus and nephritic abscess. 

Symptoms. — There are few diseases which, when well developed, produce 
a train of symptoms more characteristic than are those of acute peritonitis. 
This holds true, however, only when the disease is well advanced, and, indeed, 
is so severe that there is grave doubt as to the patient's recovery. In most 
cases of peritonitis, when the physician is first called to the patient, severe 
pain in the abdomen is the chief condition which is complained of. The 
pulse is usually quick, small, and hard, and the belly wall tender on palpa- 
tion, and distinctly rigid. The face will be found to wear an expression of 
anxiety, which seems to be far out of proportion to the length of the illness 
and its severity. In many instances, even when the pains are exceedingly 
severe, the patient considers that he is suffering from acute indigestion, 
but acute indigestion is often relieved by pressure, and is usually accom- 
panied by tumidity of the abdomen; whereas, peritonitis is characterized 
by great abdominal tenderness and by a flat or scaphoid appearance of 
the belly wall. The fever is usually not very high. The pulse is tense and 
rapid. It often does not go above 102°, and frequently not over 101°. Vomit- 
ing is frequently present. 

After* the pains have been present for a few hours, the exquisite tenderness 
of the abdomen makes the weight of the bed-clothes insupportable, and, in 
order to obtain some relief for the abdominal tension, the patient usually lies 
on his back, with the knees drawn up, and supports the bed-clothes over his 
abdomen by his hands, looking with dread upon the approach of the attendant 



644 DISEASES OF THE PERITONEUM 

lest he touch the abdomen or jar the bed. Thirst which cannot be relieved, 
because of constant retching, may add to the patient's distress, and hiccough 
of a very persistent and exhausting character often develops. 

As the disease progresses, the belly, which has been tense and scaphoid, 
becomes hard, not from muscular spasm, but from abdominal distention. In 
the flanks percussion may reveal some flatness due to the accumulation of 
the exudate in these parts. The face not only is anxious in appearance, but 
rapidly becomes pinched and peaked, the eyes appear sunken, the nostrils are 
thin and drawn, the skin pale and livid, and the tongue dry and parched, 
the typical "Hippocratic facies." The pulse at this stage is exceedingly 
rapid, running, and wiry, and, as the end approaches, loses its tense char- 
acter. A cold sweat may break out about the wrists and on the forehead. 

The bowels are usually obstinately confined, but in some instances diar- 
rhoea may be present, particularly if diarrhoea has been a symptom of the 
case prior to the development of the peritonitis. The respirations are usually 
a little quickened, but are shallow and superficial, in order that the abdom- 
inal movement may be as slight as possible. A remarkable fact in connection 
with these cases is the preservation not only of consciousness, but the develop- 
ment of intense mental activity, which in some cases persists up to the 
moment of death, the patient showing an acuteness of mind which is startling. 
In some instances during the last hours there may be a mild delirium, or even 
slight stupor. 

In septic cases pain is absent in the majority of instances, but the tem- 
perature in the early stages may be much more febrile than in the ordinary 
types of the disease. Sometimes it is distinctly like that of early septicaemia. 
By the time that the septic inflammation is well developed, however, the 
fever usually falls to the neighborhood of normal, and it may reach sub- 
normal. 

Careful examination of the abdomen in cases of well-developed peritonitis 
not only reveals the local symptoms already described, but it may also show 
localized patches of tympany where gas has accumulated in the coils of 
intestine, which are more or less fixed in one position by inflammatory adhe- 
sions. These coils, partly because of the inflammation and partly because 
of distention, may soon become paralyzed, so that distention increases. 

When the peritonitis is due to a perforation of the intestine or of the 
\ stomach, the accumulation of gas in the peritoneal cavity may mask the 
area of liver dulness or completely obliterate it. At one time this was consid- 
ered a very valuable sign in the diagnosis of perforation with secondary 
peritonitis, but we now know that in many instances this symptom is 
absent. 

Complications and Sequelae. — Peritonitis usually runs such a rapid course, 
either to recovery or death, that complications are rarely met. The most 
important and most frequent complication of a serious nature is pneumonia. 
In 100 cases of peritonitis observed in the London Hospital, Treves found 
that no less than 17 developed pneumonia or pleurisy after the peritonitis 
began. Retention of urine is frequent. 

As a sequel intestinal obstruction may develop as the result of adhesions 
or by strangulation of the bowel, produced by the slipping of a knuckle of 



ACUTE PERITONITIS 645 

intestine through an opening under a band or a false ligament, or by the 
development of a twist of the bowel through interference with its peristaltic 
movement. 

Diagnosis. — The diagnosis of acute diffuse peritonitis is usually readily 
made, even in its early stages. In its late stages its symptoms, except in the 
septic form, are so characteristic that the diagnosis can be made on a most 
superficial examination of the patient. 

In certain cases of typhoid fever in the early stages, when the inflam- 
matory process in the intestines is acute, there may be a good deal of 
abdominal pain and considerable tenderness. The apathetic expression of 
the face, the higher temperature of typhoid fever in the stage of onset, the 
tumid belly, and the coated tongue, with red edges, will aid in its differ- 
entiation. 

The separation of intestinal obstruction from peritonitis is exceedingly 
difficult; but as they often are coincident, the one following the other, and 
the treatment of such cases the same, differentiation is unnecessary. The 
rapid onset of severe pain of a cramp-like character, the complete ab- 
sence of any movement of the bowels, the presence of intestinal unrest, 
and in intussusception the palpation of a mass may make the diagnosis 
possible. 

Certain cases of hysteria at times present symptoms so characteristic of 
peritonitis that even the most skilful may be misled. Every symptom may 
be presented, yet the patient always recovers. 

Acute hemorrhagic pancreatitis may also so closely resemble peritonitis that 
a diagnosis is impossible, but this malady is exceedingly rare. In it there 
may be a preceding history of gallstone disease, whereas in peritonitis, 
unless perforation of the gall-bladder has occurred, there is no such history. 

The pain of gallstone colic and renal colic is so localized that much diffi- 
culty in diagnosis does not exist, as a rule. 

In cases of perforation of the stomach with secondary pyopneumothorax 
subphrenicus, the differentiation may be exceedingly difficult, save that 
swelling in the epigastrium and a history of gastric ulcer may be present. 

When perforation of the stomach has occurred without the formation of 
abscess, so that the gastric contents and gas escape into the peritoneum, 
great tympany and modification of the area of liver dulness is found. Not 
infrequently in subphrenic abscess a pleural effusion exists, so that serum 
may be drawn from this level and pus from the level below the diaphragm. 

Occasionally, in children suffering from pleurisy, pericarditis, and pneu- 
monia, violent pain is complained of in the abdomen, which may mislead the 
physician, if he be not on his guard. 

Prognosis. — The prognosis in every case of well-developed acute diffuse 
peritonitis is distinctly unfavorable. If the physician has reason to believe 
that the peritonitis is localized, the outlook becomes more promising. A good 
deal depends, too, upon the cause of the peritonitis, and upon the character 
of the infecting micro-organism. Thus, if it follows perforation of the 
stomach or bowels, and it is not walled off from the general peritoneal cavity, 
and again, if a skilful surgeon is not at hand to operate at once, the prognosis 
is hopeless. When the infection after perforation is localized, the mortality 



646 DISEASES OF THE PERITONEUM 

is not so great, but this form of localized peritonitis is far more fatal than 
that form which is due to appendicitis. 

The duration of life in fatal cases of peritonitis varies very greatly. Death 
may come as early as thirty-six or forty-eight hours, or may be deferred for 
a week or ten days, or even longer. 

Treatment. — The treatment depends so entirely upon the cause of the peri- 
tonitis that it behooves the physician to study the case most carefully. If 
seen shortly after the onset of the malady, the physician should at once con- 
sider the possibility of perforation of some portion of the alimentary canal 
being responsible, and should examine carefully into the history of the patient 
as to the possible presence of gastric ulcer or intestinal ulcer due to typhoid 
fever or dysentery. If the patient is an adult, careful consideration of the 
possibility of extension of inflammation from the gall-bladder should be 
followed. It is hardly necessary to state that as appendicitis and diseases of 
the Fallopian tubes are the most common causes of peritonitis, the condition 
of these two parts should be most carefully inquired into, both as to previous 
history of the patient and as to the physical signs which may be present. 
If the peritonitis is diffuse and has followed perforation or strangulation, the 
salvation of the patient depends upon immediate surgical interference, 
unless, perchance, shock prohibits operation, when it is permissible to wait 
two or three hours, in the hope that by the use of external heat and stimulants 
the patient may be enabled to bear operation. If, on opening the belly, a 
diffuse general peritonitis is found, it would seem best, in the majority of 
cases, to resort to the plan suggested by J. B. Murphy, namely, to remove 
the appendix if it can be reached, close the perforation if it exists, intro- 
duce a drainage tube into the pelvis, place the patient in a semi-recumbent 
posture and give a quart of normal saline solution by the rectum every 
two or three hours. 

When it is due to appendicitis, the age and general physical condition 
of the patient, must largely influence the decision as to operative inter- 
ference. I agree with McCosh, who states that in aged persons, particu- 
larly if they have been dissipated, medical treatment gives better chances 
than surgical interference, while the reverse holds true in young persons. 
If a surgeon of experience cannot be obtained, medical treatment will 
always give the best results. 

The question as to the procedure which should be followed if the cause 
lies in the appendix has already been discussed in the article on that dis- 
ease. Fulminating, gangrenous, or perforative appendicitis should, of course, 
be operated upon at once; whereas, on the other hand, if the appendicitis has 
simply produced an adjacent peritonitis, temporizing measures should be 
resorted to, and operation performed in the period of quiescence. 

The profession has passed through three periods of fashion in regard 
to the drug treatment of peritonitis itself. Twenty or thirty years ago 
it was extensively taught that general peritonitis should be treated by the 
administration of massive doses of opium, which were not only sufficient 
to relieve pain completely, but also to produce mental quiet. Under the 
leadership of Alonzo Clark, of New York, enormous doses were sometimes 
given, as much as 258 grains of opium being given in a day; and while 



CHRONIC PERITONITIS 647 

it is undoubtedly a fact that patients with peritonitis are able to take these 
doses without being poisoned, this plan of treatment received its deathblow 
with the discovery that nearly all cases of peritonitis are due to an infection, 
and that the source of infection must be discovered, and, if possible, removed. 
It has therefore become obsolete because it masks the symptoms, and is 
thought to have no definite influence upon the progress of the disease, save 
that it diminishes the suffering of the patient. It is probably safe practice 
to administer a sufficient quantity of morphine or opium to diminish agony, 
but not enough to mask the symptoms or make the patient so comfortable 
that he will refuse operative interference when the physician thinks it 
advisable. 

Soon after the infectious nature of peritonitis was recognized, the profes- 
sion went to the extreme of purging with saline cathartics, and even with 
vegetable cathartics, all cases in which symptoms of acute peritonitis were 
manifest. There is no doubt that this method was used to excess, and at 
the present time we know that it is unnecessary, unless there is reason to 
believe that the bowels are overloaded with fecal matter. In the writer's 
experience cases of this character are usually relieved by the bowels expelling 
the feces in the early stages of the peritoneal inflammation. 

The opium treatment was excessive, the purgative treatment was also 
excessive, when either of these plans was applied to every case, but both of 
them used in moderation may be advantageous in certain cases. 

Counterirritation applied over the abdomen in the shape of a large 
number of leeches may be useful in sthenic cases. In other instances a 
light mustard plaster may be used for relief. In still others an ice-bag has 
been employed. Thirst may be relieved by the use of small pieces of ice, or, 
better still, by rinsing the mouth with glycerin 1 part and water 3 parts, 
to which has been added a few drops of lemon-juice. Liquids should not 
be swallowed, as they increase the tendency to vomiting. If thirst is exces- 
sive, fluid may be supplied to the tissues by hypodermoclysis or by rectal 
injection. As a rule, the patient does not live long enough in well-developed 
peritonitis to make the question of feeding an important one. If the 
focus of infection is removed by operation, the feeding is that used 
after all abdominal sections. 



CHRONIC PERITONITIS. 

Chronic peritonitis occurs in four forms, namely : a local adhesive process; 
a diffuse process; one characterized by a proliferation of inflammatory mate- 
rial and connective tissue; and in a hemorrhagic form as a complication of 
severe disease in adjacent organs or malignant disease of the serosa. 

The local adhesive type is often found in the neighborhood of such organs 
as the liver, spleen, and stomach, when, as a result of an acute inflamma- 
tory process in the visceral peritoneum covering the organ, an adhesion takes 
place, and, perhaps, thick fibrous bands develop. In many of these cases this 
condition is not even suspected during life. In the neighborhood of the 
pelvic organs this type of peritonitis is exceedingly common, and is, perhaps, 



648 DISEASES OF THE PERITONEUM 

the most frequent peritoneal lesion met with by the gynecologist. Sometimes 
intestinal obstruction results from a slow, chronic, inflammatory process, 
which glues a knuckle of intestine to the omentum or the anterior wall of 
the pertitoneum. 

In the diffuse but chronic type of peritonitis a condition closely resembling 
that of fibrous tuberculous peritonitis develops, so that the peritoneal cavity 
is practically obliterated, and the coils of intestine are often matted together 
so that it is impossible to separate them. The parietal layer of the peritoneum 
is greatly thickened, and all the abdominal organs seem to be constricted 
and drawn by the cicatricial process. 

Closely allied to the last type is the 'proliferative form, in which the changes 
are not very different, except that there is, in addition, a considerable quantity 
of serum in the abdominal cavity. Sometimes this may be present in such 
quantities that the belly is greatly distended. The omentum is rolled up as 
a window-shade is rolled up, and extends across the upper zone of the 
abdomen in a round mass. The intestines may, or may not, be adherent 
to one another, the presence of the fluid serving to separate them and to 
prevent dense adhesions taking place. At times some of the fluid may be 
divided off into pockets by the adhesions. This form of proliferative peri- 
tonitis is usually due to tuberculosis, and not infrequently complicates 
alcoholic cirrhosis of the liver, but it is generally believed that in some cases 
it may arise from other causes than tuberculosis. Even if the cause is not 
tuberculosis the condition may, however, very closely resemble it on palpa- 
tion, because nodules may be found. 

In cases of carcinoma of the viscera a chronic form of peritonitis asso- 
ciated with the exudation of blood-stained or hemorrhagic serum is occa- 
sionally met with. Indeed, the obtaining of such serum from a case of 
ascites is always to be considered as indicative of that form of peritonitis 
depending upon malignant growth. As a rule, the chief lesions are found 
in the pelvis, or there may be present a general carcinomatosis of the peri- 
toneum. In other cases the pelvic viscera may be coated with fibrinous 
exudate, which undergoes connective-tissue changes, and becomes highly 
vascularized. 

Friedreich has described a form of chronic hemorrhagic peritonitis which 
follows repeated resort to paracentesis abdominis, the entire peritoneal 
surface being granular, reddened, and dotted with extravasations of blood. 



CHRONIC ADHESIVE SCLEROTIC PERITONITIS. 

This is a very rare state, apparently met with more frequently in Germany 
than in the United States. It was described by Virchow in 1853, and in more 
recent times by Riedel. It consists in an extensive subperitoneal fibroid 
infiltration or sclerosis, without ascites and without serous, or serofibrinous, 
or purulent fluid in the abdomen. In other words, it is rather a disease 
primarily involving the subperitoneal connective tissue than a true chronic 
peritonitis. This hyperplasia results in a sclerotic process, which in turn 
produces contractions and retractions, and, by the formation of adhesions, 



OTHER GROWTHS OF THE PERITONEUM 649 

fastens organs to the abdominal wall. The symptoms are those of the 
chronic fibroid type of tuberculous peritonitis already described, but the con- 
dition is not due to tuberculosis. Wetherill states that the peritoneum 
shrinks so that when abdominal section is performed it is impossible to 
approximate its edges on closing the wound. 

For a description of the so-called "iced liver of Pick" see Adhesive 
Pericarditis. 

CANCER OF THE PERITONEUM. 

This is an exceedingly rare condition as a primary lesion. In all proba- 
bility when it does occur, it is an endothelioma rather than an epithelioma. 

Carcinoma and carcinomatosis of the peritoneum are usually if not always 
secondary to cancer of some contained viscus. The primary growth may be 
so small as to escape superficial examination even at autopsy, and is com- 
monly in the stomach, pancreas, liver, or biliary passages, or, less frequently, 
in the rectum; in the female the pelvic organs are by far the commonest site 
of the primary growth. On account of the pervious nature of the diaphrag- 
matic lymphatics, the pleurae, pericardium, and peritoneum may be simul- 
taneously affected, or invasion of one may be quickly followed by extension 
to the others. 

An interesting case of colloid cancer has been reported by Ferguson. 
Both the visceral and parietal layers of the peritoneum were involved, as 
were also the omentum. The mesentery was in some places 10 cm. thick. 

The symptoms of either the primary or secondary carcinoma of the peri- 
toneum are emaciation, ascites, and, it may be, the discovery of nodules, or of 
a furled omentum, such as occurs in certain types of peritoneal tubercu- 
losis. The fact that the fluid is often hemorrhagic has already been referred 
to. In the colloid cases the peritoneum may be rilled, not with fluid, but with 
a jelly-like substance, which is so firm that it will not fluctuate. 



OTHER GROWTHS OF THE PERITONEUM. 

Hydatid cyst of the peritoneum is occasionally found, although, as a 
rule, it develops in the abdominal organs rather than in the peritoneum 
itself. A cyst the size of an orange has been reported by Jones as occurring 
in the mesocolon. It was successfully removed. Rein has reported a mul- 
tiple hydatid cyst occurring in the omentum of a woman in the third month 
of pregnancy. She was operated on and recovered. Other instances have 
been reported by various clinicians, the largest number of cases collected 
being those of Moneger, who has reported 32. He tells us that such cysts 
are nearly always secondary to rupture of cysts in neighboring organs, and 
there is usually a history of violent pain at the time of rupture. Perhaps the 
most extraordinary case is that reported by MacDonald, who has reported 
the case of a man with thirty hydatid cysts of the peritoneum. Other 
cysts of the mesentery are chylous, dermoid, serous, and sanguineous. 

Very rarely sarcoma and cystic adenoma affect the peritoneum. 



650 DISEASES OF THE PERITONEUM 



ASCITES. 



Definition.— The term ascites is applied to the accumulation of serous 
fluid in the abdominal cavity. In some cases the quantity of fluid is very 
small, but in others it amounts to several gallons. In the majority of 
instances ascites is due to atrophic cirrhosis of the liver, tuberculosis of the 
peritoneum, or cardiac disease. In cases of chronic Bright's disease of 
the parenchymatous type, ascites is often present as part of the general 
anasarca. It also develops as the result of pressure upon the abdominal 
bloodvessels, whereby the blood in the large venous trunks is obstructed in 
its flow. 

The fluid in ascites is usually of a light straw color, and does not coagulate 
when exposed to the air. 

Etiology. — The intra-abdominal causes of ascites, as just stated, are 
atrophic cirrhosis of the liver, tuberculous peritonitis, and morbid growths, 
which, by pressure upon bloodvessels, or by producing changes in the peri- 
toneum, result in a transudation of fluid. A thrombophlebitis, or other 
form of venous obstruction, may also cause ascites. Thrombosis, tubercu- 
losis, or neoplastic invasion of the thoracic duct, or its obstruction by 
parasites (filarial) , or other causes, and also wounds of the duct or of the 
receptaculum, or larger lymph-vessels or chyle-vessels may produce an 
ascites the fluid of which contains chyle. 

Symptoms. — When the abdomen of a patient suffering from ascites is 
exposed, it is seen to be greatly enlarged, this enlargement being chiefly in 
the lower and lateral zones, although if the intestines are by chance dis- 
tended by gas the upper and middle zone may be most enlarged. The 
line of the ribs is usually sharply defined, by reason of the fact that they 
do not yield readily to the pressure and are held in place by the dia- 
phragm. 

If the ascites be due to hepatic cirrhosis, the venules about the navel will 
often be found engorged (see Cirrhosis of the Liver), and in all forms of 
ascites due to venous obstruction the veins under the skin in the right and 
left hypogastrium and groins may be surcharged with blood in an endeavor 
to establish a collateral circulation, and so relieve deep pressure in the 
venous trunks. 

The signs of fluid in the abdominal cavity are dulness on percussion in 
the flanks, and in the suprapubic region when the patient is semi-recumbent, 
with tympany over the anterior and middle zone of the abdomen extending 
upward to the epigastrium, owing to the intestines being floated up against 
the anterior abdominal wall by the fluid beneath. If the hand of the nurse 
is placed with its ulnar edge upon the middle line of the abdomen, the left 
hand of the physician placed on the right flank, and the right hand used to 
lightly strike the left flank, distinct fluctuations will be felt by the left hand, 
the impulse being transmitted by the fluid from one side to the other, the 
hand of the nurse being used to prevent the transmission of this impulse 
through the abdominal wall. Changing the patient's position from the 
recumbent to the erect posture will change the area of dulness on per- 



ASCITES 



651 



cussion and the shape of the abdomen, owing to the alteration in the position 
of the fluid. Palpation will reveal fluctuation if the belly is not too 
tense. Percussion will give a tympanitic note in the epigastrium when the 
patient is sitting up and flatness below the navel and at the sides of the 
abdomen. 

A patient who has ascites to any considerable degree is usually unable to 
lie down with the head low, because if this attitude is assumed the pressure 
of the fluid against the diaphragm is such that breathing is interfered with. 
For this reason he usually sits propped up in bed or in a reclining chair. 
The face, which is usually thinner than in health and somewhat haggard, 
forms a striking contrast to the large abdomen, which is "aldermanic" in 



Fig. 86 




Ascites due to cardiac dropsy, with diastasis of the recti muscles, so that there is a subcutaneous 
hernia in the tissue around the umbilicus. There is also enteroptosis due to great relaxation of the 
abdominal wall, which actually overlies the thighs. 



appearance, and if the legs be dropsical as well, the massiveness of the lower 
half of the trunk, as compared to the upper half and to the neck and face, 
presents a striking picture. Not rarely the face bears the expression known 
as the " abdominal facies." 

Dyspncea may not be noticeable when the patient is at absolute rest, but 
it not rarely happens that so slight an exertion as conversation will develop 
this symptom, particularly if, in addition, there be some tendency to oedema 
at the bases of the lungs. As a rule, men are more uncomfortable when 
suffering from ascites than are women, because their respiration is naturally 
more diaphragmatic than that of women, whose respiratory movement is 
chiefly costal. 



652 



DISEASES OF THE PERITONEUM 



Diagnosis. — Ascites must be differentiated from distention of the abdomen 
due to a large ovarian cyst. This can usually be accomplished by palpation 
percussion, and vaginal examination. Inspection of a case of a cyst will 
usually reveal somewhat greater distention of one side of the abdomen 
than the other. The area of dulness on percussion will not be in the lower 
zone of the abdomen alone, but will extend upward toward the ribs and will 
include part of the area in the anterior and middle zone of the belly, which 
in ordinary ascites is tympanitic. Further than this, a large ovarian cyst 
of this character will usually be tense and will offer more resistance when 
the abdomen is palpated with both hands. 



Fig. 87 




Case of enormous ascites due to atrophic hepatic cirrhosis. 

From enlargement of the spleen in chronic leukaemia ascites may be differ- 
entiated, by reason of the fact that in this disease the area of dulness is chiefly 
in the upper zone instead of in the lower zone of the belly, that tympany is 
usually not present in the middle line if the spleen extends so far, and that the 
edge of the spleen can be readily palpated. In some cases, however, in which 
the spleen is enlarged in leuksemia, ascites is also present, and it may be 
impossible to feel the edge of the spleen until some of the fluid is removed. 
This removal may be more difficult than in an ordinary case of ascites, 
because the spleen may be so close to the anterior abdominal wall and may 
extend so far down toward the pubis that ordinary paracentesis cannot be 
readily performed without danger of puncturing the spleen. Ascites must also 
be separated from great enlargement of the liver, as in hypertrophic cirrhosis. 
Here, again, the presence of dulness in the right upper zone of the abdomen 



INFLAMMATION OF THE LIVER 653 

and the ability to feel the lower edge of the large liver will aid materially in 
the differentiation. In both enlargement of the spleen and enlargement of 
the liver the area of dulness and of tympany is not materially altered by 
changing the posture of the patient as it is in ascites. 

Treatment. — The treatment of ascites depends to some extent upon its 
cause. If it is due to interference with the circulation by pressure, as in 
atrophic hepatic cirrhosis, little can be done except to remove the fluid 
by paracentesis, for the purpose of giving the patient relief from distention. 
If it is due to cardiac disease an improvement in the condition of the heart 
by the use of digitalis and rest, and the judicious administration of saline 
purges, may remove the fluid. In renal disease the use of purgatives may 
also be of value, but paracentesis has usually to be resorted to if the fluid is 
present in large amount. In peritoneal tuberculosis paracentesis may be of 
value, but the best method of producing cure is to resort to abdominal 
section, permitting the fluid to escape through the incision, and then 
maintaining drainage. 

Before performing paracentesis abdominis the patient should be made to 
evacuate his bladder, in order that by no possibility can it be punctured by 
the trocar. If the patient be a woman, great care should be taken that an 
ovarian cyst is not punctured. Puncture of a papillomatous cyst not infre- 
quently results in the speedy death of the patient. 



DISEASES OF THE LIVER 

INFLAMMATION OF THE LIVER. 

Acute Hepatitis or Hepatic Abscess. Definition. — Acute exudative 
hepatitis is a state of inflammation of the liver in which, after a stage 
of hyperemia with exudation, the area involved undergoes necrosis, and 
abscess results. 

Etiology. — Inflammation of the liver, severe enough to result in suppura- 
tion, may arise from injury, from inflammation of the portal vein or of the 
bile-ducts, or from adhesions to neighboring organs which are infected and 
from which infection may spread, as, for example, in cases of gastric ulcer. 

Suppuration within the substance of the liver beneath its capsule or in 
the bile passages occurs under many varying conditions. 

Traumatic Abscess. — Liver abscess may result from traumatism. The 
traumatism may be a severe blow or contusion, or a penetrating w T ound in 
or near the liver from a bullet, knife, or other weapon. Traumatic abscess 
of the liver is usually single. When it occurs as a result of contusion in 
the absence of direct infection, the injury acts by lessening resistance and 
permitting colonization of pyogenic bacteria brought to the organ by the 
portal vein or hepatic artery. 



654 DISEASES OF THE LIVER 

Pyemic Abscesses. — Pysemic abscesses are, as a rule, multiple. One 
group of cases arises from pyogenic embolism of the portal vein. There is 
phlebitis or thrombophlebitis of the portal trunk or its branches, the infection 
being due to ulcerations in the colon and rectum, or to appendicitis, ulcera- 
tions and suppurative processes about the neck of the bladder, and typhoid 
fever. Another group of cases arises from embolism of the hepatic artery, 
as in ulcerative endocarditis and other pysemic conditions. Infection 
may also reach the liver through the lymphatics. Abscess may also arise 
from the direct extension of infection from the gall-bladder and the 
biliary ducts. Ascarides, liver flukes, echinococcus, and the Balantidium 
coli may also cause abscess of the liver, and it has also been observed as a 
sequel to measles, epidemic influenza, and ulcer of the stomach. 

Amoebic Abscess of the Liver. — In the consideration of the etiology of 
tropical abscess, we find predisposing and direct causes. As a predisposing 
cause, the passive congestion of the liver which exists, to some extent, in a 
large proportion of colonists in the tropics, must be remembered. Other 
predisposing factors in the production of tropical abscess are malaria and 
exposure to cold and wet. Abuse of alcohol is probably an important 
predisposing cause. In Waring's careful study of the subject of abscess of 
the liver, he found a clear history of the abuse of alcohol in 65 per cent, of 
the cases. 

The direct cause of tropical abscess is the aoembce dysenteric which may 
or may not have previously excited intestinal lesions. Various observers 
have found that tropical abscess of the liver has been preceded by 
dysentery in from 72 to 97 per cent, of all cases. Woodward, in 3680 
dysentery autopsies, found liver abscess in 779, or 21 per cent. Boston col- 
lected data of 2430 autopsies, with 486 abscesses, or 20 per cent. Legrand, 
of Alexandria, found that in 109 cases of hepatic abscess which occurred in 
children 31 were due to dysentery. Hepatic suppuration may develop very 
shortly after the dysentery, or may be delayed for years. (See Dysentery.) 

Pathology and Morbid Anatomy. — Abscess of the liver usually occurs either 
in one or two large purulent collections or in a number of small abscess 
cavities. 

The single large abscess is usually the result of dysentery, and the infec- 
tion reaches the liver through the veins, which closely anastomose with 
the hemorrhoidal plexus. If the cause be dysentery of the amoebic type, 
the amoeba is found in the wall of the abscess, and less constantly in the 
abscess contents. In still other cases an examination of the pus reveals the 
presence of the Bacillus coli communis, or the Streptococcus pyogenes or 
a pyogenic staphylococcus. In still other cases, if the abscess be very chronic, 
the pus may be sterile. 

In tropical abscesses the lesion is solitary in about 60 per cent of the cases ; 
it is single, from coalescence, or double in about 15 per cent, of the cases, and 
the remainder are multiple. The abscesses vary in size from a pigeon 's egg 
to a cocoanut. 

The single abscess may be very large, and often fills an entire lobe of 
the liver. The right lobe is usually affected, and as the abscess gradually 
nears the surface of the organ it bursts through the capsule into the peri- 



INFLAMMATION OF THE LIVER 655 

toneal cavity, or, as is far more common, the advancing inflammatory zone 
causes the surface of the liver to become adherent to adjacent structures, 
so that when rupture takes place the pus breaks into the bowel, as in a case 
recently under my care, or through the diaphragm into the pleura, or even 
into the lung, so that the pus from the liver escapes by the respiratory tract. 
Accumulations of pus in burrowing a way for escape often cause extra- 
ordinary effects, and cases are on record in which the pus from one of these 
abscesses has escaped into the pericardium, and even into the pelvis of a 
kidney. Still other instances have occurred in which the pus has found its 
way into the great veins of the abdomen or into the gall-bladder. Rupture 
externally is not common. 

Fig. 88 




Liver, amoebic abscess of right lobe; case of dysentery. Note the shaggy necrotic wall and that the 
abscess has approached the superior surface of the organ. 

The pus from such an abscess is often very offensive, and it generally differs 
from ordinary pus in appearance, being thin instead of creamy, reddish 
instead of yellow, and oftentimes it is quite green from the presence of bile. 
Sometimes, however, the pus is quite like that commonly found in abscesses. 

The lining of the abscess cavity is shaggy, because of the pieces of dead 
hepatic tissue which hang upon it (Fig. 88). In abscesses of long standing 
more or less imperfect encapsulations of the pus may occur. 

Large multiple abscesses are sometimes met with as the result of suppura- 
tion about an echinococcus cyst. 

Small multiple abscesses are usually pysemic — i. e., of metastatic origin. 
Septic emboli, or micro-organisms, from septic foci elsewhere are carried 
by the blood into the liver and cause multiple areas of necrosis, and 



656 



DISEASES OF THE LIVER 



suppuration. The liver, therefore, presents not one large abscess, but a 
large number well distributed through its tissues. These abscesses vary 
in size. Several small necrotic cavities, which may hold several drachms 
of pus, may be present, or a number may coalesce to form one large 
abscess. Although each abscess seems isolated, it is usually in communica- 
tion through a branch of the portal vein with others, so that by this vascular 
pathway the whole gland is riddled with pus. The pus may vary from foul, 
reddish, or greenish material to the character of what used to be called, in 
preantiseptic days, "laudable pus." 

When the infection takes place along the bile-ducts, as the result of the 
entrance of micro-organisms, the introduction of which is facilitated by the 
presence of gallstones, it is often found that the pus is not only distributed 



Fig. 89 




Chart showing septic fever and marked leukocytosis in case of hepatic abscess. (Bassett-Smith.) 

widely through the organ, but, in addition, that the gall-bladder is full of pus 
as well, so that the entire biliary tract is involved in the suppurative process. 

Small multiple abscesses may be due not only to the ordinary organisms of 
suppuration, but to infection by the Amoeba dysenterice. 

Symptomatology. — The symptoms of hepatic suppuration are usually 
marked. In some cases, however, even with the existence of large abscesses, 
the lesion is latent, and the disease is not suspected until rupture of the 
abscess occurs. The chief symptoms are fever, sepsis, enlargement of the 
liver, and pain. 

The pain is felt not only in the right hypochondrium, but in the region of 
the right shoulder blade, and, as the abscess approaches the surface and 
causes inflammation of the peritoneum, the pain may be sharp and even 
severe. 



INFLAMMATION OF THE LIVER 657 

There is loss of weight and strength and pronounced feebleness in mus- 
cular effort. Dyspeptic symptoms become marked. There is anorexia, 
nausea, morning vomiting, with a heavily coated tongue. The patient becomes 
an&mic and gradually takes on a peculiar subicteric color. The fever 
begins early and is the most constant symptom. At first it does not 
run high, but later an evening temperature of from 104° to 105° is not 
uncommon. The fever is irregular or intermitting in type. It is preceded 
by a chill and then followed by a sweat. These sweats are very severe and 
contribute greatly to the depression and exhaustion of the patient. They 
follow the fastigium of the fever and are prone to come on during sleep, whether 
it be by day or night ; so that they may be properly called sleeping sweats 
rather than night sweats. 

Enlargement of the liver is constant. It is symmetrical, and in extreme 
cases may reach as high as the third rib in front and may extend as far 
down as the crest of the ilium, or over as far as the umbilicus. The 
right hypochondrium may appear full and bulging, and there may be 
an apparent fulness or sleekness of the right side, and in marked cases 
obliteration of the lower intercostal spaces. 

When pus approaches close to the surface it is always preceded by an 
&dema of the skin overlying the abscess, and in cases with large abscess 
fluctuation may be present. Auscultation over the liver may reveal peritoneal 
or liver friction. 

Occasionally sharp pain is felt in the esophagus, when a food bolus 
passes the level of the diaphragm. A dry, hacking, unproductive cough is 
very commonly present and frequently leads to error by directing attention 
to the lungs rather than to the liver. 

The decubitus of the patient is characteristic. He lies on his right side 
with that shoulder drawn down and knee drawn up to relieve the tension on 
the abdominal muscles. 

Jaundice is not common and only appears when the enlarged liver or 
abscesses make pressure on the bile-duct. Pressure on the portal vein may 
cause a moderate degree of ascites. 

Pneumonia of the right base often occurs when the abscess is high up in 
the dome of the liver. 

Diagnosis. — The condition which in all probability most closely resembles 
hepatic abscess is infection of the gall-duct or gall-bladder, produced by the 
presence of a stone or stones, for here, too, there is septic absorption, high 
fever, chills, sweats, and tenderness about the liver, although pus may not 
be actually present. In this condition, however, there is a history of gallstone 
colic in most instances, and of jaundice. Further, the emaciation and 
anaemia are not so marked, nor is the liver so generally increased in size. A 
marked leukocytosis is present in either case. 

The absence of marked swelling of the spleen, of any history of malarial 
infection, and the lack of the malarial parasite in the blood, combined with 
the fact that the fever does not yield to quinine, all go to prove the febrile 
state not malarial. The blood condition may also aid in the diagnosis. 
There is usually a marked leukocytosis, which ranges from 12,000 to 53,000. 
Unfortunately, this symptom is not constant, but when it does occur it 
42 



(558 DISEASES OF THE LIVER 

makes a clear distinction between this disease and malaria. Other condi- 
tions that simulate liver abscess are hepatic colic with fever, suppuration 
in and about the gall-bladder, suppuration in or near the right kidney, 
subdiaphragmatic abscess, empyema or pneumonia of the right base, and 
ulcerative endocarditis. 

An empyema or pleural effusion on the right side can be excluded by the 
decrease in vocal resonance and vocal fremitus caused by that state, and by 
the presence of Skodaic resonance just above the area of dulness on per- 
cussion. 

It is important to remember that amoebic abscesses may be present with- 
out diarrhoea or dysentery, the amoeba?, nevertheless, being present in the 
stools and in the liver. 

In all obscure cases attended by the signs of hepatic disease and sepsis, 
an effort should be made to establish the condition of the liver by explora- 
tory operation. 

Prognosis .—The prognosis of abscess of the liver depends on two factors, 
the number of abscesses and the time when the case is brought to operation. 
Eighty to 90 per cent, of single abscess brought to early operation should 
recover, but often operation is postponed too long. In cases of sponta- 
neous rupture into the colon 50 per cent, recover. The prognosis is not so 
good where rupture takes place into the lung or pleura. Recovery occa- 
sionally takes place when two and three abscesses are present. 

In 162 fatal cases of hepatic abscess the mortality is given as due to the 
following causes: severity of the accompanying dysentery, 125 cases; burst- 
ing of abscess into the peritoneum 12 cases, into the pleura 11 cases; gan- 
grene of the abscess wall, 3 cases; rupture of adhesions, 2 cases; pneumonia, 
2 cases; and rupture into the pericardium, 1 case. The prognosis in multiple 
abscess is hopeless, for manifest reasons. 

Treatment. — The treatment of hepatic abscess consists in sustaining the 
patient's strength by good food and by iron and arsenic, and, if the abscess 
is single, by opening and draining it as soon as its existence is determined. 

Exploratory puncture should not be practised unless the surgeon is 
prepared to go ahead and operate at once. If pus be found, the puncture 
may spread infection or cause a leak along the wound. This is especially a 
danger with large needles, and large needles must be used on account of the 
thickness and viscosity of the abscess contents in some cases. 



CIRRHOSIS OF THE LIVER. 

Definition. — Cirrhosis of the liver is a state in which there is an overgrowth 
of connective tissue of the gland. In some instances this overgrowth results 
in an atrophy and shrinkage of the organ (atrophic cirrhosis) ; in others the 
liver becomes greatly enlarged (hypertrophic cirrhosis). 

Recently Kretz, MacCallum, Kelly, and others have called attention to 
regenerative changes in the liver cells as being a prominent feature of cir- 
rhosis. They do not regard the normal liver as made up of distinct lobules 
but as consisting of continuous mantles of cells surrounding the blood- 



CIRRHOSIS OF THE LIVER 659 

vessels. In cirrhosis, following degenerative changes, these cells regenerate 
and rearrange themselves and, according to Kretz, cirrhosis is consequently 
to be regarded as a focal recrudescent chronic atrophy of liver cells modified 
by parenchymatous regeneration and not as a disease entity. He believes 
that practical extension of our knowledge on this subject is to come from 
investigating the causes of degeneration of liver cells rather than from 
attempts further to differentiate and classify so-called types of developed 
cirrhosis. 

Cirrhosis of the liver derives its name from the Greek word Zfppoc,, mean- 
ing yellow or tawny. The term cirrhosis was first applied by Laennec, 
because the liver, when cirrhotic, is yellow or tawny in color. Cirrhosis is an 
unfortunate term, in that it in no way describes the pathological state which 

Fig. 90 




2 cm* 
A 

Liver, advanced cirrhosis; typical hob-nailed organ. A. Gall-bladder. 

is present. Further than this, the word cirrhosis is now applied to patholog- 
ical states of other organs in which no yellow hue is seen. 

Atrophic Cirrhosis. — The liver in cases of atrophic cirrhosis is often 
enlarged in the early stage of the disease, but after this primary change 
it undergoes a diminution in size, so that eventually it is much smaller 
than normal. This primary enlargement, which does not always occur, is 
perhaps due to hyperemia, cellular infiltration, and oedema. The charac- 
teristic picture of atrophic cirrhosis is. however, that of a small, contracted 
liver, tawny in hue, and possessing a roughened surface, which in some cases 
may be so irregular as to be called "hob-nail" liver, because of its resem- 
blance to a rough shoe the sole of which is filled with hob-nails (Fig. 90). 

Atrophic cirrhosis of the liver is a not uncommon malady in adults, and 



660 DISEASES OF THE LIVER 

it is by far the most frequent of all the types of cirrhosis which affect this 
organ. 

Etiology. — The causes of atrophic cirrhosis of the liver are chronic alcohol- 
ism and other chronic intoxications, of which lead is certainly one of the most 
important. There is good reason to believe that prolonged gastrointestinal 
indigestion and disorders of nutrition, such as gout and its allied states, may 
exert a similar effect. Experimental cirrhosis has been produced in animals 
by acetic, lactic, butyric, and valerianic acid, all of which are present in 
cases of gastrointestinal disorder. Syphilis may cause it (see Syphilis of 
the Liver), and hepatic cirrhosis has been known to develop after severe 
infectious fevers. Cardiac disease, with great and prolonged hepatic conges- 
tion, may also produce cirrhotic changes, and it is a noteworthy fact that 
cirrhosis may be present as a part of a general fibroid process involving the 
bloodvessels and the kidneys. 

Pathology and Morbid Anatomy. — In cirrhosis of the liver the dominant 
lesion is an increase in its connective tissue. This overgrowth varies very 
greatly in different cases. Although the fibrous overgrowth may penetrate 
the lobules, it is principally increased at the periphery of these structures. 
Again, it may be equally distributed throughout the entire liver or affect 
certain areas very much more than others, and, finally, the overgrowth 
of fibrous tissue may be so great that bands, both large and small, may 
traverse the liver substance, separating it into masses of compressed gland- 
ular tissue. 

The fibrous tissue formed in this process, like fibrous tissue formed 
elsewhere in the body, undergoes cicatricial contraction, and by this means 
fatty degeneration or atrophy of the liver cells composing the lobules is 
facilitated. These changes are due, not only to the pressure exerted on the 
lobules, so that their cells are flattened and deformed, but also to the effects 
produced on the circulation of blood in the liver. 

It will be recalled that the hepatic artery carries to the liver the blood 
which is to nourish its cells, just as the bronchial arteries carry the blood 
which is to nourish the lungs. The blood from the branches of this vessel in 
performing its nutritive function passes through the so-called interlobular 
vessels, and from these into the intralobular vessels, which carry blood 
from the digestive organs. 

The overgrowth of fibrous tissue in the interlobular spaces, in the fibrous 
sheath of the interlobular veins, and sometimes even between the cells about 
the intralobular veins results in obstruction to the flow of blood. The 
arterial supply is little affected, but the venous flow is interfered with, and in 
this manner the cells suffer, not only from the pressure of the fibrous tissue, 
but from the pressure in the vessels and the lack of fresh blood as well. 
Nor is this all, for the fibrous tissue obstructs the smaller bile-ducts and so 
prevents the escape of bile, with the result that atrophy takes place from 
retained secretion, and the tissues of the liver become bile-stained. 

Many pathologists adhere to the view that the destruction of the paren- 
chyma of the organ takes place first, and that the overgrowth of the con- 
nective tissue already described is secondary to this change. 

The remote effects of the interference with the circulation of blood in the 



CIRRHOSIS OF THE LIVER 661 

liver is catarrh of the stomach and duodenum, due to the obstruction of the 
blood in the portal veins. This state, finally, may cause varicosities in 
the gastric or oesophageal vessels, and hsematemesis may ensue, or it may 
cause fatal hemorrhage from the bowels because of similar varicosities 
in the intestinal wall. The marked portal obstruction leads to trans- 
udation from the peritoneal vessels, constituting the ascites of hepatic 
cirrhosis. 

Not rarely in well-developed cases of hepatic cirrhosis the veins of the 
abdominal wall will be found enlarged in an endeavor to supplement the 
deep abdominal veins in the transfer of blood from the portal area to 
the vessels of the thorax. Still another state, called the "caput medusa?" 
is the development of a bunch of enlarged veins about the umbilicus. This 
has been generally considered as due to the stasis in the paraumbilical vein 
or in the umbilical vein, which has not closed, as it usually is after birth. 
As a result a collateral circulation is established by an anastomosis with 
the internal mammary, epigastric, and cutaneous veins. 

From the description which has just been given of the effect of cicatricial 
contraction, it is easily seen why the liver presents upon its surface so many 
excrescences or projections (the so-called "hob-nail liver"), for parts of the 
gland are pressed out of place, or irregular bands pulled in, by the ever- 
growing fibrous bands. (See Fig. 90.) 

The atrophy of the parenchyma of the liver in the true atrophic form 
causes a very great diminution in the size of the organ, so that the organ may 
be less than one-half its natural dimensions. 

The spleen is usually enlarged, and arteriosclerotic changes are often 
present. Secondary fibroid changes in the pancreas have also been described. 

In the so-called fatty cirrhosis, in which the deposit of fat is more pro- 
nounced than the cicatricial contraction of fibrous tissue, the gland may not 
be decreased in size, and it may be very much larger than the normal. Such 
a liver is rarely hob-nailed, but smooth, or but slightly roughened. 

Peritoneal and pleural tuberculosis is a very common complication of 
atrophic cirrhosis of the liver. 

Symptoms. — The symptoms of atrophic cirrhosis of the liver are, to a large 
degree, dependent upon the obstruction to the circulation of blood in the 
intralobular and interlobular vessels, and if the effects of this obstruction are 
relieved, or prevented from developing, by the establishment of an efficient 
collateral circulation, there may be no symptoms at all for many months, or . 
indeed, for years. Occasionally we meet with cases in which an extreme 
degree of atrophy of the liver seems to be present with no symptoms of 
any importance, and yet the patient is taking far more alcohol than is good 
for him. It is scarcely conceivable that the establishment of a collateral 
circulation can be responsible for the absence of all systemic disturbance, 
but there is no other explanation for it. 

When obstruction to the flow of blood in the portal vessels is produced 
gastric catarrh develops, and this causes indigestion and distress in the 
epigastrium, with morning nausea and vomiting. Usually the patient loses 
strength and is prone to become spare and lean if previously stout. 

The occurrence of hemorrhage from the stomach, and bowel has already 



662 DISEASES OF THE LIVER 

been mentioned when discussing the secondary lesions of the disease, as 
has also the presence of enlarged abdominal veins and the caput medusce on 
the abdominal wall. (See also the article on Hsematemesis.) The skin of 
the trunk is often more sallow and yellow than normal, but it is rarely dis- 
colored by a true jaundice. At times the temperature may be subnormal, 
and at others slightly febrile. 

In some cases which have manifested few or none of these symptoms, the 
patient, with little warning, develops a state of delirium, which is often of a 
noisy and joyous type, but he soon sinks into a state which proceeds to coma, 
and then to death. To this state the term " hepatic coma 7 ' has been applied. 
It was thought at one time to be due to cholestersemia, but this view has now 
been cast aside without any satisfactory explanation of the state being offered. 
I have so often seen this condition follow free drainage of ascites that I believe 
this operation predisposes to its development. 

The physical signs of atrophic cirrhosis consist in an inability to palpate 
the lower margin of the liver by ordinary effort, and in the small area of 
hepatic dulness on percussion. In those cases in which ascites is marked, it 
is often impossible to discover the state of the liver until the fluid is with- 
drawn. 

Some have held that the ascites is really the result of an associated low- 
grade peritonitis. 

Hess has lately directed attention to obliterating endophlebitis of the 
hepatic veins as producing symptoms almost identical with those of cir- 
rhosis. Most of the 23 cases on record, as also the one he reports, were 
diagnosed cirrhosis of the liver. The signs leading one to suspect oblitera- 
tion of the hepatic veins are absence of the history of a cause of cirrhosis, 
pain over the hepatic area or localized in the upper abdomen, and rapid 
swelling of the liver and development of ascites. 

Prognosis. — The prognosis as to the duration of life depends entirely upon 
the degree of obstruction to the circulation and upon the severity of the 
patient's symptoms. If ascites is well developed the outlook for more than 
a few months of life is bad, yet there are cases on record in which repeated 
tappings have resulted in the prevention of recurrence of ascites and in the 
apparent recovery of the patient. Probably in these cases the ascites was not 
due to the cirrhosis, or the relief of pressure has permitted the establishment 
of a collateral circulation. The occurrence of hemorrhages is always a most 
grave omen, yet patients often live for months after severe bleedings. On the 
other hand, I know of one case in which a man, in apparently perfect health, 
while washing in his bath-room bled so freely from the stomach as to die in 
half an hour, although he had never had a hemorrhage before. 

Treatment. — The treatment consists in removing the cause of the disease, 
if it be alcohol, and in an endeavor to prevent intestinal fermentation and 
disorder by mild purgatives, digestive stimulants, acids, and antiseptics. 
Each morning the patient should have the bowels well moved by a glass of 
hot Hunyadi or Carlsbad water, and while this is acting he should receive a 
few drops of Fowler's solution for the nausea and lack of appetite at break- 
fast. During breakfast, luncheon, and supper he should take a capsule 
made up as follows : 



CIRRHOSIS OF THE LIVER 663 

1£ — Paucreatin, 

Taka-diastase, 

Sodii bicarbonat aa gr. ij. — M. 

S. — Take with each meal. 

In some cases the catarrhal state of the stomach and bowels is benefited 
by the use of small doses of iodide of potassium, 5 grains three or four times 
a day, or of ammonium chloride in the same amount. 

Within the last few years it has been proposed by Talma and others that 
an endeavor be made to relieve the obstructive symptoms of atrophic cirrhosis 
by establishing a collateral circulation by surgical procedure. The anterior 
surface of the liver, of the spleen, and of the parietal peritoneum and intes- 
tines are roughened by being rubbed with surgical gauze, and the omentum 
is attached to the parietal peritoneum of the anterior abdominal wall by 
sutures. By this means it is hoped to cause adhesions through which the col- 
lateral circulation may be established. According to Greenough's statistics, 
only 9 cases have been cured in 105 operated upon. The operation is not 
devoid of danger because of the malnutrition of the patient. 

Ascites should be treated by tapping. (See Ascites.) The use of violent 
hydragogue cathartics, in the hope that the quantity of fluid will be materially 
decreased, is not very successful, as a rule, and may weaken the patient. It 
is, however, important to keep the bowels opened freely to avoid distention 
and pressure. 

Hypertrophic Cirrhosis. Definition. — Hypertrophic cirrhosis is a condi- 
tion in which the liver is very much enlarged, its surface is smooth, jaundice 
develops, but ascites is absent. It is called by the French cirrhose hyper- 
trophique avec ictere, or hypertrophic cirrhosis with jaundice. 

Etiology. — The causes of this malady are unknown. Alcohol is not a 
factor. In the cases I have seen a history of severe and prolonged malarial 
infection has been present in several instances. It is a disease of young adult 
and early middle life, but cases occur in children of tender years. 

Pathology and Morbid Anatomy. — An essential difference between atrophic 
and hypertrophic cirrhosis is that in the former the connective tissue which 
is developed undergoes contraction, whereas in the hypertrophic form it 
remains more cellular and does not contract. The second difference lies in 
the fact that in hypertrophic cirrhosis there is a very considerable increase of 
connective tissue about the biliary ducts (biliary cirrhosis), with compara- 
tively little or no increase of this tissue about the bloodvessels. For these 
reasons we do not find any marked decrease in the blood supply of the gland, 
but we do find jaundice because the biliary ducts are obstructed. In the 
atrophic form, therefore, venous obstruction causes ascites; in the hyper- 
trophic form biliary obstruction causes jaundice, but there is usually no 
ascites. Between these two types of cirrhosis intermediate cases develop, 
in which sufficient overgrowth of connective tissue about the bloodvessels 
may be present to cause ascites, for in hypertrophic cirrhosis there is an 
overgrowth of connective tissue about the interlobular vessels, and even 
between the cells of the lobules. 

Although the liver is enlarged, it does not present the hob-nailed appear- 
ance of atrophic cirrhosis because contraction does not occur. On cross- 



664 DISEASES OF THE LIVER 

section it presents a firm surface of a yellowish-green hue, and strands of 
connective tissue can be seen traversing it. 

It has been shown that in some instances hypertrophic cirrhosis is a 
secondary condition arising from disease of the bile-ducts, and that in 
others it is a primary state without connection with any direct cause yet 
discovered. As a consequence, some writers have divided this disease into 
two types and have asserted that these are separate entities. • The patholog- 
ical changes in each case are so nearly identical that this separation is not 
justifiable. To the primary form the term " Hanot's cirrhosis " has been 
applied. In this form there is pigmentation of the skin in addition to jaun- 
dice, there is usually more pain than in the commoner variety, and the 
spleen is usually very large. It is better to call such cases instances of 
Hanot's type of hypertrophic cirrhosis. 

Symptoms. — The predominant symptom of this disease is enlargement of 
the liver, which often extends to a lower level than that of the navel and far 
to the left of the middle line. When the liver is palpated it is found to be 
hard and its surface fairly smooth, its edges rounded, and its movement 
heavy and difficult when it is pressed upon. Percussion reveals the fact that 
it not only extends downward, but upward far above the ordinary hepatic 
level, and laterally even to the sixth rib, pushing the diaphragm and lung 
before it. The spleen is usually considerably enlarged. Jaundice is generally 
present and varies from a faint lemon-yellow to a dark-olive hue, but it is a 
noteworthy fact that the stools are not without bile, as in ordinary jaundice. 
The urine, of course, contains bile. At times attacks of severe hepatic pain 
develop, and the liver may seem more enlarged than usual at these periods. 
Pruritus is often a most persistent symptom, and xanthoma may be developed 
to an extraordinary degree. In a case now under my care the yellow xan- 
thomatous patches about the eyes form a striking contrast to the dark-olive 
hue of the rest of the face. More or less disturbance of digestion, due to gastric 
catarrh, from an impaired circulation in the stomach, is nearly always present. 

Diagnosis. — An enlarged liver, like that seen in hypertrophic cirrhosis, is 
also seen in leuksemia, but the association of profound anaemia and pallor 
of the skin separate it from the condition now under consideration. Great 
enlargement of the liver also occurs in heart disease from hepatic congestion, 
and in cases of adherent pericardium. The state of the heart makes the 
diagnosis possible in this instance. Malignant growth of the liver can often 
be differentiated by the presence of a primary growth in the gall-bladder or 
stomach, and by the nodules felt in the liver substance. 

Prognosis. — The prognosis as to cure is hopeless. As to duration of life, 
it varies from one to ten years. Death comes from some terminal infection, 
from a hemorrhage into the bowel or stomach, or from an ever-increasing 
feebleness. At times coma develops. 

Treatment. — There is no treatment for the disease itself. The digestion 
should be kept in good order by the line of treatment outlined for this 
function under Atrophic Cirrhosis. 

Syphilitic Cirrhosis. — Syphilis may produce, in its inherited form or ter- 
tiary stage, a remarkable degree of cirrhotic change in the liver. The over- 
growth of connective tissue in this type projects itself everywhere between 



PERIHEPATITIS 665 

the lobules and between their cells, or forms large bands which, as they con- 
tract, produce extraordinary irregularities in its surface, so that the organ 
appears to be as well covered with knobs as a tuberous root is covered by 
projections, a polylobed organ. (See Syphilis.) 

Because of the frequency of syphilis, this form of cirrhosis is not very rare. 
The importance of recognizing it lies in the fact that while we cannot cure 
the state already developed, by active antisyphilitic treatment we may be able 
to arrest or delay its progress, and in this sense the prognosis is better than 
in the non-syphilitic type. In some cases, however, this peculiar nodular 
formation does not occur, and the course of the disease may be identical 
with ordinary atrophic cirrhosis. Sometimes tumors due to the formation 
of gummata can be felt. The symptoms differ in no way from those of 
ordinary cirrhosis, except when gummata are present. 

Treatment. — The treatment of syphilitic cirrhosis, while it presents greater 
opportunities than are offered by therapeutic measures in ordinary cirrhosis, 
cannot be expected to produce very remarkable alterations in the liver. 
Wonderful as are the effects of the iodides and mercury in the treatment 
of syphilis, they cannot regenerate tissues which have been destroyed, and 
the most that we can expect from them is that they will do something to 
arrest the progress of the disease, and, perhaps, cause a removal of some of 
the cells which have been proliferated, but which have not as yet become 
organized tissue. In those cases in which there are any evidences of active 
syphilis, it is hardly necessary to state that the specific treatment should be 
carried out most thoroughly. (See Syphilis.) 



PERIHEPATITIS (CAPSULAR CIRRHOSIS). 

Inflammation of the capsule of the liver and of the tissues immediately 
beneath it, when it occurs in a chronic form, may be associated with chronic 
peritonitis and with hepatic cirrhosis. More rarely it develops as a result 
of chronic pleurisy on the right side. The thickening which ensues may, 
by its contraction, result in deformity of the surface of the liver. This 
effect is increased by the fact that abnormal projections of connective tissue 
dip downward from the capsule into the liver substance and divide it into 
masses of parenchyma, which undergo atrophy from pressure. The condi- 
tion is, therefore, in some cases, at least, not very different from that met 
with in ordinary atrophic syphilitic cirrhosis. 

The condition is very rare and is thought by Hale White to be due to, 
or a sequence of, contracted kidney. Unlike most instances of chronic 
contracted kidney, the patient often has marked ascites because of the 
state of the liver. As already stated, it sometimes happens that the 
capsule of the liver is secondarily involved in cases of chronic peritonitis, 
particularly in cases of adherent pericardium and chronic inflammatory 
changes in the mediastinum. (See Adherent Pericardium and Mediastinitis.) 



DISEASES OF THE LIVER 



AFFECTIONS OF THE HEPATIC BLOODVESSELS. 

These consist, aside from those already considered when discussing the 
subject of cirrhosis, in three chief changes. 

Hyperemia occurs physiologically whenever the liver is actively engaged 
in disposing of foodstuffs. Pathologically, it probably takes place when 
an extra amount of stimulating food and irritant drink are taken. Neither 
condition is capable of being diagnosticated. 

A much more important state is the congestion, due to cardiac disease, or 
to other causes which retard the egress of blood from the gland. We find, 
therefore, that all the causes which tend to result in interference with the free 
flow of blood in the inferior vena cava above the liver may cause hepatic con- 
gestion. Disease at the tricuspid orifice of the heart, pulmonary emphysema, 
fibroid lung, bronchiectasis, and valvular disease of the left side of the heart, 
with secondary obstruction in the right side, all produce it. 

The congestion is, of course, due not to an increase of blood in the 
portal vein but in the hepatic veins. As a result of this, the centre of 
each lobule is congested, and its periphery contains relatively less blood. 
Frequently the cells in the areas of greatest congestion are pigmented. As 
a result of this, the homogeneous hue of the normal liver is altered, and it 
presents what is called a "nutmeg" appearance, particularly if the cells at 
the periphery become still paler from fatty changes. In some cases, however, 
nothing more than the appearance of intense congestion is present. When 
the continued pressure by the excess blood causes atrophy of hepatic cells, 
the condition is known as "red atrophy" of liver. 

During life the congested liver is usually much larger than normal, and 
may attain enormous dimensions, but not rarely, when the congestion has 
lasted for a long time, it grows smaller than it is in health, and its surface 
may be roughened, so that it may somewhat resemble the roughened sur- 
face seen in early stages of atrophic cirrhosis. In fact' the connective 
tissue is usually increased. 

A third vascular change is thrombosis of the portal vein. The formation 
of this thrombus may be due to pressure on the vein produced by a tumor, 
by gallstones, by traumatism, and in some instances it may arise from 
septic infection. When the thrombus forms from pressure, and is not infec- 
tious, it may become organized and gradually close the vessel permanently. 
This does not necessarily work much havoc in the liver, because the 
nutrition of this organ is carried out by the branches of the hepatic 
artery, which speedily enter into anastomosis with the neighboring vessels. 
While the liver itself may not suffer very greatly, the abdominal circula- 
tion is usually much disturbed by obstruction of the portal vein, and the 
spleen, the kidneys, and the veins of the entire abdominal network become 
engorged, so that ascites usually occurs and hsematemesis or bloody stools 
may be produced. 

If the thrombus is infectious (suppurative pylephlebitis) , the pathological 
and clinical picture is quite different, for in this case the clot does not act as 



AMYLOID LIVER 667 

a mechanical obstruction alone, but as a source of septic disease. Necrosis 
and suppuration take place in the wall of the infected vessel and in the 
hepatic tissues around it. The thrombus may break down and minute 
pieces of the infected mass pass into smaller divisions of the portal vein, and 
so spread the disease until multiple abscess of the liver develops. 

The sources from which such septic infections arise are found in ulcer of 
the stomach and bowels, appendicitis and suppuration of the lymph nodes 
in the mesentery. Another origin is suppurative angiocholitis. (See Abscess 
of the Liver.) In infants infection may take place by way of the umbilicus. 

Symptoms. — The symptoms of congested liver consist in finding its lower 
margin below the ribs to an abnormal degree and distinct tenderness on 
pressure, particularly in the epigastrium. Pain in this region is often com- 
plained of by the patient even when he is at rest. If tricuspid regurgitation 
is present, the liver may have systolic expansile pulsation, which must not 
be confounded with movement of the liver due to direct transmission 
of the impulse of the apex beat of the heart. In some cases distinct evi- 
dences of gastrointestinal catarrh develop, and the congestion of the gastric 
vessels may be so great as to cause rupture and hamiatemesis. Ascites due 
to the interference with the venous return in the lower parts of the body, and 
oedema of the legs from the same cause may be present. 

Treatment. — The treatment consists in unloading the gastroduodenal and 
hepatic glands and bloodvessels by a full dose of blue mass (10 grains), 
followed, if need be, by a saline purge. This is to be followed by the use 
of digitalis to support the heart, and, if the arterial tension is high, by the 
administration of nitroglycerin, to lower the arterial pressure and so relieve 
the heart of work. (See Valvular Disease of the Heart.) 

AMYLOID LIVER. 

Amyloid disease of the liver occurs as the result of severe and prolonged 
suppurative changes in other parts of the body, as in chronic bone disease, 
in pulmonary tuberculosis, and in syphilis, particularly if the latter disease 
has caused suppuration over a long period of time. The liver is usually very 
large and may be easily felt far below the ribs, presenting a smooth surface. 
Occasionally an amyloid liver is small. When it is cut across it is found to 
be hard and infiltrated by amyloid material, which stains a mahogany hue 
when it is touched with a watery solution of iodine. 

Symptoms. — The symptoms are not typical. Indeed, it may be said that 
the changes in the liver produce no manifestations that call attention to 
hepatic disease, for there is no jaundice and no pain, neither is there any 
ascites. The presence of enlargement of the liver, with a smooth surface of 
the gland, and the presence of a suppurative focus, combined with an absence 
of any of the signs of hypertrophic cirrhosis and morbid growth, make the 
diagnosis easy. 

Treatment. — There is no treatment for amyloid liver, except the removal, 
if possible, of the suppurating area, which is the underlying cause of the dis- 
ease, and in the maintenance of as great a degree of health as possible by the 
use of fresh air, sunshine, iron, arsenic, and good food. 



DISEASES OF THE LIVER 



FATTY LIVER. 



Fatty liver, like fatty heart, occurs in two forms, namely, as a true fatty 
degeneration of the hepatic cells and as an infiltration of fat into the 
cells. The true fatty degeneration without cirrhosis is rarely met with, 
except as a result of the ingestion of some poison, such as phosphorus, anti- 
mony, iodoform, sulphate of copper, and carbolic acid. A similar change is 
present in acute yellow atrophy of the liver. 

In uncomplicated fatty infiltration the liver is enlarged and smooth. On 
autopsy it is pale and yellow and renders the incising knife greasy. Its 
specific gravity is so low that the organ may almost float in water. No 
distinctive hepatic symptoms are present. 

Often fatty infiltration is part of general obesity, and the large deposit of 
fat in the abdominal wall and in the tissues near the liver make a diagnosis 
difficult. 

Large, fatty, cirrhotic livers have been recorded, and fatty liver accom- 
panying alcoholism, severe anaemia, and cachexia, as in tuberculosis, also 
occurs. In such cases the change is thought to be due to faulty oxidation. 



TUMORS OF THE LIVER. 

The most important morbid growth in the liver is carcinoma. It is 
rarely primary. 

Secondary carcinoma is quite common and is nearly always due to metas- 
tasis from the alimentary viscera, as from carcinoma of the gall-bladder, 
of the stomach, of the pancreas, or of the intestines. In rare instances the 
metastasis is from more distant organs, as the uterus or mammary gland. 

Carcinoma of the liver rarely occurs as a solitary nodule. Usually 
it is in the form of multiple growths, which vary in size from a small seed 
to an orange. When these growths are immediately subcapsular they 
appear as large protuberances on the surface of the organ, which may be felt 
as nodules through the belly wall, or they lie buried in the tissue of the 
liver and present a disk-like surface upon the level of the capsule, so that 
they may be felt in thin persons as a slightly flattened or umbilicated eleva- 
tion. The nodules are sometimes very hard, at other times quite soft, and 
in the centre softening may take place, so that an apparent cyst is formed 
(Fig. 91). 

The liver is sometimes enormously enlarged and may extend far below the 
navel, thereby causing great distention of the belly. A very rare form of 
hepatic cancer is that in which the liver diminishes in size with the develop- 
ment of the growth. 

Sarcoma of the liver is rarely encountered. 

Cavernous angiomata have been described, and cysts, single and large, or 
multiple and small, have been found in this organ. The latter are congenital, 
the so-called " cystic disease of the liver." (See also Hydatid Disease.) 



TUMORS OF THE LIVER 669 

Symptoms. — The evidences of tumor of the liver may be so easily observed 
in many cases that there is no difficulty in making a diagnosis, particularly 
if emaciation, amemia, and profound cachexia are present. In other cases 
the fact that the patient is still well nourished, and the growths deeply 
situated, may render it impossible to discover the existence of a mass by 
palpation. In some instances there is present nothing more than a vague 
sense of distress in the hypochondrium, with loss of weight and strength. 
In still others, if the gall-ducts are obstructed, jaundice may come on, and if 
the pancreas is involved, fatty stools may be present, or glycosuria is found. 
Pain may be severe, but usually it is not. At times the veins of the leg 
on the right side may be obstructed by a thrombus, or a phlebitis may be 
present. Moderate fever may occur. 

Fig. 91 




Liver, secondary carcinoma. Even the smaller nodules show more or less umbilication, which is 
marked in the larger masses. 

Diagnosis. — The diagnosis requires that we exclude hypertrophic cirrhosis, 
which can be done by the more rapid development of the enlargement of the 
liver in carcinoma, and by the presence of cancerous cachexia. From 
echinococcus cyst it must be separated, by the fact that the cyst usually 
fluctuates, or, at least, is not so hard as is nodular cancer. From gumma 
of the liver other tumors can be differentiated only by the history of the 
patient and the response to antisyphilitic treatment. 

Prognosis. — When the growth is malignant, the outlook is, of course, hope- 
less as to recovery. 

Treatment. — If the growth is a gumma, antisyphilitic treatment is of great 
value. (See Syphilis.) If it is a cyst or non-malignant, surgical interference 



670 DISEASES OF THE LIVER 

is a possible source of relief. If it is malignant, no efficient treatment 
except the relief of pain can be instituted. 



ACUTE YELLOW ATROPHY OF THE LIVER. 

Definition. — Acute yellow atrophy of the liver is a condition characterized 
by marked fatty degeneration of the organ and violent headache and 
delirium. It is a very rare disease. 

Etiology. — The causes of acute yellow atrophy are unknown, but it occurs 
more frequently in women than in men, and has been associated in many 
instances with the puerperal state. A micrococcus has been found in the 
liver in some cases, but the suspected bacterial origin of the disease has not 
been proved. Some pathologists regard it as a local state representing a 
general infection, and others as a distinctly local disease, but its toxic nature 
is generally admitted. 

Pathology and Morbid Anatomy. — The changes which take place in the 
liver are a rapid decrease in its size due to necrosis, fatty degeneration, and 
cellular fragmentation. So rapid may be the process that after three or four 
days the organ is not one-half its normal size. The gland is soft and its cap- 
sule shrivelled, as if it were too large for the organ. If an incision is made 
into the viscus the lobules will be found almost destroyed, and the cut surface 
is mottled, softened, and gray, red, or yellow, according to the stage of the 
disease. In the gray areas the forms of the hepatic cells are recognizable, 
and their protoplasm is granular in appearance. In the yellow areas the 
cells are more or less filled with fatty globules and yellow pigment, and in 
the red areas the cell outline may be lost, and only cell debris, or the remains 
of broken-down cells, may be found. The spleen is usually enlarged, the 
kidneys are the seat of parenchymatous degeneration, and the heart muscle 
is also degenerated. Hemorrhagic extravasations may occur, not only in 
the liver, but in the stomach, bowels, bladder, and kidneys as well. When 
death has been long delayed, evidences of universal tissue degeneration may 
be found. 

If the urine is examined, it will be found loaded with bile and an excessive 
quantity of leucin and tyrosin, or, perhaps, only one of these products. 
Leucin appears in round disks, and the tyrosin in needle-shaped crystals, 
which are usually bunched together. 

Symptoms. — The symptoms of this malady are jaundice, severe headache, 
vomiting, and finally delirium, fibrillary muscular tremors, convulsions, and 
death. As a rule, there is little or no fever, but cases with high temperature 
have been recorded. Petechial spots and large hemorrhages may develop 
beneath the skin. 

Diagnosis. — The development of what might be called fulminating jaun- 
dice in a woman during the puerperium should awaken a suspicion of this 
disease at once, but such an onset does not necessarily prove the presence of 
acute yellow atrophy, unless there is marked decrease in the size of the liver, 
and leucin and tyrosin are present in the urine. Even these additional signs 
are not pathognomonic. Particular care must be taken that the coma of 



ACUTE CATARRH OF THE BILE-DUCTS 671 

hypertrophic cirrhosis is not taken for acute yellow atrophy of the liver, for 
sometimes hypertrophic cirrhosis belies its name, in that the liver is not 
greatly enlarged, and acute yellow atrophy may occur without the liver being 
greatly decreased in size. 

Prognosis. — Death nearly always occurs. A few cases are said to have 
recovered. 

Treatment. — Beyond the use of mild purgatives, diuretics, and stimulants 
there is no treatment for this malady. 



DISEASES OF THE BILIAEY TEACT. 

1. Acute Catarrh of the Bile-ducts, or Acute Cholangitis. — As its name 
indicates, this is a condition in which the mucous membrane lining the gall- 
ducts becomes inflamed and swollen, and its secretion thick and tenacious. 
These two conditions produce partial or complete occlusion of the ducts, 
which in turn results in biliary stasis and jaundice. In the liver itself 
marked pigmentation also occurs, because of the accumulation of pigment 
granules in its cells. When the inflammatory process affects the gall- 
bladder, it is called catarrhal cholecystitis. Acute catarrh of the bile-ducts 
is the cause of most attacks of jaundice which last for a few days. 

Etiology. — This condition nearly always arises from a primary catarrh 
of the duodenum, which extends to the common bile-duct. It may follow 
exposure to cold, particularly if the exposure follows heavy eating and drink- 
ing. It usually accompanies the presence of gallstones if they arise in 
or enter the common or hepatic duct. It also is a result of infection in 
many cases, as in influenza, or more rarely in pneumonia. Still more 
rarely jaundice occurs after a severe fright or a paroxysm of intense anger. 
Any cause which interferes with the circulation in the liver and duodenum 
may also indirectly produce this state, as, for example, mitral stenosis. 

In nearly all cases the inflammation does not extend beyond the lower part 
of the larger ducts. 

Symptoms. — The symptoms vary very greatly. In some persons a well- 
marked jaundice develops, with such slight general symptoms that the patient 
does not know he is ill until he sees his reflection in a glass or a friend 
remarks upon his yellovj hue. In other cases the patient may feel and seem 
wretchedly ill, probably because he has in the intestine certain substances 
which, in the absence of bile, develop toxic materials which the torpid liver 
does not destroy. Headache is often marked, and profound weakness may 
be felt. The stools are putty color because of lack of bile, and the urine is 
the hue of porter, because of the presence of this secretion in excess. The 
color of the skin varies from a faint lemon to a much deeper hue, but the 
deep olive-green jaundice of chronic hepatic disease is not met with. The 



672 DISEASES OF THE BILIARY TRACT 

pulse and respiration are remarkably slow, owing to the pathological action 
of the retained biliary salts. The temperature may be subnormal, but if the 
condition is due to an acute infection it may reach 102° or more. The 
liver on palpation and percussion is usually found to be moderately enlarged, 
about two to three fingers' breadth below the ribs, and it is often tender on 
pressure. 

Catarrhal jaundice usually lasts from a few days to several weeks. After 
the patient has been ill for some days he usually loses weight very rapidly. 
There is no mild, brief acute illness which causes a greater loss of weight in 
a few days than this affection. 

Diagnosis. — The development of jaundice in persons under forty without 
any signs of grave disease renders a diagnosis of acute catarrh of the bile- 
ducts probable. In older persons, particularly if the jaundice develops 
gradually, the possibility of malignant growth being present must be excluded. 
In other cases when jaundice comes on suddenly, the cause may be gall- 
stone, and in such instances a history of colic may be given. If distinct 
enlargement of the gall-bladder is present, the probability of carcinoma is 
great. (See Tumors of the Gall-bladder.) 

Prognosis. — In cases of acute catarrh of the simple form the prognosis is 
always good. 

Treatment. — In acute catarrh of the bile-ducts the treatment consists in 
placing the patient in bed, and in the application of hot compresses over the 
liver, renewing the compresses as rapidly as they become cooled. In some 
instances it is advantageous to wet the compresses with hot water which 
contains a drachm of dilute nitromuriatic acid to the pint; or, in other cases, 
for the purpose of producing counterirritation, a turpentine stupe may be 
employed. 

The kidneys should be kept acting freely by the administration of large 
quantities of Vichy water, or in other instances Poland water, if Vichy water 
is not to be had. In some instances, if the kidneys are inactive, it is 
advantageous to add to the water 5 grains of bicarbonate of potash in 
each glass. 

If the bowels are at all confined, as they are prone to be, they are best moved 
by one of the saline purgatives, of which sodium phosphate is usually con- 
sidered most advantageous. This may be given in quantities varying from 
20 grains to a drachm in half a glass of hot water every two hours until the 
bowels are thoroughly moved. 

The administration of calomel in the early stages of catarrhal jaundice 
is not rational. The object of the physician is to re-establish biliary flow, 
and the difficulty which exists is that the liver is unable to get rid of the bile 
which it secretes. To stimulate this gland to a greater secretion of bile by 
calomel, when its ducts are blocked, is manifestly not good therapeutics. 

After the acute stages of jaundice have passed by, it is often advantageous 
to give broken doses of calomel, in order to overcome the natural inactivity 
of the liver after acute inflammation in its bile-ducts, and these should be 
followed by the doses of phosphate of sodium, already named. 

Patients with jaundice frequently insist upon getting up and going about. 
This is not a safe thing for them to do, as it is entirely possible for them, if 



SUPPURATIVE INFLAMMATION OF THE BILE-DUCTS 673 

the cause be gallstones, to convert an attack of acute catarrhal jaundice 
into one of acute cholecystitis. 

In regard to diet, the patient had better subsist upon nutritious broths, 
thickened it may be with barley or rice, partly digested with pancreatin, 
and well flavored with salt. Milk is usually not well digested by patients 
suffering from this condition, particularly if it contains any considerable 
quantity of cream. All fatty articles of food should be avoided, as the 
emulsification of fats in the intestines in the absence of bile is imperfectly 
carried out. 

2. Chronic Catarrh of the Bile-ducts.— This state rarely arises as a 
sequence of the acute type just described. More commonly it is due to 
obstruction of the common duct caused by the presence of gallstones, 
growths, or stricture. Two results ensue from such a state, depending 
upon the degree of obstruction. When the duct is totally blocked, we find 
on opening it that it is not filled with bile, but with clear or slightly tinged 
mucus which is devoid of bile, and that the mucous membrane is not 
much affected, for it remains smooth. Such patients present marked and 
persistent jaundice, the skin often being olive-green in hue. When the 
duct is not quite occluded, the retained mucus is bile-stained; it is cloudy, 
not clear, and it may contain micro-organisms from the bowel. Because of 
the infection of this mucus from the bowel marked fever may be present, 
characterized by sharp intermittency, and associated with fever and sweats, 
just like those met with in the suppurative type about to be described. 

Treatment. — Chronic catarrh of the bile-ducts cannot be materially modi- 
fied by medicinal measures. Prolonged counterirritation in the form of 
tincture of iodine over the liver may be tried, but it must be continued for 
long periods of time before any possible influence can be expected from it. 
If constipation exists, the bowels should be relieved, preferably by saline 
purgatives, of which the phosphate of sodium, Hunyadi water, or some 
similar mild purgative, are considered the best. 

The diet should be composed of easily digested meats and easily digested 
starches, the digestion of which should be aided by the use of pancreatin and 
taka-diastase. Milk and fatty foods are usually not well digested by such 
patients, and are prone to cause fermentation and distention of the bowels 
by gas. The best treatment for these patients is operative interference, 
for the presence of fever indicates infection and hints at the existence 
of pus. 

3. Suppurative Inflammation of the Bile-ducts. — When infection of 
the mucous membrane results from the growth of the Bacillus coli com- 
munis, or more rarely the Streptococcus pyogenes or other pyogenic organ- 
isms, suppuration occurs. It is sometimes called " suppurative cholangitis." 
The solution of continuity in the mucous membrane which permits infec- 
tion may be due to gallstones. In some cases typhoid fever, cholera, 
typhus fever, or pysemia may be the cause. 

This form of inflammation extends much farther into the smaller biliary 
passages than the acute catarrhal form, and by this means the liver may be- 
come generally infected, the ducts containing pus and the gall-bladder also 
being filled with the same material. In some cases the suppurating ducts 
43 



674 DISEASES OF THE BILIARY TRACT 

may cause small abscesses in the liver substance outside their walls, and these 
again may grow large enough to communicate, and so abscesses of consider- 
able size develop. When the process is severe the ducts may be perforated, 
and the pus and bile escape into the peritoneal cavity, causing peritonitis, 
or fistulous tracts may communicate with the bowel or the exterior of the 
body. 

Symptoms. — The symptoms are usually so sharply developed that there is 
little difficulty in deciding that pus is present in the liver. The fever ranges 
from high to low, as in sepsis; the liver is enlarged and very tender; the gall- 
bladder may be palpable, and jaundice is also well marked in some cases, 
but slight in others. The presence of pus in so vascular and important an 
organ causes profuse sweats and rapid loss of flesh, but pain is usually not 
severe. 

Diagnosis. — Suppurative cholangitis must be differentiated from abscess 
of the liver, and, more important than all, from severe catarrhal cholangitis 
without the formation of pus. 

In hepatic abscess there will be found, on careful examination of the 
patient's history, that at some time in the near or remote past there has been 
an attack of dysentery or of an infection in some part of the body from 
which pyogenic micro-organisms have been carried to the liver. Very 
rarely there may be a history of trauma. While such a history may be 
found in a case of suppurative cholangitis it is much more indicative of 
abscess. A history of gallstone colic is indicative of cholangitis, and it must 
be recalled that only moderate attacks of pain in the hepatic or gastric region 
may be present in cases of gallstones. In other words, every person that 
has passed a gallstone does not give a history of severe colic. Finally, the 
presence of jaundice is a sign of cholangitis, for this symptom is usually 
absent in abscess. In both cases the liver is enlarged and there is a distinct 
leukocytosis. 

From severe catarrhal cholangitis suppurative cholangitis is separated 
by the facts that in the former state the leukocytosis is not so marked as in 
the suppurative type, there are no marked chills, sharp fevers, or sweats, 
nor is there so much tenderness and enlargement of the liver. 

Treatment. — There is no medicinal treatment for this condition. The 
same rule holds good in regard to pus here as for pus elsewhere ; whenever it 
is present, the safety of the patient demands that it should be given an exit, 
but if the suppurative process is diffuse this, of course, cannot be done. 

4. Occlusion and Constrictions of the Bile-ducts. — Occlusion of the 
bile-ducts sometimes takes place by the entrance of an intestinal worm, by 
the impaction of a gallstone, or by the pressure produced by an aneurysm, a 
carcinoma, or other growth, such as enlargement of the lymph nodes, 
enlargements or tumors of the head of the pancreas, inflammation and 
fibroid changes around the ducts, and twisting or angulation, caused by 
hepatoptosis or other changes in the visceral relations. If the cystic duct 
is obstructed the gall-bladder is greatly enlarged, but no jaundice is present, 
but if the common or biliary ducts are closed, intense jaundice is developed. 
(See Tumors of the Gall-bladder.) 

Congenital occlusion of the ducts sometimes is met with. When it is com- 



ACUTE CHOLECYSTITIS 675 

plete death occurs within a few weeks after birth. Hemorrhages from the 
navel and other parts of the body are usually present in these cases. 

Symptoms. — The symptoms are those met with in chronic catarrh of the 
bile-ducts and vary as these vary with the degree of obstruction and the 
degree of infection. Cases occur, however, in which life is prolonged for 
long periods if the ducts are not completely closed and infection does not 
take place. A remarkable instance of this character has been reported by 
Cocking, of Sheffield, in which a woman was jaundiced for fifty years from 
her third week of life, yet was in perfect health otherwise. 

Treatment. — The treatment is surgical. 



ACUTE CHOLECYSTITIS. 

Definition. — This is a state in which the gall-bladder suffers from an acute 
inflammatory process, which varies from catarrh of the mucous mem- 
brane to suppuration, and even to phlegmonous change in the walls of the 
viscus. The process may be catarrhal, pseudomembranous, gangrenous, or 
suppurative. It may be restricted to the lining mucosa and submucosa, 
or extend to all the coats. When the overlying serosa is affected the process 
is called pericholecystitis or paracholecystitis. 

Etiology. — Cholecystitis arises from the presence of gallstones, which, by 
injuring the gall-bladder, permit infection to occur, and by the entrance of 
pathogenic organisms, which, by reason of lowered vitality of the patient, 
or other causes, are able to produce more or less severe inflammatory changes 
by their presence. The time at which the micro-organism enters the gall- 
bladder and that at which it makes its presence felt may be widely sepa- 
rated ; for while it is true that bile is antiseptic in its influence under certain 
conditions, the germ may remain alive but quiescent for months or even for 
years, and produce its effects only when some illness or other cause offers 
an opportunity for it to develop. This period of inactivity, so far as inflam- 
matory action is concerned, may be utilized in the formation of gallstones 
about the nucleus formed by those bacilli which have become agglutinated. 
(See Cholelithiasis.) The organisms found in the gall-bladder are very 
numerous as to kind. The typhoid bacillus, the tubercle bacillus, the Bacil- 
lus subtilis, the streptococcus, the staphylococcus, and the colon bacillus 
have all been found here, although it is probable that the latter does not 
remain active, except for a short time. 

Morbid Anatomy. — The gall-bladder is found to be filled with dark, muco- 
purulent material, in which, if the wall of the gall-bladder is seriously involved, 
there may be traces of blood. Occasionally the distention of the gall-bladder 
is due not only to blocking of the cystic duct by a stone, but the canal is 
closed by the intense inflammatory process. Perforation of the gall-bladder 
or gangrene of its walls may develop if the inflammation is very severe, and 
it not rarely happens that adhesions form between it and the nearby tissues. 

Riedel states that such adhesions develop in no less than 75 per cent, of 
cases of cholecystitis. These adhesions are of importance because as a 
result of their formation a gallstone perforating the gall-bladder may find 



676 DISEASES OF THE BILIARY TRACT 

its way into adjacent organs. (See below.) Riedel also states that the adhe- 
sions depend as to their location to a large extent upon the position at which 
the stone exists. Thus, if it be in the gall-bladder the adhesions are between 
this viscus and the colon or the omentum. If it be in the cystic or common 
duct the adhesion is to the stomach, in the region of the pylorus. These 
adhesions are also of importance because they may cause pain or obstruc- 
tion of the pylorus or duodenum. 

Symptoms and Diagnosis. — The symptoms are those of acute inflammation 
in the hepatic area, varying in severity from a slight discomfort and soreness 
to violent and alarming pain and collapse. There is tenderness, particularly 
about the region of the gall-bladder, and this speedily may amount to 
exquisite pain on pressure. The point at which the greatest tenderness is 
felt is where the lower third of a line drawn from the navel to the ninth 
rib joins the middle third. With these symptoms there is fever, often 
ushered in by a chill. When the development of the condition is sudden, 
as it very frequently is, the patient may be seized with nausea and vomiting, 
threatened collapse, and other symptoms of fulminant abdominal disease. 

The pulse is rapid; the belly is distended and its walls rigid. 

Diagnosis. — Unless the pain is so localized as to aid materially in diagnosis, 
and unless the physician is provided with a history of gallstone colic, or of 
an inflammation in the gall-bladder after one of the acute fevers, as typhoid 
fever, the symptoms may mislead him into a diagnosis of intestinal obstruc- 
tion or acute appendicitis; for paralysis of the bowel may be present, on 
the one hand, and in appendicitis the pain is often referred to the region 
of the epigastrium or liver. In certain cases of appendicitis, with a history 
of recurrent attacks or of a recent attack, the physician must also recall 
the fact that pain in the hypochondrium may arise from a septic focus, 
carried there from the appendix by the lymphatics. So, too, a gastric ulcer 
with perforation and subdiaphragmatic abscess may simulate acute chole- 
cystitis. When palpation reveals an elongated gall-bladder projecting 
below the edge of the liver, which is very tender on palpation, the diag- 
nosis is readily made. Jaundice may or may not be present. It is often 
absent. It is important to bear in mind the fact that attacks of hepatic colic 
may occur in cases of cholecystitis without any gallstones being present. 

But in hepatic colic an examination of the blood will not reveal leuko- 
cytosis of polymorphonuclear cells, which will be notably increased by 
the presence of an acute inflammatory process in or about the gall- 
bladder. In questioning the patient as to the possible presence of gall- 
stones it should be remembered that mild attacks of pain in this region 
may be as indicative of the passage of these bodies as a history of typical 
gallstone colic. Acute cholecystitis is rarely characterized by the sud- 
denness of onset of pain and abdominal tenderness which are met with 
in acute pancreatitis or perforation of the stomach due to ulcer. If these 
symptoms are present they may, however, be due to perforation of the gall- 
bladder due to chronic cholecystitis arising from gallstones. (See Chole- 
lithiasis.) Sometimes when there is an infection of the gall-bladder, as in 
the third or fourth week of typhoid fever, the onset of cholecystitis may be 
as severe as that of perforation. Occasionally during the course of acute 



CHOLELITHIASIS 677 

ulcerative endocarditis with secondary Cardiac failure the liver becomes 
enlarged and tender and chills and fever are met with. Pyopericardium 
must also be excluded if possible. 

Treatment. — The treatment in all cases in which the symptoms are severe 
is prompt operative interference. Temporizing measures consist in the 
use of rest in bed, counterirritation over the region of the gall-bladder, and 
the use of gentle saline purges to unload the bowels. 



CHOLELITHIASIS. 

Definition. — The term cholelithiasis is applied to a condition in which the 
gall-bladder or the other parts of the biliary passages contains one or more 
gallstones. 

Etiology and Pathology. — The predisposing causes of gallstone formation 
are all conditions which produce catarrh of the stomach and duodenum and 
biliary passages. A sedentary life with high living is a factor. So, too, 
enteroptosis may aid in its development. The condition is commonly met 
with after forty years of age, but cases have been seen in childhood and even 
in the newborn. More than 75 per cent, of all cases occur in women, and 
90 per cent, of these women have been pregnant one or more times. 

Biliary calculi are formed as the result of the deposit of certain of the 
ingredients of the bile about a nidus, which we now know is often, if not 
always, an accumulation of micro-organisms. The presence of these infecting 
agents has already been discussed in the article on Cholecystitis, but it is 
particularly important to bear in mind the fact that typhoid bacilli are fre- 
quently the origin of stone, probably because they often remain in the gall- 
bladder for years, and because, when they agglutinate, they form with 
epithelial cells a good nidus for the deposition of biliary materials. That 
micro-organisms play this part is now proved not only by many observations 
on man, but by experiments on animals. 

The mere presence of micro-organisms, however, is not sufficient for the 
formation of stone. It is necessary that a catarrhal state of the mucous 
membrane be present, since in this condition three ingredients of the stone 
are excreted by the walls of the gall-bladder, namely, mucus, cholesterin, 
and a substance called "bilirubin calcium." Healthy bile prevents the depo- 
sition of bilirubin calcium, but if albumin is present this action is arrested 
and the deposit is made. When inflammation is present enough albumin 
enters the bile from the diseased mucous membrane to permit of this effect, 
and the small quantity of cholesterin present in normal bile is also much 
increased. It is evident, then, that for the deposit of the materials forming 
a gallstone an unhealthy mucous membrane is primarily essential. 

Gallstones when composed chiefly of cholesterin are transparent or slightly 
tinged by bile. If broken, such a stone appears crystalline, with radiating 
lines. In other cases the stone is composed not only of cholesterin, but of 
biliary pigment and salts of magnesium and calcium. Such stones are 
usually dark in color, brown or green. They may be round or marked by 
facets, due to attrition, where they have rubbed against other stones. 



678 DISEASES OF THE BILIARY TRACT 

In these stones also a radiating crystalline formation is present on fracture. 
These dark-faceted stones are the ones commonly found. More rarely 
stones of small size are found, composed almost entirely of bile pigment. 
Calcium carbonate stones are still less frequently met with. 

In size gallstones vary from fine gritty sand to masses as large as a small 
banana. 

In the vast majority of cases of cholelithiasis biliary calculi are formed 
in the gall-bladder. Very rarely small particles of biliary sand form in the 
bile-ducts of the liver itself. The large stones found in the cystic and common 
duct have formed in, and then slipped from, the gall-bladder. 

The number of stones found in the gall-bladder may vary from one or two 
to several thousand, if the tiny, sand-like pieces are counted. When the 
number is large, they usually show signs of lateral pressure, but sometimes 
several may exist without facets being developed. 

If a gallstone lodges in the common gall-duct so as to completely occlude 
it, there is usually found at autopsy a condition of dilatation of this duct, 
which is filled with a clear, mucus-like fluid. (See Occlusion of the Bile- 
ducts.) If the obstruction is not complete and infection of the duct takes 
place, the state is one of cholangitis, already described, or even of sup- 
purative angiocholitis. 

When the cystic duct is completely obstructed by a stone, the gall-bladder 
may be greatly enlarged and filled with clear fluid or with other gallstones. 
If the gall-bladder is infected suppurative cholecystitis develops, and perfor- 
ation may occur. (See Symptoms.) In other cases the gall-bladder undergoes 
atrophy, and may be so shrunken as to be nothing but a small mass of fibrous 
tissue the size of a large nut, hidden in the hollow naturally occupied by 
the gall-bladder. Less commonly a process of calcification is developed, and 
the gall-bladder becomes coated or infiltrated by lime-salts. 

Symptoms. — It is important to bear in mind the fact that the mere presence 
of gallstones in the gall-bladder does not necessarily cause any symptoms 
whatever. The records of autopsies in Germany, in particular, show that a 
very large proportion of all women who come to autopsy in the later years 
of life have gallstones, and yet there has been no suspicion of their existence 
prior to death. Only about 5 per cent, suffer from distinct symptoms due 
to this cause. On the other hand, if the biliary tract becomes infected, or 
if an acute congestion of its mucous membrane occurs, more or less severe 
symptoms may be at once produced and fever may develop; or if a stone 
becomes dislodged from the gall-bladder and slips into the cystic or common 
duct, this mechanical difficulty may at once produce biliary colic. 

The symptoms of biliary colic usually consist in severe pain, which amounts 
to an agony in most instances. Occasionally, however, the pain is very 
moderate, and is thought to be due to indigestion. The patient often 
vomits and sweats profusely. The pain manifestly originates in the gall- 
bladder, but is radiated to the right shoulder-blade and to the epigastrium. 
The facial expression is one of anguish and anxiety, and the color of the 
skin is pallid. 

After the attack has lasted for some hours, or on the day after an attack, 
a moderate degree of jaundice may appear, but it is rarely well marked 



CHOLELITHIASIS 679 

unless the attack lasts for several days or the obstruction is persistent. If 
the stone is in the cystic duct, no jaundice occurs unless the neighboring 
raucous membrane in the common, or hepatic duct, becomes swollen and 
inflamed, or unless the stone is so placed in the cystic duct that it presses 
upon the hepatic duct. The presence of jaundice in a case which suffers 
from severe pain in the region of the gall-bladder is a positive diagnostic 
sign of much value, but the absence of jaundice does not in the slightest 
degree negative the view that gallstone is present. Kehr states that in 
720 cases operated on for gallstone, 80 per cent, showed no jaundice. 

The urine, if the stone is in the common duct, may soon show the 
presence of bile, and not rarely albumin is found in it. In still other 
cases red blood cells may be found in the urine, and this may lead us into 
the belief that the pain is due to renal colic. 

An attack of biliary colic lasts, as a rule, for but a few hours, but occa- 
sionally the patient suffers from a prolonged seizure lasting over several 
days and marked by temporary remissions, which are, perhaps, due to ex- 
haustion of the irritated gall-bladder or to temporary restoration of biliary 
flow. 

The presence of a stone or stones in the common or cystic duct produces 
not only symptoms of biliary colic in some cases, but other signs as well, 
which may be of use in diagnosis. If the stone blocks the common duct 
completely, the jaundice which develops is persistent and well marked, and 
further attacks of colic may never occur, or, indeed, there may not be a 
single attack in the patient's history. Febrile movement is usually absent, 
because the complete obstruction of the duct prevents infection from the 
intestine. The gall-bladder is usually not distended. 

When the common duct is not completely closed, and in the majority 
of cases it is not occluded, the attacks of biliary colic are more frequent, 
and the degree of jaundice varies. This is due to the fact that at 
times, when the mucous membrane surrounding the stone is not acutely 
inflamed or congested, bile is permitted to escape into the bowel, so that 
the pressure is relieved and the stools become bile-stained. Such a condition 
of repeated attacks of colic with varying degrees of jaundice may also be 
due to the stone becoming so fixed in the ampulla of Vater that it forms a 
ball-valve, which sometimes permits the passage of bile and sometimes pre- 
vents it. In rarer instances the stone becomes encysted in the w T all of the duct, 
and so acts as a valve, and in still other cases it may become lodged at 
the junction of the cystic and hepatic duct, and by pressure cause symptoms 
characteristic of obstruction in both the cystic and common duct. 

These cases of partial obstruction differ from those of complete obstruction, 
in the fact that they not rarely develop fever, owing to infection of the com- 
mon and hepatic duct by micro-organisms from the bowel. The febrile 
attacks which ensue may be so irregular or so intermittent in type that they 
closely resemble those of malarial fever, but they are in reality septic fever, 
the so-called "intermittent hepatic fever of Charcot." Such attacks may 
persist for years with no more serious changes in the ducts than a chronic 
catarrh with thickening and the proliferation of an exudate about the parts. 

In some cases, however, the degree of infection is so severe that suppura- 



680 DISEASES OF THE BILIARY TRACT 

tion takes place, not only in the common duct, but in the hepatic duct as 
well, and even in the gall-bladder, producing suppurative cholecystitis and 
suppurative angiocholitis. (See Suppurative Inflammation of the Bile-ducts 
and Acute Cholecystitis.) 

The additional symptoms, to those of biliary colic, which arise when the 
cystic duct becomes the lodging-place for a stone are chiefly enlargement of 
the gall-bladder from distention and the negative, but nevertheless valuable, 
evidence of absence of jaundice. The size of the gall-bladder in cases in 
which the obstruction is complete is sometimes marvellous. Instances have 
been recorded in which the enlarged gall-bladder has been mistaken for an 
ovarian tumor, and not rarely the enlarged, pear-shaped mass can be felt 
near the median line of the abdomen. (See Diagnosis.) On the other 
hand, the facts in regard to atrophy of the gall-bladder, already named in 
the discussion of the pathology of this affection, should be recalled; in other 
words, the absence of a large gall-bladder does not exclude obstruction to 
the cystic duct. 

If the gall-bladder, which is distended by retained bile and gallstones, can 
be palpated, it may be possible to produce what is called "gallstone crepitus" 
by the rubbing of the stones one upon the other. 

Complications and Sequelae. — A stone may perforate the gall-bladder, 
and, by way of an adhesion, gain the cavity of the duodenum and 
escape with the feces. In still other cases the perforation takes place 
through an adhesion to the colon, but very rarely does the stone escape 
into the small bowel below the duodenum. In other instances the gall- 
bladder becomes adherent, by an inflammatory exudate, to the abdom- 
inal wall, and the stones finally escape from the fistulous opening. I had 
a case in my clinic at the Jefferson Hospital some years since in which the 
patient passed almost daily a little pus and a little bile with one or more 
stones through such an opening, yet seemed in excellent health, probably 
because nature had established free drainage. More commonly the perforation 
takes place so that the stone enters the peritoneal cavity and then the asso- 
ciated infectious material causes fatal peritonitis. When the gall-bladder 
becomes adherent to the diaphragm and perforation ensues, the stone with 
pus and bile may escape into the pleura or into the lung. In the Transactions 
of the Association of American Physicians for 1897, Graham, of Toronto, 
reports 10 cases of cholelithiasis perforating into the lung, and in 4 of them 
the stone passed through an adhesion which existed between the gall-bladder, 
the diaphragm, and the pleura. 

The spitting of bile, with a distressing cough, and dulness on percussion in 
the area just above the liver, where pulmonary resonance is usually present, 
make the diagnosis certain. 

Gallstones have been carried far away from the gall-bladder by suppura- 
tion after perforation, and have even been found in the urinary bladder as 
a result of this process. Perforation of the gall-bladder with fatal syncope 
has been reported during an attack of biliary colic. 

Diagnosis. — This is not difficult if we are able to exclude appendicitis, 
diaphragmatic pleurisy, gastric ulcer, gastralgia, the gastric crisis of ataxia, 
and renal stone. Appendicitis is detected by finding even greater pain on 



CHOLELITHIASIS 681 

palpation in the appendicular area; pleurisy is excluded by careful auscul- 
tation to reveal a friction sound. In gastric ulcer there is a history of pain 
immediately after the taking of food, and perhaps of hsematemesis ; and the 
patient is usually a young woman, whereas gallstones are usually present 
in women past forty years of age. A person with an ulcer is usually poorly 
nourished and anaemic, whereas the patient with gallstones is usually plump 
and possessed of a thick abdominal wall. Hyperchlorhydria is present in 
ulcer, but absent in cholelithiasis, as a rule. In those cases, however, in 
which there are adhesions between the gall-bladder or its duct and the 
pylorus or duodenum, these differential signs may fail because pyloric 
obstruction causes pain after taking food and produces hyperchlorhydria. 
Gastralgia is pointed to by the fact that the patient is subject to neuralgia, 
and is neurotic in type, rather than stout, as are most gallstone cases. An 
attack of gastric crisis in ataxia, while often associated with vomiting, 
can be detected by the history of an ataxic gait and by the presence of an 
Argyll-Robertson pupil or other signs of that disease. Renal stone causes 
pain to be radiated to the inside of the thigh and to the testicle. Movable 
kidney may, by dragging or pressing upon the common biliary duct, cause 
obstruction, and so produce an attack of biliary colic and jaundice not due 
to stone. Further, the pain due to twisting of the ureter in such a case may 
simulate hepatic colic. The finding of a floating kidney clears up the 
diagnosis. A new-growth may produce similar symptoms, and it may be 
impossible to differentiate the obstruction from that due to gallstones. In 
none of these states is the greatest degree of pain on pressure over the gall- 
bladder. 

It is essential that attention be paid to one very important differential 
point, which must always be borne in mind, the so-called " Courvoisier's 
law," namely, that an enlarged gall-bladder with jaundice is a sign of 
malignant growth of the gall-bladder rather than that of obstruction due 
to stone. 

Treatment. — The treatment of biliary colic, like that of renal colic, con- 
sists in the administration of a hypodermic injection of J of a grain of mor- 
phine, with y^-g- of atropine, and y^-Q of a grain of nitroglycerin, to relieve 
pain and to relax spasm. If the first injection does not give relief at the end 
of fifteen or twenty minutes it may be repeated, the atropine being left out. 
After the attack is over the patient should rest quietly in bed for two or 
three days, in order to hasten the disappearance of the inflammation of the 
mucous membrane, which is usually associated with the attack, and thereby 
decrease the danger of a subacute or chronic inflammatory process develop- 
ing in the gall-bladder or common duct. 

No medicines have any effect upon the gallstones which are already 
formed, but a number of remedies may be given to patients who suffer 
from gallstones, with the object of preventing the formation of others, and 
with the hope that by their use catarrh and irritation of the mucous mem- 
brane lining the gall-bladder and the common duct may be materially 
diminished. These remedies consist in the mild saline purgatives, such 
as the various imported purgative waters, which are gentle in their action, 
and which may be preferably taken hot in the dose of one or two teacupfuls 



682 DISEASES OF THE BILIARY TRACT 

before breakfast. Chloride of ammonium, in the dose of 5 to 10 grains three 
times a day, is useful for its effect upon mucous membranes, and is, perhaps, 
best given in equal parts of fluid extract of licorice and water. 

Until within recent years the physician was content when a case of chole- 
lithiasis escaped month by month from a return of biliary colic, deeming it 
inexpedient that any radical measure of relief should be instituted. With our 
present knowledge, however, it cannot be doubted that the question of opera- 
tive interference must be carefully considered in every case in which a positive 
diagnosis of cholelithiasis can be made. The time for operation is, of course, 
during a period of quiescence, since at the time of an attack the acute inflam- 
mation which exists in and around the gall-bladder may seriously complicate 
the work of the surgeon. 

The question as to how frequently the patient should be allowed to 
suffer from gallstone colic before operative interference is urged is one which 
varies with each individual case. If the jaundice which is present with the 
first attack is not severe and lasts but a very short time, and if the temper- 
ature of the patient is not disturbed, or returns to normal within a period 
of twenty-four hours, and if, again, palpation in the neighborhood of the 
gall-bladder some days after the attack fails to reveal evidence of a low-grade 
inflammation, as manifested by tenderness or pain, it is then permissible, 
and, indeed, advisable, that the patient should not be operated upon. Even 
when as many as two or three such mild attacks have occurred at long inter- 
vals, the condition may not be such as to require that the physician should 
strongly recommend surgical aid. When, however, the attack of biliary colic 
is violent or repeated, when the jaundice persists for a long period, and 
when distinct evidence of persistent cholecystitis continues, then operation 
should be resorted to, particularly if a mass, caused by the gall-bladder being 
distended by stones, can be distinctly felt. To delay operation in a case of 
this kind until frequent attacks have resulted in the formation of a large 
amount of inflammatory material about the gall-bladder is very unwise. By 
this means cases which would offer under ordinary circumstances no surgical 
difficulties may become almost inoperable, and what should be an easy con- 
valescence may be instead a difficult and prolonged illness, testing the skill 
of both the physician and surgeon to the utmost. 

Mayo has performed 510 operations for gallstone, with a mortality of 
only 3 per cent. On 208 cases in which stones were present in the gall- 
bladder alone, and which were uncomplicated by any other condition, there 
were 2 deaths — a mortality of less than 1 per cent. 

Grouping together all cases complicated by the presence of stones in the 
common or cystic ducts, cases of cholelithiasis in which infection occurred, 
cases of biliary infection and malignant disease, Mayo finds the mortality 
to be 5 per cent., or 16 deaths out of 326 cases which he operated on. He 
believes these figures to be a strong argument in favor of early operation in 
cases of cholelithiasis. 



MALIGNANT GROWTHS OF GALL-BLADDER AND BILIARY PASSAGES 683 



MALIGNANT GROWTHS OF THE GALL-BLADDER AND BILIARY 

PASSAGES. 

Etiology. — The cause of the development of morbid growths in these parts 
is unknown, and only some of the predisposing causes are recognized. 

In the case of carcinoma of the biliary ducts and the gall-bladder, there can 
be no doubt that age has a very distinct influence. The growth usually 
develops later in life than does carcinoma in any other part, namely, about 
the fifty-sixth year; whereas, the period of greatest frequency of cancer of 
the mammary gland is, according to Kelynack, about the fortieth year. It 
would also seem probable that gallstones very distinctly predispose to the devel- 
opment of carcinoma in these parts, for they are found present in from 90 to 
95 per cent, of all cases; whereas, the frequency of gallstones in persons 
dying from other diseases than cancer of these parts is from 6 to 12 per cent. 
(Kelynack). On the other hand, it has been claimed that the presence of 
carcinoma of the gall-bladder leads to the rapid formation of stone. Prob- 
ably the pathological condition of the mucous membrane which aids in the 
formation of stone (see Cholelithiasis) also predisposes to the development 
of a morbid growth, and this effect may be increased by the irritation pro- 
duced by the stones after they are formed. 

In women carcinoma of the gall-bladder is far more common than it is in 
men. Musser, in his classical paper upon this subject, found that out of 98 
cases 75 were in women and only 23 in men, and other clinicians have noted 
an even greater percentage among women. Curiously enough, this is not the 
case when the growth affects the biliary passages other than the gall-bladder, 
for in such instances the number of men and women affected is practically 
the same. 

Pathology and Morbid Anatomy. — Carcinoma of the gall-bladder is usually 
of the type of cylindrical-cell epithelioma, but in statistics there is much 
contradiction as to this point. This form of cancer is also the type which 
most commonly affects the biliary ducts. When the gall-bladder is affected 
the fundus is the part that usually suffers. If the biliary passages are in- 
volved, the common duct is the part that is usually affected, and that 
portion of it where it enters the bowel is the favorite site of the growth. 
(See Fig. 92.) 

When cancer attacks the gall-bladder, as already pointed out in the article 
on Cancer of the Liver, the liver is affected in a large percentage of cases 
by secondary growths (Musser says 54 per cent.). The pancreas is also 
very commonly involved. When the growth is in the biliary ducts, metas- 
tasis to other parts is rare. 

Carcinoma of the gall-bladder may also result in the formation of 
adhesions, by which it becomes attached to the abdominal wall, the colon, 
and even the stomach and small intestines. In other instances a suppurative 
cholecystitis may develop. 

Symptoms. — The symptoms of cancer of the gall-bladder are most varied. 
If the growth is so situated that it interferes with biliary flow, the manifes- 
tations of hepatic disease may develop while it is still a very small mass; 



684 



DISEASES OF THE BILIARY TRACT 



whereas, if no pressure is produced, the tumor may reach a very considerable 
size before its presence is suspected. 

As soon as the tumor reaches any size it can be palpated below the border 
of the last rib in most instances, particularly if it affects the fundus of the 
gall-bladder, as it does in the majority of cases. Its position is usually 
along the outer edge of the right rectus muscle and about the neighborhood 
of the normal gall-bladder. It may extend downward toward the pelvis, or 
it may be erect and protrude through the abdominal wall, as an aneurysm 
protrudes from the chest. The tumor feels hard and is usually somewhat 
pear-shaped. It varies in size from that of a child's head to that of a small 
walnut. 

Fig. 92 




Primary carcinoma of the duodenal papilla seen at the upper end of the rod running through 
the duct. (Kast and Rumpler.) 



If the growth is so placed near the neck of the gall-bladder that it pre- 
vents the cystic duct from draining that viscus, the resulting distention of 
the gall-bladder may cause the formation of a greatly distended sac, which 
may extend far below the ribs, and by its pressure upon the bowel cause 
intestinal obstruction. 

Jaundice and pain are very constant symptoms of cancer of the gall- 
bladder. Musser found jaundice in 69 per cent, of his cases, and pain in 
62 per cent. When the growth invades the gall-bladder alone, it does not 
of itself cause icterus, but the neighboring glands are often involved very 



MALIGNA XT GROWTHS OF GALL-BLADDER AND BILIARY PASSAGES 685 

early, and by this means, or by secondary growths in the common duct, jaun- 
dice is produced. In this connection " Courvoisier's law" is to be recalled, 
namely, that given an enlarged gall-bladder with jaundice the cause is 
carcinoma, not gallstone. 

Wasting is usually well marked, not only by reason of the malignant 
growth, but because of the jaundice and gastroduodenal catarrh which are 
usually present. Ascites may develop (18 per cent, of cases, Musser). Death 
is due to exhaustion, and sometimes to cholsemia. 

Diagnosis. — A growth in the gall-bladder can usually be differentiated 
from one in the bile-ducts by its size, the readiness with which it can be pal- 
pated, and the absence of jaundice until it is of some size. Given a case in 
which jaundice develops in a woman well along in years, in which the jaun- 
dice remains persistent and in which no tumor can be felt, and the diagnosis 
is in favor of growth in the duct. If metastatic masses can be found in 
the liver, the primary growth is probably in the gall-bladder, for they rarely 
develop from a growth in the duct. 

An even more important differential point is that between cancer of the 
gall-bladder with cystic enlargement and enlargement due to hydrops 
of the gall-bladder. In the latter case the gall-bladder is distended with a 
clear fluid as the result of the presence of stone or other cause, completely 
closing the cystic duct. As Courvoisier found this state of hydrops 79 times 
in 91 cases of impacted gallstone, it is not a very rare condition. The dif- 
ferentiation between these two states is made as follows: In hydrops of the 
gall-bladder there is usually no jaundice, and the tumor presents a smooth, 
pear-shaped surface, and there may be a history of gallstone colic. Bile is 
present in the stools and the degree of wasting is not marked. 

In some rare cases the gall-bladder undergoes thickening and presents a 
small, hard mass, which may be palpated. This has already been described 
elsewhere as calcification of the gall-bladder. The absence of metastasis 
and of other signs of cancer also aids us in excluding the morbid growth 
in these cases. 

Other causes of tumor in the region of the gall-bladder are aneurysm, 
cancer of the pylorus, cancer of the head of the pancreas, and tumor of the 
kidney. A fecal mass in the bowel may also mislead the physician. 

Prognosis. — Life, in a case of cancer of the gall-bladder, usually does not 
last beyond a year, and in many instances death comes earlier than this. 

Death usually comes much earlier in cases of malignant growth in the 
duct than of malignant growth in the gall-bladder. 

Treatment. — The treatment of malignant growth of the gall-bladder, of 
necessity, does not offer much promise for ultimate and complete recovery, 
for medicinal measures are, of course, entirely useless, except for the pur- 
pose of relieving pain. Operative procedures, even if they result in the 
complete removal of the diseased gall-bladder, are nearly always followed 
by the development of secondary growths in neighboring parts, where they 
are inoperable and where they straightway proceed to destroy the patient. 
Nevertheless, given a case in which the gall-bladder is greatly enlarged, and 
in which evidences of the presence of a growth in nearby parts is not marked, 
it is certainly permissible, and, indeed, advisable, that operation shall be 



686 DISEASES OF THE BILIARY TRACT 

performed, with the hope that the growth can be removed, or that the opera- 
tion will reveal the fact that the enlargement of the gall-bladder is not can- 
cerous in origin, but dependent upon the presence of gallstone, or other 
cause, or obstruction of the cystic or common duct. 

In all of these cases in which jaundice is present, the very grave influence 
of this complication upon operative procedure must be taken into considera- 
tion, for while, on the one hand, we are learning every year that operations 
upon the gall-bladder can be performed with a surprising degree of impunity, 
we have also learned with increasing experience that jaundiced persons 
withstand operations badly, and that the presence of bile in the blood pre- 
disposes the patient to obstinate and persistent capillary hemorrhage during 
and after operation. This has not infrequently resulted in death, although 
the mere operative procedure itself was a success. 

When the growth involves the bile-duct the outlook is, of course, even 
more discouraging, for the bile-duct cannot be excised, and the jaundice is 
usually so extreme that the condition of the patient scarcely justifies opera- 
tive interference. The most that can be done for a patient with a malignant 
growth in the bile-duct is to operate with the idea of providing drainage and 
relieving pressure. 

ICTERUS NEONATORUM. 

Jaundice of the newborn is a very common condition, and usually appears 
about the third or fourth day after birth. It is noticeable in the skin and in 
the conjunctiva, but it is never intense, and in many cases may be so slight 
as to be overlooked. Holt states that it occurred 300 times among 900 
babies, and Kehrer asserts that in his statistics it was present in 75 per cent. 
The last of these estimates is much too high a proportion for private prac- 
tice. Hofmeier and others believe that it is hematogenous in origin, and 
results from the destruction, shortly after birth, of a large number of red blood 
cells. On the other hand it not rarely happens that the urine is slightly bile- 
stained, and the stools are lacking in bile, which would indicate disordered 
hepatic action. In some instances the portal vein may have been overdis- 
tended in birth, and in this way the finer bile-ducts may have been obstructed. 
Whatever the cause, in its simple form the condition possesses no evil import 
whatever. 

A severe and rare form of icterus of the newborn may, however, develop 
and cause the death of the child. It is due to sepsis following infection of the 
umbilical vein, with phlebitis, to congenital syphilis of the liver, or to con- 
genital atresia of the biliary ducts, so that the bile cannot escape into the 
bowel. 



PANCREATITIS 687 

DISEASES OF THE PANCREAS. 

PANCREATITIS. 

Definition. — Pancreatitis, as its name implies, is an inflammation of the 
pancreas. It occurs in three forms, although it must be understood that no 
hard and fast lines separate these conditions one from the other. These 
three forms are the acute, the subacute, and the chronic. 

Acute Pancreatitis. History. — As long ago as 1672 Tulpius described 
an acute abscess of the pancreas due to pysemia. In 1799 Baillie studied 
what was evidently a case of chronic interstitial pancreatitis. In 1804 Portal 
recorded an instance of acute suppurative pancreatitis, as did Percival in 
1818. In 1879 Balzer reported a case of acute pancreatitis, with fat-necrosis 
but it was not till the epoch-making paper of Fitz appeared in 1889 that the 
profession recognized the frequency and importance of lesions of this gland, 
although in 1886 another American practitioner, Senn, had written a paper 
upon its surgery. Von Mering and Minkowski made valuable contributions 
in 1889 and 1890. 

Chronic pancreatitis was not recognized till Birch-Hirschfeld described it 
in 1895. Since that time the literature on pancreatitis has become quite vol- 
uminous, and a number of studies have appeared, of which the most notable, 
from the surgical standpoint, have been those of Robson and Moynihan, of 
Leeds, and, from the pathological standpoint, one by Opie, of Baltimore,who 
has done more than anyone else to throw light on diseases of this organ. 

Etiology. — By far the more common cause of pancreatitis is infection of the 
gland by way of its duct. This results usually from the presence of a gall- 
stone in the ampulla of Vater, which prevents the flow of bile into the 
bowel, but does not occlude the opening of the pancreatic duct. Again, 
the presence of a gallstone is prone to result in the development of a septic 
process in the surrounding mucous membrane, and this results in infection 
of the bile, which fluid passes along the duct of Wirsung and so enters the 
pancreas. This is particularly apt to occur if the gall-bladder is so 
shrunken by disease that it cannot readily expand when the bile is dammed 
back into the ducts. Further than this, bile alone entering the pancreas, 
even if it be free from micro-organisms, may cause hemorrhagic pancrea- 
titis and fat-necrosis. 

It has been argued that if these causes are active in the production of pan- 
creatitis, this state would be met with much more frequently. The explana- 
tion of the fact that so many cases suffer from gallstones and gall-bladder 
infections without pancreatitis lies in the fact that in a certain proportion of 
individuals the bile-duct and pancreatic duct do not enter the bowel by one 
opening, but through separate openings. In a few cases the chief secretion of 
the pancreas escapes by way of the duct of Santorini. (See Fig. 93.) 

Acute pancreatitis may result from several other causes, such as one of the 
acute infectious diseases, or, again, in the course of septicaemia. Another 



G88 



DISEASES OF THE PANCREAS 



cause is infection from a neighboring lesion, as in direct extension from 
a gastric ulcer or cancer, or a subphrenic abscess. Still another cause is 
injury by blows or by surgical procedure. 

Pathology and Morbid Anatomy. — Acute pancreatitis is characterized not 
only by a primary hypersemia of the gland, but in some cases by the 
escape of its ferments into its own tissues, and adjacent tissues as well. As a 
result of this accident, a condition of " fat-necrosis " develops in the fatty 
tissues in the immediate region of the pancreas, and often in other parts of 
the body to which the pancreatic ferment may escape in the lymph. The fat 
is split up into glycerin and fatty acids. The glycerin is absorbed; the acids, 
being insoluble, are not eliminated, but combine with calcium salts, and with 

Fig. 93 




Portion of human pancreas and duodenum from a person who had been executed (after Claude Bernard 
Physiologie Experimentale, 1856, tome ii. p. 185), showing a condition in which pancreatic juice may- 
enter the intestine, although the gall-duct is obstructed : A, duodenum showing the projections formed 
by Brunner's gland; B, B, the large pancreatic duct ; C, C, anastomoses between the small pancreatic 
duct and the large pancreatic duct; D. opening of the superior pancreatic duct into the intestine ; 
E, opening of the small inferior pancreatic duct into the bile-duct. 



the necrotic fat form yellowish-white patches in the retroperitoneal fat, and 
in the fat of the omentum, mesentery, abdominal wall, and it may be in other 
parts. 

In a certain number of cases of acute pancreatitis, but not in all cases, 
hemorrhage into the body of the gland occurs, forming what is known as 
acute hemorrhagic pancreatitis. (See also Hemorrhage into the Pancreas.) 
Whether this hemorrhage is the result of the action of the ferment of the 
gland upon its own vessels is not known. 

Acute pancreatitis may proceed to suppuration (suppurative pancreatitis) 



PA NCREA TI TIS 689 

or to gangrene (gangrenous pancreatitis). The suppurative form may be 
circumscribed or diffuse. In some cases the pus may be confined to the 
pancreas or peripancreatic structures, but the lesser peritoneum, or even the 
general peritoneum, may be involved. 

Symptoms. — In acute pancreatitis the patient is suddenly seized by a 
severe pain in the epigastric region, which is associated with faintness, or 
even collapse, and it may be active vomiting. Inquiry reveals the fact that 
constipation is present, and so the physician may be misled into a diag- 
nosis of intestinal obstruction, but doubt is thrown upon this belief by the 
fact that gas can be passed by the anus. The pain may be paroxysmal in 
type, and there is great tenderness in the epigastrium upon pressure. This 
area becomes swollen and tense, and as the case progresses the entire abdo- 
men may become distended. The face is pinched and anxious-looking, and 
the upper lip drawn as in acute peritonitis. The vomit may become black 
and tarry from the presence of altered blood. 

If the patient survives more than a few hours, a more or less marked jaun- 
dice develops, provided that the bile is prevented from escaping into the 
bowel by swelling of the mucous membrane or the presence of a stone. 
Hiccough may be an annoying symptom, and the pulse is rapid and running. 
The temperature may be febrile, normal, or subnormal. The urine may 
contain casts and albumin. Death in collapse with profound asthenia 
usually occurs by the second to the sixth day, but recovery may occur in 
mild cases, and it sometimes happens that these acute symptoms gradually 
merge into the subacute type of the malady. 

Subacute pancreatitis cannot, of course, be sharply separated from the 
acute form, yet cases occur in which the symptoms are sufficiently modified 
to indicate that another form of pancreatitis is present. The malady is not 
so sudden in its onset, the pain is not so excruciating, and the epigastric 
swelling is neither so great nor so rapid in its development. The pulse is less 
rapid, and the constipation is more prone to give place to diarrhoea, the stools 
containing pus, tarry blood, and undigested food. Chills also occur, and 
after a few days a swelling, due to abscess, may be felt. This abscess may 
burrow in such a way as to form a perirenal abscess, a psoas abscess, or a 
subphrenic abscess, or it may burst into the stomach or bowel. The symp- 
toms of sepsis are, of course, present in such a case, and if surgical relief is 
not given death is due to this cause or to profound asthenia. Such a case 
must be separated from perforation of a gastric ulcer, from abscess due to 
caries of the spine, from suppurating cholecystitis, and from perirenal 
abscess. 

Diagnosis. — Fitz gives the following rule for the diagnosis of this state: 
"Acute pancreatitis is to be suspected when a previously healthy person, or 
a sufferer from occasional attacks of indigestion, is suddenly seized with 
violent pain in the epigastrium, followed by vomiting and collapse, and in 
the course of twenty-four hours by a circumscribed epigastric swelling, 
tympanitic or resistant, with slight rise of temperature." These symptoms 
are still more indicative if there is a history of gallstone colic. 

Acute pancreatitis must be separated from intestinal obstruction, per- 
foration of the duodenum, and the perforation of a gastric ulcer. It must 
44 



690 DISEASES OF THE PANCREAS 

not be confused with rupture of the gall-bladder, suppurative cholecystitis, 
and fulminating appendicitis. The differential diagnosis from intestinal 
obstruction has already been touched upon. If doubt exists an operation 
will reveal the true cause of the symptoms, for in pancreatitis fat-necrosis 
may be evident as soon as the belly is opened. The operation is justified, 
because it ought to be performed in either instance to save life. When per- 
foration of the stomach or duodenum is considered, the history of an old 
gastric ulcer or of hemorrhage from the bowel, in which dark, tarry blood is 
passed, will be of importance, and here, again, an operation to save life is 
necessary, whether the condition be pancreatic disease or perforation. 

When suppurative cholecystitis is suspected, it may be confirmed by the 
discovery that the early swelling is in the neighborhood of the gall-bladder, 
and a history of typhoid fever or of gallstones will be presented. However, 
this latter history may be equally suggestive of secondary pancreatic disease. 
Here, again, an operation primarily for diagnosis and secondarily for relief 
is indicated. 

Perhaps the most important differential diagnosis lies between acute 
pancreatitis and fulminating appendicitis, because appendicitis is a common 
disease, because the pain accompanying it is often referred to the epigas- 
trium, and because an incision in the pancreatic region is far removed from 
that required for appendectomy. 

Palpation of the appendix will usually elicit pain over its site, and, perhaps, 
localized swelling. Examination by the rectum may reveal marked iliac 
tenderness and a history of repeated attacks of appendicitis may be found. 

A valuable aid to diagnosis in these cases is the examination of the urine 
for leucin and ty rosin, which are not present in healthy urine, although they 
may be present in other conditions than pancreatitis. The urine is pre- 
cipitated with basic lead acetate and filtered. The filtrate from which the 
excess of lead has been removed by hydrogen sulphide is now evaporated 
almost to dryness and allowed to stand for crystallization to take place, when 
crystals of leucin and tyrosin may be found. (For a valuable article on the 
chemistry of the urine in disease of the pancreas see Cammidge, British 
Medical Journal, April 2, 1904.) 

Opie has described a test for lypolytic substances in the urine, and 
Cammidge has advocated a test for glycerin derivatives in the urine as 
aids to diagnosis; but neither of these methods is readily employed by 
the general practitioner. 

Prognosis. — Acute pancreatitis is always an exceedingly grave state. Death 
ensues in the majority of cases. Recovery occurs in the very mild cases, as 
has been proved by instances in which a subsequent operation has revealed 
the evidences of the disease. 

Treatment. — The treatment of acute pancreatitis consists in the prompt 
institution of surgical proceedings as soon as the shock of the onset of the 
disease has been overcome. Robson insists that the surgeon should not wait 
until collapse passes off, as the collapse may be due to septic absorption, 
which only an operation can relieve. By the relief of pressure, the pro- 
viding of drainage, and the removal of the cause of the attack, if it exists 
in the gall-duct, relief may be given the patient and the process arrested 



PANCREATITIS 691 

before it has proceeded too far. In a certain proportion of cases, however, 
the state of the patient from the onset is too grave to permit of surgical inter- 
vention. Excessive pain is to be relieved by morphine given hypodermically, 
and collapse is to be treated by the employment of strychnine and atropine. 

The treatment of the subacute form of the disease consists in supporting 
the nutrition of the patient by the use of predigested foods and stimulants, 
and by surgical intervention for the relief of tension and removal of pus as 
soon as the diagnosis is made and the patient is strong enough to stand 
operative procedures. 

Chronic Pancreatitis. — This form of pancreatitis has been in the past 
considered quite rare, but it would seem probable that it exists more com- 
monly than is generally thought. It is usually developed as a result of 
chronic catarrh of the duct of Wirsiing, which, in turn, is caused by chronic 
gastroduodenal catarrh or by cholelithiasis, pancreatic lithiasis, or by gastric 
ulcer. 

Of chronic pancreatitis, Opie, of Baltimore, thinks there are two types. 
One is an interlobular pancreatitis, with increase in the connective tissue 
between the lobules ; the intralobular tissues being unaffected and the islands 
of Langerhans escaping until very late in the pathological process. This is 
the type of chronic pancreatitis which follows blocking of the pancreatic duct 
by a morbid growth or by pancreatic or biliary calculi. Glycosuria is rarely 
present, because the islands escape. This is the common form. In the 
second form there is an interacinar pancreatitis, that is, new connective- 
tissue formation in the lobules themselves. The islands of Langerhans are 
seriously affected in this type, and hence glycosuria is usually present. This 
form is not due to obstruction of the ducts. 

These pathological facts show why it is that glycosuria does not appear 
as a sign of pancreatic disease in most cases in which, as the result of gall- 
stone disease or other sources of infection or obstruction, we suspect the 
presence of pancreatitis. For a recent and exhaustive consideration of the 
Relation of the Islands of Langerhans to Morbid Conditions of the Pan- 
creas and Diabetes Mellitus see Finney's article in the Medical Chronicle 
for June, 1903. 

The interstitial type, like the more acute forms, may be diffuse or local- 
ized. When localized a single area may manifest the change. A somewhat 
subacute form is also recognized, and in some of these cases there is 
a conspicuous enlargement of the area involved, so that the head of 
the pancreas when affected may be mistaken for a neoplasm. Presum- 
ably this enlargement represents a cellular infiltration, which later passes 
on to a fibrosis. The typical fibroid pancreas is small, dense, resists incision, 
and may creak when under the knife. Fatty infiltration is usually also 
present, and evidences of a primary acute process may be manifest. On 
microscopic examination there is a notable increase in the fibrous tissue, 
which, as already stated, may be perilobular or interlobular, or it may be 
interacinar. In the latter form the islands of Langerhans show hyaline or 
fibrohyaline transformation, or they may be absent from certain areas, or, 
perhaps, cannot be demonstrated in any part of the organ. The ducts 
may show dilatation, and in some instances be stained with bile. 



692 DISEASES OF THE PANCREAS 

Symptoms. — Chronic pancreatitis may be divided into those cases in which 
the symptoms are mild and those in which they are severe. In one case 
there may be little if any pain, but there is present persistent loss of flesh, 
and in the epigastrium, near the gall-bladder, may be found a hard mass 
which may be mistaken for a malignant growth in the stomach or gall- 
bladder. The patient complains of epigastric distress, such as that which 
follows taking food which is difficult of digestion, and attacks of vomiting 
may occur. Sometimes jaundice appears. Fever may be present if the 
infection of the ducts is marked. 

In the more severe form of chronic pancreatitis, the symptoms are in 
close accord with those of the subacute form, in that the symptoms may 
begin with severe pain in the epigastrium, as if the patient had gallstone 
colic. There is tenderness in the midepigastrium. Chills and fever may be 
well developed. 

Diagnosis. — Chronic pancreatitis is to be separated from gallstones in the 
ductus communis choledochus, from cancer of the head of the pancreas, 
from cancer of the gall-bladder and of the liver, and from subphrenic abscess. 
From impacted gallstones in the common duct the differentiation is prac- 
tically impossible. Tenderness on deep pressure will usually be found 
over the gall-bladder in the case of gallstones and over the epigastrium in 
pancreatic disease, and etherization may permit sufficiently deep palpation 
to feel the enlarged head of the pancreas if chronic pancreatitis is present. 
The distribution of the pain may be of value in the differentiation. In 
gallstone cases the pain is in the gall-bladder area and radiates around to 
the right scapular region; whereas, in pancreatic disease it is central and 
travels directly backward to a space between the ends of the scapula. 

Cancer of the head of the pancreas is a disease of advanced life; its onset 
is usually painless, and the jaundice that may ensue is gradual in onset and 
persistent, because the growth primarily, or secondarily, presses continually 
on the gall-ducts. The presence of great swelling of the gall-bladder in asso- 
ciation with jaundice and with the other symptoms of pancreatic disease 
already named indicates cancer. Sometimes in these cases secondary can- 
cerous nodules are to be found in the liver and in other organs. The liver 
may be much enlarged from the damming back of bile and from second- 
ary growths. Robson and Moynihan lay stress on the fact that the absence 
of pancreatic secretion from the stools causes them to be clay-colored, even 
when bile is present, and this may aid in diagnosis. If on testing the stools 
bile is found, and the feces are, nevertheless, light in hue, it is a fair sup- 
position that pancreatic secretion is absent. The test of the urine for leucin 
and ty rosin, already described, should also be used. 

There are two other facts which, if present, will decide the diagnosis posi- 
tively, namely, fatty stools due to the lack of pancreatic juice in the bowel 
and the presence of glycosuria due to the invasion of the islands of Langer- 
hans in the pancreas by the pathological process. Both of these signs are 
often absent, but if they are present they are pathognomonic of pancreatic 
disease. (See Diabetes Mellitus.) 

Prognosis. — Patients suffering from chronic pancreatitis in moderate degree 
may live for months or even for years. If glycosuria develops the prognosis 



PANCREATIC CALCULUS 693 

becomes very grave, not only because this symptom is grave in itself, but 
because the glycosuria indicates that the involvement of the gland in the dis- 
ease process is well-nigh universal, for as long as but a few islands of Langer- 
hans exist glycosuria does not ensue. Great emaciation, marked jaundice, 
and the development of a tendency to have multiple hemorrhages are evil 
signs. 

It is in this form of pancreatitis that surgery has given its most valuable 
results, often producing perfect recovery. 

Treatment. — The treatment of the mild form of chronic pancreatitis 
depending upon catarrh of the biliary and pancreatic ducts may be medi- 
cinal for a time in the hope that the condition may be relieved. The 
measures instituted are practically identical with those advised in cases of 
chronic cholangitis (which see). It is, however, a vital mistake to permit 
these cases to drift along in a state of chronic ill health, because the condi- 
tion is one which will eventually lead to pancreatic cirrhosis, and this in 
turn results in great emaciation and the development of glycosuria, which 
causes death. In other words, if the patient does not improve surgical 
measures should be adopted to give relief. 

The treatment of chronic pancreatitis of the severe type is wholly surgical, 
for it is cured in the majority of instances by abdominal section and drainage 
of the pancreatic and gall-ducts. Robson gives the mortality of operations 
in chronic pancreatitis as 12.9 per cent, in 62 cases. Operations in all cases 
of jaundice are of a grave character, because persistent oozing hemorrhage 
is prone to follow. Robson and Moynihan are firmly convinced that the 
danger from oozing hemorrhage after operation in cases of jaundice without 
pancreatic lesions is less than in those cases in which the pancreas is affected. 
They strongly advise the use of full doses of calcium chloride in all these 
cases prior to operation, to increase coagulability of the blood. They advise 
20 to 60 grain doses three times a day for one or two days. It is not to 
be forgotten that the persistent use of this salt finally decreases the coagu- 
lability of the blood. 

To sum up the subject of treatment, it may be said that all forms of pan- 
creatitis should be operated upon if the condition is such than an operative 
procedure can be supported. While in acute pancreatitis the operation can 
do little good directly, it permits drainage and it may remove some provok- 
ing cause, and so lead to recovery. In any case it is the patient's only chance. 
In the hemorrhagic or suppurative cases, the relief of pressure or of pus is, 
of course, advantageous. 

PANCREATIC CALCULUS. 

Pancreatic calculus is an exceedingly rare condition. The stones are 
composed of phosphates and carbonates. They vary in size from two and 
a half inches in length to fine sand, and they may be single or multiple. 
As many as 300 have been reported in one case. 

Symptoms. — There are no pathognomonic signs of the presence of pan- 
creatic calculus. Pain in the upper zone of the abdomen near the middle 
line or, as in Minnich's case, near the left costal border may be present. It 



694 DISEASES OF THE PANCREAS 

is often colicky in character, and with the pain there may be vomiting, sweat- 
ing, and collapse, as in gallstone colic. Fatty stools from the absence of 
pancreatic juice may be present, and glycosuria may occur. Occasionally 
pieces of the stone or small stones can be found in the stools. 

Treatment. — The treatment consists in removal of the stones from the 
duct by operation. Hypodermic injections of pilocarpine have been advised 
to increase the flow of the pancreatic fluid, but this, of course, cannot 
remove the stone if it is embedded. 



PANCREATIC CYSTS. 

These occur in four forms, namely, as retention cysts, proliferation cysts, 
hydatid cysts, and pseudocysts. Such cysts are, however, exceedingly rare. 
Hale White states that in 6000 autopsies at Guy's Hospital cysts of the pan- 
creas were found only 4 times. 

Retention cysts arise from blocking of the flow of secretion by calculi or 
by a single calculus, by the formation of cicatricial tissue, which narrows the 
duct, and by pressure from neighboring morbid growths. If no infection 
accompanies the retention of the fluid a cyst results instead of pancreatitis. 

Proliferation cysts occur as cystadenoma, or multilocular tumors, with a 
lining of cylindrical epithelium, and as cystic epithelioma. Hydatid cysts of 
the pancreas are very rare indeed, particularly in the United States and 
England; Hale White has reported one in England. 

Hemorrhagic cyst results from the occurrence of a hemorrhage into the 
gland tissue. Its existence is doubted by many pathologists. 

Pseudocysts are not real cysts of the pancreas, but small cystic accumula- 
tions of fluid in adjacent tissues. Sometimes a pancreatic pseudo-cyst is due 
to effusion into the lesser peritoneal cavity. They are thought to follow some 
injury to the epigastrium. 

Pancreatic cysts occur at all ages from infancy to old age, and are met with 
more frequently in men than in women, but the difference in the two sexes 
is very slight. The fluid varies very greatly in appearance. It may be as 
clear as water, or it may be opaque, or yellow, or coffee-colored, and even 
green or black. Its specific gravity is from 1.010 to 1.020, and it contains 
albumin. Sometimes it contains all the digestive ferments of the pancreas. 
The presence of any of them is of value in diagnosis, but their absence does 
not negative the pancreatic origin of the fluid. Nor does their presence 
prove that the cysts arose from the pancreas. Pressure upon the pancreas 
and secondary changes in a cyst wall may cause communication with the 
pancreas and admit its secretion to the cyst cavity. 

Symptoms. — The symptoms of pancreatic cyst are dependent upon the 
pressure which is produced, and, therefore, more or less discomfort may be 
the only sign of its existence. If the pressure is great pain is present. If 
the cyst be large enough to palpate it will be found to fluctuate, to be flat 
on percussion, and to transmit an impulse as in ordinary ballottement. 
Puncture with a fine aspirating needle may reveal the character of the 
fluid. 



HEMORRHAGES INTO THE PANCREAS 695 

Diagnosis. — Pancreatic cysts must be separated from cystic kidney, horse- 
shoe kidney, ovarian cysts, cysts of the liver, hydrops of the gall-bladder, and 
cysts of the suprarenal capsules. It must also be separated from mesenteric 
cysts, omental cysts, and retroperitoneal cysts. 

Prognosis. — Pancreatic cyst may last for years without causing discom- 
fort or death. On the other hand, cases occur in which the cyst ruptures 
into the peritoneal cavity or into the bowel or stomach, and when this hap- 
pens death ensues, preceded by vomiting and diarrhoea. Rarely hemorrhage 
takes place into the cyst, and this is accompanied by sudden increase in 
its size, and by faintness and collapse. 

Treatment. — The treatment consists in aspiration, evacuation and drainage, 
or complete extirpation of the cyst wall. The second procedure is usually 
that of election 



PANCREATIC TUMORS. 

These growths are exceedingly rare. Park states that in 53,000 autopsies 
only 226 showed primary malignant disease of this gland. Tumors of the 
pancreas consist in carcinoma, sarcoma, adenoma, and gumma. The infre- 
quency of carcinoma is shown by the fact that in 23,581 autopsies made in 
various parts of the world, in only 29 instances was pancreatic carcinoma 
present. The relative frequency of these growths is scirrhus, encephaloid 
and colloid. 

Carcinoma is the most frequent primary growth, according to Osier, and 
sarcoma is a more common secondary tumor because of involvement of 
the retroperitoneal glands by this disease. 

As nearly all cases of pancreatic malignant growth are secondary to disease 
of the gall-bladder, a tumor in the region of that viscus will usually be found 
to confirm the diagnosis. 

The prognosis in the case of malignant tumors is, of course, hopeless. In 
benign tumors the outlook depends upon the pressure symptoms. If a 
gumma is present, antisyphilitic treatment is, of course, indicated. 

HEMORRHAGES INTO THE PANCREAS. 

This condition is to be distinctly separated in the physician's mind from 
" acute hemorrhagic pancreatitis." Local hemorrhages may take place into 
the pancreas without any injury being received and without the patient being 
a sufferer from hemorrhages elsewhere. The hemorrhage may occur in a 
person who has seemingly been in excellent health without any other symp- 
toms than collapse, with a feeble pulse and evidences of shock. Sometimes 
hemorrhage into the pancreas occurs as the result of aneurysm of nearby 
vessels, or of cancer of the head of the gland. When hemorrhage into the 
pancreas occurs, it may be a limited extravasation of blood into the gland, 
from which the patient may recover, or it may be so profuse as to flood the 
retroperitoneal space, extending back to the kidneys and up to the posterior 
insertion of the diaphragm. 



696 DISEASES OF THE KIDNEYS 

The differentiation between the symptoms produced by hemorrhage into 
the pancreas and acute pancreatitis is practically impossible if there is no 
previous history of hepatic and duodenal disorder. If the condition is due 
to hemorrhage, an operation to relieve local tension is indicated, as death is 
due rather to this cause than to the loss of blood. 



DISEASES OF THE KIDNEYS. 

MALFORMATIONS OF THE KIDNEY. 

It happens not very rarely that one kidney is absent, its place being 
occupied by a little fibrous tissue or by atrophied renal tissue and fat. In 
order that the blood may be relieved of effete materials the other kidney is 
often very large, and, as it is usually lower down in the loin for this reason, 
it may be mistaken for a dislocated or cystic kidney, and removed, which 
means death to the patient. Not uncommonly one kidney is larger than the 
other, even if both are functionally active. In other cases one kidney has two 
pelves and two ureters. Perhaps the most common of these malformations 
is the so-called " horseshoe kidney," in which the two kidneys are joined 
across the vertebral column by a mass of renal or connective tissue. Some- 
times this horseshoe kidney is displaced into the pelvis, or it may be altogether 
on one side of the vertebral column. 

Again, the kidneys may be fused into a single mass, usually occupying a 
median position much below the normal level, or even in the pelvis. 

MOVABLE KIDNEY. 

Definition. — Aside from the renal malpositions incident to malformation, 
and, therefore, essentially of congenital origin, the kidney may wander from 
its normal position. Several forms of such displacement are recognized. 

The movable kidney lies behind the peritoneum, and usually can be made 
to assume its normal position, but descends during the erect posture ; its mal- 
position may be parallel to the axis of the body, or it may show a lateral 
movement, or the two may be combined — the "cinder-sifting" kidney. The 
organ may be pushed from its place and anchored in its new position — the 
" incarcerated kidney.'" 

When the kidney falls forward and develops a pedicle, consisting of the 
ureter, vessels^ and peritoneum, the last also covering the organ, it then 
becomes a "floating kidney," the pedicle forming the so-called mesone- 
phron. 

Kidneys enlarged from any cause are prone to displacement, and displaced 
kidneys, on account of obstruction of the ureters and veins, are frequently 
subject to enlargement. 



MOVABLE KIDNEY 697 

Movable kidney is far more frequent in women than in men, in the pro- 
portion of about 7 to 1. Again, the right kidney is the one at fault in the 
majority of cases, or in the proportion of about 7 to 1. Sometimes both kid- 
neys are movable. 

Etiology. — The most important etiological factor is undoubtedly bodily 
configuration. Women of the lean, lank type with floating ribs that slope 
markedly downward and who are hollow in the flank, like a hunting dog in 
training, are the most frequent subjects. Their muscles are usually poorly 
developed, and, if they have been pregnant, as a rule, the abdominal wall 
is relaxed. If to the natural configuration and these other causes is 
added the effect of a tight corset and a sudden effort or fall, the needful 
etiological factors are all present, and a sharp pain in the side may be the 
sign that the kidney has made its maiden movement from its natural site. 
In one case the woman says she has had a fall and has wrenched her side in 
falling; in another she has reached high above her head, as in playing tennis; 
and in a third case a blow or jar in a railway accident may have been the 
needed trauma. 

Symptoms. — Many patients have no symptoms of this condition for years. 
If on examining the belly in the region of the gall-bladder a floating kidney- 
is found in a person ignorant of its existence, and anything is said of it, the 
patient not rarely becomes a hypochondriac on this subject, and goes from 
physician to surgeon, insisting on relief of symptoms which are often 
not really in existence. As the condition is, to a large extent, harmless, it 
should be ignored, unless it is causing symptoms. 

When symptoms are present they vary over a wide degree of severity. In 
some they consist of a sensation of dragging in the back and side, in others 
they amount to keen suffering, and in still others they may consist in attacks 
of agony due to twisting or angulation of the ureter by the kidney becoming 
rotated on its axis or bent by great displacement. These paroxysms of pain 
have been called i( Dietl's crises/' Nausea, vomiting, chills, and collapse 
are present, and after the attack the urine is found loaded with urates and 
perhaps pus and blood cells. Sometimes even free hematuria may be present. 
When by postural change or manipulation the kidney assumes its normal 
position, a distinct renal pelvis may suddenly be emptied and a gush of urine 
overdistends the bladder and escapes by the urethra. 

Diagnosis. — There are several states that resemble the pain of floating kid- 
ney. Violent pain in the epigastrium may be due to this cause or to appen- 
dicitis, or gastric ulcer. I have seen a "Dietl's crisis'' closely resemble a severe 
attack of acute appendicitis. It also may resemble gallstone or renal colic, 
or the symptoms produced by abdominal aneurysm. The presence of the 
mass in the abdominal cavity may lead to a diagnosis of malignant growth 
or of impacted feces. 

The dislocated kidney may be felt on careful palpation in thin women 
just below the border of the ribs and back of the area in which the tip 
of the gall-bladder can be felt when that viscus is enlarged, but gentle 
pressure often causes it to disappear. A floating kidney may, however, be 
found almost anywhere in the abdominal cavity, and has even been dis- 
covered in the pelvis. When found in the belly it is usually so movable 



698 DISEASES OF THE KIDNEYS 

as to be easily pushed about, and it is so free and slippery that it is often 
elusive, being found one moment and lost the next. Not rarely some move- 
ment of the patient may cause it to slip into its normal position. This fact 
often leads the physician to overlook its presence, and only when the patient 
is repeatedly examined is the kidney found "away from home." In other 
words, inability to find a floating kidney at one examination does not prove 
that the patient is not a sufferer from this state. 

Pressure upon the kidney gives rise to a sickening sensation, which causes 
the patient to wince. 

To examine the patient properly the woman should be placed on her back 
with the knees drawn up so that the belly wall is relaxed. If the right side 
is being examined the left hand of the physician is so placed that the tissues 
of the right side can be grasped close to the last rib, between the thumb in 
front and the fingers behind. The patient is then told to take a deep breath, 
when the kidney may be felt to slip out between the fingers and thumb, as a 
watermelon seed slips when pressed upon in this way. The left hand remain- 
ing in situ to block the pathway of return, the fingers of the right hand can 
now feel the smooth, rounded surface of the organ below the area grasped by 
the left hand. If the pressure by the left hand be relaxed and pressure 
upward is produced by the right hand, the kidney may be felt to slip back 
into its place. While the kidney is wandering deep palpation in the flank 
may reveal a lack of resistance due to absence of the kidney. When the left 
kidney is examined the same process is followed, save that the right hand 
takes the place of the left. 

Treatment. — No treatment is needed unless the kidney really causes pain. 
If it does it can usually be kept in place by the avoidance of tight lacing and 
of severe exercise, or by wearing a properly adjusted pad and bandage to sup- 
port the tissues just below the floating ribs. Operative interference, with the 
object of stitching the kidney in place, is needed in bad cases, but the diffi- 
culty is that the relief obtained by operation is not permanent in all cases, 
the kidney wandering away from where it is sutured. Further than this, the 
operation is not entirely devoid of danger. My colleague, Dr. Keen, has 
placed the mortality at 2 to 3 per cent. Out of 137 cases which were 
operated upon and collected by Watson there were 5 deaths, but 4 were not 
the result of the operation. In neurasthenic patients operation should be 
avoided, at least until a rest cure is instituted, when not rarely all signs of 
renal tenderness may disappear. Even in those cases which have had one 
attack of severe pain (Dietl's crisis) the kidney may give no further trouble 
if a belt and pad are worn. 



CIRCULATORY DISTURBANCES IN THE KIDNEY. 

Changes in the circulation in the kidneys produce very great alterations 
in the urinary flow, both as to its quantity and quality. If the vessels of the 
kidney, and particularly those of the Malpighian tufts, are poorly supplied 
with blood, the urinary secretion is scanty, even though the amount of solids 
in the urine may be fairly large. On the other hand, any cause which sends 



CIRCULATORY DISTURBANCES IN THE KIDNEY 699 

a large amount of rapidly flowing blood to the kidneys results in free diuresis. 
Thus, chilling the surface of the body often causes a profuse urinary flow, 
and nitroglycerin, by dilating the renal vessels, may do likewise. 

Any substance which acts deleteriously upon the delicate cells of the 
Malpighian tufts causes them to permit not only the transudation of fluid, 
but of albumin as well. 

Acute Hyperemia. — An acute hyperemia of the kidneys may follow 
exposure to cold, or the ingestion and attempted elimination of irritating 
substances, such as cantharides, turpentine, and a host of other drugs 
capable of damaging the kidney epithelium. It is also generally accepted 
that a similar state of these organs may exist in the course of acute 
infectious diseases, like scarlet fever, but it is exceedingly doubtful if this is 
the case even in a modified form. 

Treatment. — The treatment of this state consists in the use of a few dry 
cups on the back over the kidneys and in the liberal administration of some 
water, like Poland water, to flush these organs. Rest in bed is, of course, 
essential. An old-fashioned and useful remedy is watermelon-seed tea or the 
infusion of flaxseed. Often the use of an alkaline diuretic, such as 2 drachms 
of liquor potassii citratis, with 1 drachm of sweet spirit of nitre, is valuable, 
if given every three hours. 

Chronic Hyperemia. — Chronic hyperemia is a very much more common 
condition, and occurs in nearly every case in which the circulation becomes 
sluggish by reason of cardiac weakness, as in valvular disease with rupture 
of compensation, in cases of ascites with pressure on the kidneys, and when 
tumors produce a mechanical interference with the flow of blood in these 
organs. 

Symptoms. — Albuminuria is a prominent symptom of this state, and 
hyaline casts and tube casts containing blood cells may be found. The 
amount of urine passed in each twenty-four hours is often very scanty. 
If such kidneys are seen at autopsy, they will be found to be cyanotic 
in the early stages, somewhat enlarged and heavier than normal, but the 
capsule is not adherent and the surface of the kidney is not roughened. 
Later the connective tissue increases, and when the kidney is incised it is 
found to be firm and tough, due to overgrowth of interstitial tissue. The 
pyramids are dark and purple in appearance. A more minute examination 
will reveal the fact that the capillaries forming the Malpighian tufts are 
greatly engorged, their walls thickened, and that the vasa recta, the inter- 
lobular veins, and the stellate veins of the cortex are also in a similar 
state. 

Diagnosis. — Such kidneys may lead the physician to a diagnosis of neph- 
ritis complicating cardiac disease, but the renal symptoms often disappear 
entirely under rest and proper cardiac treatment, although developed fibroid 
changes in the organ are, of course, irremediable. 

Treatment. — The treatment consists in giving the patient digitalis in full 
doses if the heart is feeble, and in applying a hot compress over the kidneys; 
or in the use of dry cups over these organs, and in the employment of gin and 
digitalis as an alcoholic stimulant to the heart and kidneys. Rest in bed 
for the tired heart and for the congested kidneys is essential. Another very 



700 DISEASES OF THE KIDNEYS 

useful remedy is fluid extract of apocynum cannabinum in the dose of 5 to 
10 minims twice or thrice a day. (See Valvular Disease of the Heart.) 



ACUTE BRIGHT'S DISEASE. 

Definition.— By acute Bright 's disease is meant a state in which the tissues 
of the kidney are involved in an acute inflammatory process, that is to say, 
it is an acute diffuse nephritis. The condition is not far removed from that 
of acute hyperemia already described. 

Etiology. — The causes of acute diffuse nephritis are the acute infectious 
diseases, particularly scarlet fever, and also diphtheria, croupous pneumonia, 
and septicemia. Sometimes typhoid fever or malaria act as exciting causes. 
In other cases an acute infection gains access to the body through the tonsils, 
and it is remarkable how often evidences of renal irritation follow the onset 
of tonsillitis. Still another cause is exposure to cold, particularly if the circu- 
lation is disturbed by violent exercise, and if the kidneys are irritated by the 
process of eliminating alcohol and other waste products after a Bacchanalian 
revel. So, too, the ingestion and elimination of irritant poisons may cause it. 
Severe burns or scalds may also produce acute nephritis. 

Acute and subacute nephritis are exceedingly rare in children, unless 
produced by one of the acute infections, and by this term is included not 
only the eruptive fevers, but infections such as bronchopneumonia and the 
various forms of severe summer diarrhoea, in all of which nephritis is by no 
means unusual. Thus, in 70 cases of gastrointestinal disorder Morse found 
signs of renal inflammation in no less than 15 per cent., and Holt states that 
in every case in which these conditions become severe the kidneys suffer. 

Pathology and Morbid Anatomy. — As with all acute inflammatory processes, 
great variations as to the severity of the alterations in the kidney are met 
with in different cases. In mild cases the organ may show no gross changes. 
The essential point to be remembered is that the texture of the kidney is 
inflamed through and through, although not uniformly so. The glomeruli, 
the tubules, the connective tissue, and the bloodvessels all share in the 
process. In typical cases, for this reason, the kidney is more or less congested, 
enlarged and cedematous, pitting on pressure, and if it is cut it oozes free 
blood in excess. The capsule strips readily and is often less firmly attached 
than normal. As a rule, the more cedematous the organ the less adherent is 
the capsule. Often the pyramids are red and engorged, while the broadened 
cortex is comparatively pallid. 

In some instances (glomerular nephritis) the glomeruli appear to bear the 
brunt of the process. Under the microscope the vessels forming the tuft are 
seen to be distended and contain leukocytes and larger cells having large 
nuclei, which are probably endothelial in origin. Degeneration of these 
cells ensues, and as this change progresses they are shed into Bowman's 
capsule with large mononuclear leukocytes, which fill it so completely that 
the vessels of the tuft are compressed. The epithelium lining the capsule 
may escape, although it usually undergoes proliferation, degeneration, and 
exfoliation. Added to these different sets of cells we find an albuminous 



ACUTE BRIGHT'S DISEASE 701 

exudate, due to the acute inflammatory state of the surrounding tissues, 
mixed with both red and white blood cells. 

In the tubules there is also degeneration and necrosis of the epithelium 
lining their walls, so that the cells become albuminous or fatty, and 
desquamate. In this way the tubules are more or less distended, not 
only with these cells, but with red and white cells and granular detritus. 
Fusion of these materials results in the formation of casts of the tubules, 
which appear in the urine as blood casts, and as casts of desquamated 
epithelium. 

As with inflammations elsewhere, there is an extravasation of fluid into 
the tissues, and when this occurs the interstitial portions of the kidney 
become cedematous, filled with outwandering leukocytes, and, in addition, 
a considerable number of small spheroidal cells, many of which, in 
some cases, as shown by Councilman, are of the plasma-cell type. If the 
inflammation is very severe, there is an actual hemorrhage into the tissues — 
"hemorrhagic nephritis." When the extravasation of serum and leukocytes 
is particularly copious, Delafield calls the condition "exudative nephritis." 
This is the form prone to occur during or after scarlet fever. 

Symptoms. — The symptoms of acute diffuse nephritis are usually rather 
sudden in onset. A child convalescing from scarlet fever, or a man suffering 
from an acute infection, or after exposure, suddenly suffers from scanty 
urinary flow, and almost before the scantiness is noticed the face may be 
seen to be edematous and the ankles swollen. The patient may go to sleep 
with a normal visage and awaken with a puffy one, the puffiness being par- 
ticularly marked on the pendent side. In children, if the nephritic irrita- 
tion be severe, a convulsion may develop as one of the early signs. Fever 
may or may not be present. 

It is an interesting fact that severe anaemia develops with extraordinary 
speed, so that the swollen face becomes pallid and white in appearance as 
soon as it is puffy. Nausea and vomiting are often early symptoms, and 
are to be regarded with some alarm, as they are indicative of toxaemia. 

The scanty urine is heavily loaded with solids, and if examined micro- 
scopically it shows red blood cells, epithelial cells from the uriniferous 
tubules, and tube casts composed of blood cells, epithelial cells, and 
hyaline material. When the heat and nitric acid test is applied to the 
urine, the amount of albumin present is found to be very large, forming a 
thick and heavy, curd-like mass, which, in the heat test, gradually settles to 
the bottom of the tube. The pulse is usually hard and the tension high, but 
sometimes the high tension is more apparent than real, the pulse being full, 
but gaseous in resistance. 

Auscultation will reveal, in the cases which have a high arterial tension, 
an accentuated aortic second sound, and a comparatively feeble first sound 
at the apex. Sometimes acute cardiac dilatation develops, and secondary 
pulmonary congestion aids in the destruction of the patient. In other cases 
in which oedema is particularly marked a rapid effusion of fluid takes place 
into the pleural spaces and into the peritoneal cavity, and pulmonary cedema 
develops with remarkable rapidity. The only vessels which do not leak 
freely are those of the skin, the kidneys, and the bowels. The skin is 



702 DISEASES OF THE KIDNEYS 

dry and harsh, the urine scanty or suppressed, and the bowels are usually 
constipated. 

These are the symptoms of what may be called a severe attack of the 
disease, but it is important to bear in mind that very often no oedema is 
present, and that in others the urinary flow is not greatly diminished. Often 
anaemia and pallor may be the first sign during convalescence from an acute 
infectious malady, to show that all is not well with the kidneys. In other 
cases some giddiness may be present, and, if the patient is an adult, uraemic 
symptoms are more prone to develop than if he is a child. 

The urine of persons suffering from the infectious diseases should be 
examined repeatedly, in order that the earliest signs of renal involvement may 
be recognized. There is no excuse for letting the condition run on unrecog- 
nized until it is forced upon the physician by marked objective symptoms. 

Diagnosis. — It is evident that this state does not present signs or symptoms 
which are often presented by other maladies, but, on the other hand, it is 
important for the physician to recall the fact that certain prominent symptoms 
may be absent without casting doubt on the diagnosis. Thus the amount 
of albumin in the urine may be small, the degree of oedema slight, and the 
urinary flow may not be greatly decreased. Again, the mere presence of 
large amounts of albumin is not alone indicative, because, as already 
pointed out in the article on circulatory disorders of the kidneys, it often 
happens that scanty urine and a large amount of albumin are present in 
renal congestion. 

Prognosis. — The outlook in cases of acute diffuse nephritis, if the patient 
has previously had healthy kidneys, is favorable, particularly if his habits 
of life have been satisfactory. This statement holds true of the acute condi- 
tion following exposure in young adults rather than in children and in young 
adults who have nephritis from acute infectious maladies, particularly scarlet 
fever. The younger the child the more grave the danger in scarlet fever. 
(See Scarlet Fever.) Evil symptoms are drowsiness from toxaemia, a tendency 
to pulmonary oedema, a feeble heart, and a free transudation into the subcu- 
taneous tissues. Suppression of urine is, of course, a most serious symptom. 

The renal lesions in those who survive the acute stage of the inflammation 
vary greatly in their persistency. In some cases all signs of renal trouble 
clear up in a fortnight, but in others albuminuria in some degree persists for 
months and returns whenever the patient is chilled or takes excessive exercise. 
When anaemia is persistent and resists fresh air and tonics, even if the albu- 
minuria is scanty, suspicion of subacute or chronic lesions following the acute 
stage is aroused. In other cases the acute nephritis is but an exacerbation of 
a hitherto unrecognized chronic parenchymatous nephritis, in which case 
the outlook is most grave. Sometimes, just as the most encouraging progress 
is being made, a terminal pneumonia occurs, and death ensues. 

Treatment. — The treatment of acute diffuse nephritis consists in putting 
the patient to bed at absolute rest and in the ordering of a liquid diet con- 
taining nothing which can irritate the kidneys, such as condiments like 
pepper or mustard. Counterirritation over the kidneys in the shape of fre- 
quently renewed hot compresses are of value, but, as a rule, it is unwise to 
add any irritating drug to these compresses, for it may be absorbed and cause 



CHROMC BRIGHT'S DISEASE 703 

renal irritation. If the pulse is quick, small doses of tincture of aconite 
(1 minim every one or two hours) may be given, with a teaspoonful of sweet 
spirit of nitre in cool water. 

During convalescence tincture of the chloride of iron and tincture of nux 
vomica may be used as tonics and to combat ansemia. Great care should 
be taken that the patient is not exposed to cold and dampness, and that 
woollen garments are worn next the skin to protect it from being chilled, 
since chilling of the surface may produce secondary renal congestion. 



CHRONIC BRIGHTS DISEASE. 

Definition. — The term "chronic Bright's disease" is applied to several 
types of slow, persistent, inflammatory process in the kidney which result 
in very definite alterations from the normal in these organs. Each type is 
also so distinct from the other in its rapidity of progress and results that it is 
difficult to regard them as related in any way, yet in each instance we find 
inflammation and degeneration forming the chief pathological change. 

The two chief forms of chronic Bright's disease are called " chronic paren- 
chymatous nephritis" and "chronic interstitial nephritis," because in the first 
the pathological process is chiefly concerned with the parenchyma of the 
organ, and in the second form the conspicuous changes are in the connective 
tissue. 

There are also cases in which these two forms of nephritis exist simultane- 
ously, that is, the kidneys present the changes found in both types. Indeed, 
these cases are much more numerous than is generally thought, because 
physicians, having been taught in student days that nephritis is capable of 
being divided into two forms, are continually trying to force cases that come 
to them into one of these categories, it being forgotten that while classification 
and division are artificial methods devised for teaching purposes, nature does 
not adhere to any such boundaries, but presents cases which may partake of 
more than one type at the same time. It is perhaps well, then, to consider 
that chronic Bright's disease is a chronic diffuse nephritis, although some- 
times the parenchyma and sometimes the interstitial tissues suffer chiefly. 

On the other hand, the clinical pictures afforded by the two classes of 
cases constitute adequate grounds for recognizing chronic parenchymatous 
nephritis as different from the chronic interstitial form. There can be no 
doubt that we have been laying too much stress on the results obtained 
from an examination of the urine in differentiating the two conditions. 
Sometimes a urinary examination at once settles the diagnosis, but Cabot 
is clearly right in his contention that the urine, in many cases, offers no 
information as to the exact type of change going on in the renal cortex. 
Differentiation, when possible, must rest upon symptoms considered with the 
results of urinary examination. 

Etiology. — Chronic nephritis may follow acute nephritis, but this is 
very rarely the case. Its most common causes are alcoholism and exposure, 
and in the upper classes alcoholism and overfeeding, with lack of exercise. 
Gout and syphilis, chronic lead poisoning, and chronic digestive disorders 



704 DISEASES OF THE KIDNEYS 

are also causes, in all probability. While the latter are not as yet proved 
to be definite causes, there is good reason to believe that the continued 
absorption of toxic materials from the bowels for long periods of time may 
cause renal lesions in the effort of these organs to eliminate the noxious sub- 
stances. A very important cause, in all probability very closely allied to those 
just named, is arteriosclerosis, it being considered that the changes in the 
bloodvessels are responsible for renal changes, although, on the other hand, 
the renal lesions are often the cause of the vascular degeneration. In 
many cases it is probable that the same causes produce both the arterial and 
the renal changes simultaneously. In some cases, indeed, it may be said in 
the majority, the exciting cause of the renal changes is undiscoverable, and 
perhaps may depend upon some congenital defect, which as yet we do not 
understand. This defect may be localized in the kidneys, or lie in other 
organs whose imperfectly performed labor results indirectly in renal dis- 
ease. 

Chronic parenchymatous nephritis is a disease of early and middle life, 
while chronic interstitial nephritis is observed in patients of more advanced 
years, but exceptions to this rule, of course, occur. 

Frequency. — Chronic renal disease is one of the most common maladies 
affecting man, a large proportion of the deaths of all persons over thirty 
years of age being due to this cause. Not only do the mortality statistics 
prove the correctness of this statement, but it is now becoming a well-recog- 
nized fact that many cases which die of acute pneumonia are in reality cases 
of chronic nephritis, in which the pneumonia acts as a terminal infection and 
destroys the patient when his powers of resistance have diminished as a result 
of his renal state. The United States census for 1900 shows that disease of 
the kidneys stands sixth in the list of diseases causing death, pneumonia, 
tuberculosis, heart disease, diarrhceal affections, and unknown causes only 
leading it. 

Of 41,924 medical cases treated in five large Philadelphia hospitals, 1395, 
or 3.32 per cent., were affected with nephritis, and of 24,624 medical cases 
treated in four large Philadelphia hospitals in which the form of the lesion 
was stated, 797, or 3.23 per cent., were affected with chronic nephritis. On 
the other hand, of 228,232 cases treated in the medical dispensaries of four 
large Philadelphia hospitals, only 1902, or 0.9 per cent., were affected with 
some form of nephritis. This remarkable difference in frequency in the 
wards and in the out-patient departments is probably due chiefly to the fact 
that most of the cases of renal disease presenting themselves for treatment 
were so ill that they became in-patients, and are so recorded. 

From this point on it will be best to consider the two chief forms of chronic 
renal disease separately. 

Chronic Parenchymatous Nephritis. — Chronic parenchymatous nephritis 
is sometimes called " chronic desquamative nephritis," because of the des- 
quamation of the epithelial cells lining the tubules; "chronic tubular 
nephritis/' because the uriniferous tubules are involved, or in certain 
cases, " chronic glomerulonephritis," because the glomeruli of the kidney 
are chiefly affected in this malady. It is also called " chronic diffuse 
nephritis." 



CHRONIC BRIGHT S DISEASE 705 

Pathology and Morbid Anatomy. — In typical cases the kidney is found to 
be large, pale, its subcapsular veins conspicuous, and the capsule easily 
detached. The organ offers little resistance to incision, and inspection of the 
incised surfaces shows that the marked enlargement of the organ is due to 
broadening of the cortex. The medullary pyramids, while often lighter in color 
than normal, never attain the pale yellowish hue of the cortex, and may be 
dark from associated congestion. In this form the microscope shows the 
epithelium, especially that of the convoluted tubules, granular or even fatty, 
desquamating, and coalescing to form casts, which may readily be recognized 
in position, or, having been passed, these casts leave tubules which are imper- 
fectly lined by epithelial cells. There is a less conspicuous, but fairly con- 
stant, change of a similar character involving the glomerular epithelium, and 
also the epithelial cells of some of the pyramidal tubes. Hemorrhages in the 
interstitial tissue are sometimes present. This is the form called " large white 
kidney." 

In some cases the interstitial tissue is but slightly involved, but in others it 
is notably increased and irregularly distributed, with unequal contractions, 
giving rise to a more or less bossed or granular surface, not unlike that 
seen in typical interstitial nephritis. In this form (small white kidney) the 
organ may not be enlarged, and may be even smaller than normal. It resists 
incision, due to the increase in fibrous tissue, which, with the unaided eye, 
may be seen as grayish patches in the yellow cortex. Hemorrhages may be 
present, mottling the incised surface with reddish or reddish-brown areas. 

Microscopically, the changes in the epithelium are similar to those seen 
in the large white kidney, but the increase in fibrous tissue constitutes a con- 
spicuous difference. It has not been definitely decided whether the small 
white kidney is a later stage of large white kidney, an independent affection, 
or a form of nephritis which having been primarily interstitial has had 
parenchymatous disease superimposed. 

The cardiovascular changes of chronic parenchymatous nephritis are 
similar in kind, but do not approach in degree those found in chronic 
interstitial nephritis. With the small white kidney, cardiac hypertrophy 
and slight arteriosclerotic changes are not of infrequent occurrence. There 
is usually an excess of fluid in the serous cavities, a varying quantity of 
oedema in the subcutaneous fat, and also in the lungs and meninges. 
Retinal hemorrhages are occasionally observed. 

Symptoms. — When chronic diffuse nephritis of the "large white type" is 
well developed there are few clinical pictures which are so typical. The more 
or less sivollen visage; the greasy, pallid skin; the stupid fades, and the 
dyspnoea on exertion strike the eye at once. Not rarely the partly buttoned 
waistcoat and the loosely laced shoes show that sufficient anasarca exists to 
cause the patient some discomfort. 

"If the pretibial tissues are pressed upon, they pit on pressure. Percussion 
may show the presence of fluid in the pleural and peritoneal cavities, although 
large effusions are not commonly met with in these cases. 

If the heart is examined, its sounds are found to be altered, so that the 
first sound lacks good quality, and the second sound is usually accentuated. 
The pulse is rapid, and the arterial tension higher than normal. The 
45 



706 DISEASES OF THE KIDNEYS 

patient is prone to be sleepy during the day and restless at night, and may 
be dyspn&ic on lying down. The urine is scanty and heavily laden with 
solids, and under the microscope shows a large number of fatty, granular, 
hyaline, and epithelial casts, leukocytes, and even red blood corpuscles. Occa- 
sionally the granular casts are particularly opaque to light, forming the " big 
black, granular casts," which are so significant of severe parenchymatous 
nephritis. Tested with heat or nitric acid, the urine is found to contain an 
excessive amount of albumin, so that the coagulum may equal half the urine. 
The specific gravity of the urine is high — about 1.025. With the advent of 
marked interstitial fibrosis, the quantity of urine increases and may equal or 
even exceed the normal amount. At this time the albumin diminishes, the 
casts often lessen in number, and cardiovascular changes occur, the chief 
sign of which is increased arterial tension. 

When the function of the kidneys is seriously disturbed, apathy, stupor, 
and finally coma may ensue from urwmia, and in some cases convulsions 
occur. These may vary from a slight twitch followed by stupor to a severe 
general convulsion, in which all the voluntary muscles are involved. Some- 
times a fleeting monoplegia, aphasia, or hemiplegia comes on as the result 
of the ursemic poisoning and without any connection with an actual apoplexy. 
(See Uraemia.) 

Patients suffering from chronic parenchymatous nephritis are sometimes 
seized by a severe serous diarrh&a, which is an effort at elimination on 
the part of the economy, and should be cautiously checked only when it 
becomes severe enough to be dangerous in itself. 

Comparatively rarely in the course of chronic parenchymatous nephritis 
an albuminuric retinitis develops, but when the nephritis complicates preg- 
nancy this ocular symptom is very common. 

The combinations of symptoms just recited are met with in the well- 
developed cases which present characteristic manifestations of the disease. 
It is to be distinctly recollected that in many cases few or none of these signs 
develop until the patient is suddenly overwhelmed by the climax of his 
malady, and that of all the chronic and grave maladies which affect man 
none advance and develop as insidiously as does chronic parenchymatous 
nephritis in many cases. In one instance a persistent indigestion which fails 
to yield to appropriate digestive remedies is found to be due to renal disease; 
in another anoemia fails to yield to ordinary chalybeates and is found to be 
renal in origin; in still another a persistent failure of health without appar- 
ent cause has its origin in bad kidneys. In yet another group of cases a 
persistent bronchitis is founded on this cause. If consulting physicians could 
be polled, I feel confident that they would universally state that the average 
case of grave ill-health seen by them in consultation, when the diagnosis is 
obscure, is not really difficult of diagnosis if the state of the kidneys is 
carefully studied. It is not sufficient to examine the urine once. It should 
be done repeatedly before deciding that it throws no light on the case. 

An important clinical fact to bear in mind is that a latent chronic parenchy- 
matous nephritis may exist for a long time, and finally be recognized by the 
sudden development of uraemia due to an acute congestive nephritis coming 
on as a complication. 



CHRONIC BRIGHT'S DISEASE 707 

Diagnosis. — The diagnosis of chronic parenchymatous nephritis is reached 
by the following symptoms and tests : The face is puffy and pallid ; there is 
often dyspnoea, even without exertion, and the second sound of the heart is 
usually accentuated. If the case is well developed, general anasarca may 
be manifest. The chief diagnostic factor, however, is the state of the 
urine. It is less than normal in quantity, of high specific gravity, and 
contains very considerable quantities of albumin. (See Albuminuria.) A 
microscopic examination of its sediment reveals fatty, granular, and hyaline 
casts, red blood cells, and large amounts of desquamated epithelium from the 
uriniferous tubules. The gravity of the disease is usually in direct propor- 
tion to the quantity and quality of the casts, the large, dark, granular casts 
being indicative of grave disease. Quantitative analysis reveals marked 
decrease in the total elimination of urea in each twenty-four hours. 

Prognosis. — The prognosis of chronic parenchymatous nephritis is inevi- 
tably fatal, and the patient's life is rarely prolonged over a few months, when 
once the disease is well developed. In those cases of chronic parenchymatous 
nephritis characterized by early dropsy which rapidly develops into general 
anasarca, Senator states that the duration of life varies from a few months to 
a year. In those cases in which the development of dropsy is gradual and 
irregular, varying in degree from time to time, he says that death ensues in 
from one to two years after the beginning of the malady. Strumpell gives 
the average duration of life in chronic parenchymatous nephritis as from one- 
half to one and one-half years. Every clinician of experience will, however, 
agree with Senator in recognizing another class of cases which extend over 
several years, and which are characterized by mildness of symptoms. In these 
cases there is not much albumin in the urine, but slight headache, and little 
swelling of the lower extremities or of the face. Gradually these patients 
become worse, until they finally fall into one of the well-defined classes 
already described. They are probably representative of that form of the 
disease characterized by moderate changes in the parenchyma of the kidney 
with associated interstitial disease. 

Treatment. — It has been generally held that diet is a very important factor 
in the treatment of this form of renal disease. While it is somewhat icono- 
clastic to say that this general belief is untrue, it is, nevertheless, a fact that a 
generous diet which does not strain the digestion and the eliminating organs 
can usually be allowed in most cases. We have before us a patient who is 
bound to die within a few months, and the question arises as to whether we 
can so regulate the diet that we will obtain results which compensate for 
the discomforts and unhappiness of the rigid milk diet, which is usually 
ordered, or one which causes the patient to regard his food with loathing 
and which is a constant reminder that he is ill. 

Although skimmed milk is theoretically capable of maintaining nutrition, 
it is practically incapable, because such enormous quantities must be 
consumed, to provide an adult with a sufficient amount of nutriment. 
Again, milk lacks the quantity of iron which ordinary food contains. It pre- 
sents to the patient the same quantities of calcium, magnesium, potassium, 
and phosphorus as is found in the ash of newborn animals, but it contains 
six times less iron ; this lack of iron being made up in the young by the 



708 DISEASES OF THE KIDNEYS 

storage of this metal in the liver, and possibly in other organs during 
intrauterine life. Again, the quantity of proteid which is present in milk 
is excessive. A normal adult requires approximately 3000 calories a day 
to maintain full nutrition. One quart of milk has a caloric value of about 
700, and therefore it takes about four to four and a half quarts of cows' milk 
to present sufficient nourishment. This large quantity of milk contains 
nearly 170 grams of proteid, whereas the normal average quantity of proteid 
ingested by a healthy adult does not exceed 100 grams a day. A milk diet, 
if taken in the quantities which are necessary for the maintenance of nutri- 
tion, forces the kidneys to eliminate enormous quantities of liquid, which 
they are illy prepared to do when suffering from disease, and if the patient 
does not take these quantities his vitality is impaired by nephritis and 
starvation combined. Again, such a diet causes the kidneys to eliminate 
large quantities of urea and much phosphates, and so, again, kidneys which 
are impaired in function because of disease are forced to perform an ex- 
cessive amount of work. 

It is entirely possible to arrange a suitable diet for cases of nephritis with- 
out in any way throwing undue stress on any of the organs of digestion or 
elimination, and at the same time maintain the nutrition of the body. Un- 
skimmed milk — that is, milk containing cream — is useful, since the fats 
add a very considerable number of calories to the milk, and by the use 
of starchy food an additional number of calories can be provided the 
patient, who, at the same time, does not receive an excess of fluid. As 
Croftan well says, one litre and a half of milk, plus a quarter of a litre of 
cream, for instance, contains approximately 50 grams of proteids (equal to 
225 calories), 75 grams of carbohydrates (equal to 337 calories), and 150 grams 
of fat (equal to 1350 calories), or a sum total of about 1912 calories. In order 
to make up the difference of 1088 calories, a little meat, eggs, sugar, butter, 
toast, zweiback, rice, fresh vegetables, etc., may be allowed with impunity, 
care being taken that the caloric value of 3000 is not greatly exceeded, 
and that all articles of diet that lead to the formation of irritating urinary 
end-products, and spices, condiments, etc., are avoided. These views are 
in accord with opinions expressed by Robin, of Paris, Bradford, and Hale 
White, of London, and other clinicians of experience. 

The fact having been established by several investigators that in many 
cases of parenchymatous nephritis with oedema there is a retention of 
sodium chloride in the tissues, it has been suggested that this salt be 
temporarily removed from the diet. The ground for this is that the excess 
of salt in the tissues requires an excess of fluid to keep it in the normal 
molecular concentration. When the patient is deprived of salt increased 
diuresis takes place and the dropsy often diminishes. 

Much discussion has occurred among physicians as to the quantity of water 
which should be allowed patients suffering from Bright's disease. Some 
believe that the amount should be as small as possible, on the ground that 
copious draughts of water engorge the vessels and increase the labor of the 
heart. That this cardiac influence is an important one we doubt, but as 
Edsall and others have shown that excessive water-drinking increases nitrog- 
enous metabolism, and as the kidneys in Bright's disease are unable to fully 



CHRONIC BRIGHT S DISEASE 709 

deal with the products of normal metabolism, it would seem evident that 
excessive quantities of water must be harmful. On the other hand, there 
can certainly be no good results from depriving the patient of water to the 
extent of making him suffer. 

The remedial measures other than diet consist in the use on each alter- 
nate day, if the heart is strong enough, of a moderate Turkish bath, in order 
that the skin may aid the kidneys in eliminating fluids and solids from the 
body. Fresh air and sunlight are essential, and severe exercise is to be 
prohibited. 

Drugs are of little value, except to relieve symptoms which may be annoy- 
ing. It has been the custom of physicians for many years to prescribe iron, 
usually in the form of Basham's mixture, for the purpose of combating the 
anaemia of chronic parenchymatous nephritis. This method of treatment 
does not possess the advantages with which it has been credited. The 
anaemia depends upon the toxaemia of the disease, and this, of course, is not 
removed by the administration of iron. Further than this, iron has a tendency 
to produce constipation, and constipation is prone to increase anaemia, and, 
again, constipation is a particularly undesirable condition in Bright's dis- 
ease, since it prevents the bowels from aiding the kidneys in eliminating 
impurities. 

The administration of very large doses of Basham's mixture is, therefore, 
unwise. It should be borne in mind that iron has no curative effect upon 
the renal condition, and therefore it is useless to administer more than 
the system can utilize for the relief of the secondary anaemia in the blood. 
Small doses of Basham's mixture are, therefore, as useful as large ones, so far 
as the anaemia is concerned. If the effect of Basham's mixture as a diuretic 
is desired, the liquor ammonii acetatis of the United States Pharmacopoeia 
may be added to a teaspoonful of Basham's mixture and given three or four 
times a day, as in this way the diuretic effect is obtained without an excess of 
iron being given. 

Should evidence of cardiac dilatation develop digitalis is indicated, and 
may be given in the dose of 5 or 10 minims of the tincture three times a day 
until some evidence of its physiological effect is obtained, when the dose 
should be cut down one-half. While the infusion of digitalis has the repu- 
tation of being more diuretic than the tincture, it is so much more prone to 
disorder the stomach that the tincture is usually preferable. 

A useful formula in place of digitalis will be found on page 519. 

If uraemic symptoms develop, the patient should be given a hot pack, and 
if there is any reason to believe that pulmonary oedema is threatened, or that 
the heart is too feeble to endure the hot pack, a hypodermic injection of 
strychnine, ^ of a grain, should be given before the pack is begun. Some- 
times a cup of strong black coffee is also useful at this time. Pilocarpine 
should not be employed, as it is too depressant and prone to produce pul- 
monary oedema. 

The question as to whether the bowels should be thoroughly purged 
by one of the hydragogue cathartics is debatable. On the one hand, it is 
claimed that by this means the intestines are unloaded and a large quantity 
of liquid and toxic material is removed from the body, and, on the other, 



710 DISEASES OF THE KIDNEYS 

that the purging may cause concentration of the blood, and so increase 
toxaemia. Probably the best rule to follow is to administer a hydragogue 
cathartic only when there is reason to believe that the bowels are con- 
fined and are consequently loaded with fecal matter. Hypodermoclysis, 
which is so useful in the uraemia of chronic contracted kidney, is worse than 
useless in chronic parenchymatous nephritis, owing to the presence of 
oedema. 

A valuable drug for the purpose of diminishing arterial tension and so 
decreasing the work of the heart, and also because it diminishes the loss of 
albumin through the kidneys, is nitroglycerin, which should be given in the 
dose of y^-q of a grain three or four times a day. This drug often increases 
the urinary flow when it is scanty. 

In regard to the treatment of uraemic convulsions, it is commonly held 
that the administration of morphine hypodermically for this purpose is 
dangerous, although there are some active practitioners who believe that 
it is a useful drug. It is probably more dangerous in the parenchy- 
matous than in the interstitial form of the disease. If the convulsion is 
severe chloroform or nitrite of amyl should be given by inhalation. (See 
Uraemia.) 

Comparatively recently it has been suggested that cases of chronic renal 
disease should be treated by decapsulation of the kidney. This plan of treat- 
ment is more indicative of surgical enthusiasm than of a clear conception of 
the pathology of the disease. A knowledge of the pathology and the results of 
experiments on animals show its futility, if not its danger. These views will 
be found in detail in the editorial columns of the Therapeutic Gazette for 
January, 1904, and June 15, 1904. 

Chronic Interstitial Nephritis. — To this form of chronic renal disease 
the terms "contracted kidney," "granular kidney," " cirrhosis of the 
kidney/' and "sclerotic kidney" are applied. 

Pathology. — Chronic interstitial nephritis is usually a primary process, 
although the small white kidney is really a combination of the fibroid and 
the chronic parenchymatous form. In this type the overgrowth of the con- 
nective tissue of the kidney is the dominant part of the pathological process, 
and the degeneration of the parenchyma, as represented by the glomeruli 
and the tubules, plays a secondary role. 

When kidneys affected by this state are examined, it is found that they 
contain large masses of fibrous tissue extending through the organ, which 
by contraction cause a shrinkage in size and a puckering of the surface. 
The capsule becomes thickened and exceedingly adherent, and the 
tissues beneath it are torn if it is stripped off. The surface of the cortex 
is roughened by rounded granules of varying size and cysts may appear 
at various points on its surface (Fig. 94). When an attempt is made to 
cut through the kidney, it is found to be tough and difficult to incise. 
After the organ is split open it is seen that the cortical portion is very 
much wasted. 

When the renal tissues are placed under the microscope, they show 
an irregularly distributed increase in the connective tissue, involving in 
particular the cortex and the interlobular vessels. There is also an asso- 



CHRONIC BRIGHTS DISEASE 



711 



ciated atrophy of the epithelium lining the uriniferous tubules. Casts are 
seen in the tubules, but not to the degree in which they are met with in 
the parenchymatous form of nephritis. The glomeruli in advanced cases 
may be converted into thick, fibrous bulbs; the walls of the bloodvessels 
forming the tuft may be thickened, and the capsule is seen to be dense 
and fibrous. Nor does the fibroid process affect the finer bloodvessels and 
the connective tissue alone. It extends to the large bloodvessels, and even 
to the renal arteries and veins. 



Fig. 94 




2 cm 



Kidney of chronic interstitial nephritis. The surface is granulated and irregular, and contains 
numerous cysts. The contraction is quite marked, the organ being but little more than half the 
normal size. 



It is also a noteworthy fact that while cardiac hypertrophy and arterio- 
sclerosis are often met with to some degree in parenchymatous nephritis, 
they are constantly found in a well-developed degree in the interstitial type of 
the disease. This cardiac hypertrophy is not limited to the left ventricle, 
as it is in the parenchymatous form. It affects the whole heart and 
it is often very great. The cause for the hypertrophy has been the sub- 
ject of much debate, but the conditions present in the bloodvessels seem to 
offer an adequate explanation of the state. These vessels are always fibroid 
and lacking in normal elasticity, and this, of course, offers greater resistance 



712 DISEASES OF THE KIDNEYS 

to the flow of blood through them and into the capillary networks. As the 
process is a gradual one, there is a gradual increase in the demands made 
upon the heart, and this is met by an increasing hypertrophy. The difficulty 
in forcing blood through the renal vessels also aids in producing this effect, 
but such influence has no doubt been overestimated. 

This is not the place to dilate upon the relationship of these vascular 
changes to the renal lesions. Many persons think that the renal changes 
are the cause of the vascular lesions, and others hold that the vascular 
degeneration causes the renal state. A most striking illustration of the 
relation between arterial disease and contracted kidney was shown by 
Welch at the meeting of the American Medical Association in 1904. He 
presented a specimen which consisted of a kidney supplied by two renal 
arteries, one of which was sclerotic. The area of the kidney supplied by 
this vessel was typically fibroid, while the other pole of the organ nourished 
by the uninvolved trunk was but slightly changed. 

Again, it is held by many that the overgrowth of connective tissue takes 
place to fill gaps made by the atrophy of the parenchyma, and by others the 
view is taken that the overgrowth of the connective tissue destroys the paren- 
chyma by pressure. The latter view seems the more probable, but the former 
opinion is adhered to by many pathologists, who believe the primary change 
is in the parenchyma. 

Symptoms. — This is the type of renal disease which is found in the iron- 
master or stock broker who boasts that he has never had a sick day in his 
life, and who begins to find himself, at forty or fifty, lacking in initiative, 
and who suffers from vertigo or dizziness, which he thinks are due to a club 
dinner or a strong cigar. This is the disease of the hard-working, " high-ner- 
vous-tension " individual who has lived hurriedly, and perhaps quieted him- 
self between periods of great exertion by a drink or two of whiskey, repeated 
it may be many times. Often it develops in those who have not used 
alcohol, but given a man who takes little exercise, some whiskey, and who is 
managing one or more large business interests, and he is the individual who 
is paving the way for or has already developed chronic contracted kidney. 
Very rarely, indeed, the disease develops in early life, but cases have been 
reported by a number of clinicians in children as young as from two to 
seven years. Most of the instances have occurred about puberty. Suther- 
land and Walker have reported 2 cases, aged eight and sixteen months, 
respectively, who had contracted kidney due to congenital syphilis. 

The symptoms of contracted kidney are, in a large proportion of cases, 
absent until the disease progresses so far that grave secondary changes take 
place. Indeed, it not rarely happens that the patient continues in what he 
considers good health until an acute attack of urcemia or cardiac failure sends 
him to the hands of the physician, who may be misled into the diagnosis of 
acute syncope, due to overexertion, by the fact that the heart seems to be 
feeble, and because the urine shows little or no albumin. The number of 
diagnoses that have been wrecked upon the shoal of "no albumin" is a 
multitude, because it is a peculiarity of chronic contracted kidney that 
albumin is often absent for brief periods, or present in such minute amounts 
that it is overlooked. It is only when the heart begins to fail so that some 



CHRONIC BRIGHTS DISEASE 713 

congestion of the kidney develops that the albumin becomes more copious. 
The albuminuria of contracted kidney is, as a rule, as scanty as it is profuse 
in the parenchymatous form. Again, the scanty urine of the parenchymatous 
type is replaced by a profuse flow in the contracted type, and the patient in 
consequence is disturbed in his sleep by having to get up at night to empty 
the bladder. The specific gravity of the urine is low, about 1.005 to 1.012, and 
it is clear and lacks color. If the urea is estimated this ingredient is usually 
much reduced, not only relatively, but actually, so that the patient in many 
cases does not excrete half the normal output per day. Casts may not be 
found and rarely are abundant, and often the centrifuge has to be employed 
to reveal them. Further, these casts are readily overlooked, for they are 
chiefly hyaline and so transparent that if careful focusing and illumination 
are not resorted to they are not seen. In some cases granular casts are 
only periodically demonstrable. 

The circulatory symptoms of contracted kidney are as important in reach- 
ing a diagnosis as the renal signs. The pulse is hard and tense, and so high 
is the blood pressure that it may be almost impossible to occlude the vessel by 
pressing upon it. If the radial artery is rolled under the fingers, it feels like 
a piece of thick rubber tubing, and it is easily recognized as being distinctly 
fibrous when it is palpated carefully. In other words, the blood tension 
is high and the vessel is thick. If the heart is examined, there is found, as 
a very constant symptom, a sharply accentuated aortic second sound at the 
second right costal cartilage, which is due to the high arterial tension. On 
inspection the apex of the heart is found to be displaced downward and out- 
ward because of the cardiac hypertrophy. At the apex a more or less dis- 
tinct systolic murmur is heard in many cases, due, as a rule, to stretching of 
the mitral orifice under the stress of high pressure in the ventricle, resulting 
from great arterial tension. When compensation fails, either because the 
heart becomes exhausted or because of fibroid or other myocardial degen- 
eration, these symptoms may be replaced by weak heart sounds and by a 
feeble pulse. It is only while the heart has vigor that high tension can 
exist 

The respiratory system does not offer much that is characteristic, but com- 
plicating lesions often develop in these parts. One of the most common is 
pneumonia, which finds a fair field for its development in all cases of renal 
disease. Indeed, in every case of acute pneumonia the physician should 
study the renal condition. Often the routine examination of the vessels 
and of the urine in a case of pneumonia is the first evidence that chronic con- 
tracted kidney is present. Perhaps the most common respiratory manifesta- 
tion is difficult breathing resembling asthma, which, coming on in persons 
not previously asthmatic, should always raise the suspicion of renal disease. 
Effusions into the lung or pleural spaces may occur with suddenness and cause 
death. When the toxaemia is well marked, Cheyne-Stokes breathing may 
develop. 

The cerebral symptoms consist in vertiginous attacks, migraine-like seizures, 
and persistent, dull, or throbbing headache. Apoplexy due to the degener- 
ative arterial changes may take place. 

It is a most interesting fact that cedema is as rare in contracted kidney as 



714 



DISEASES OF THE KIDNEYS 



it is common in the large white kidney. When it occurs it is not renal in 
origin, but due to the failure of the heart. The skin in this type of renal dis- 
ease is usually dry, and is chalky in hue. 

Next in importance to the examinations of the urine and the study of the 
peripheral circulation in these cases is the observation of the state of the 
retinal vessels. They very commonly reveal the renal condition. 



Fig. 95 




Retina showing Hirschberg's vessels. The high tension in the arteries can be seen to be narrowing 
the veins by pressure, (de Schweinitz.) 



Different observers give varying percentages of occurrence of retinal lesions. 
Out of 935 cases of renal disease, Groenouw found retinal lesions in 209, 
or 22.4 per cent. The age at which they most frequently are met with is from 
fifty to sixty years, but they have been seen in adolescents. 

Five types of these lesions are recognized by ophthalmologists : (a) typical 
albuminuric retinitis; (b) degenerative albuminuric retinitis; (c) hemorrhagic 
albuminuric retinitis; (d) albuminuric neuroretinitis, and (e) albuminuric 



CHRONIC BRIGHTS DISEASE 



715 



papillitis. In the first form irregularly shaped white dots or spots appear in 
and around the macula, and may take a stellate form. When the condition 
is well developed a zone of whitish-yellow may surround the head of the 
optic nerve. Flame-like hemorrhages may also appear. The condition is at 
first one of hypenemia, then of degeneration, and finally one of atrophy. In 
the second form the white spots are small, and hemorrhages are more limited, 
and the white zone about the nerve head is not well developed. The 
third form, as its name indicates, is chiefly hemorrhagic in type, and the 
hemorrhages are large or profuse, while the other changes are insignificant. 
Only when the hemorrhages are absorbed do these areas become whitish. 
The fifth form shows that the process has been confined to the optic nerve, 
so that a papillitis or choked disk is present, the retina being but little 
involved. 

Fig. 96 




Albuminuric retinitis. Granular kidney. Note hard-edged "asterisk" exudation and the silver-wire 
condition of the arteries, and the punctate and linear hemorrhages. 



In some cases detachment of the retina or hemorrhagic glaucoma develop as 
complications. 

Of even greater importance than the states just described in the early 
diagnosis of renal and cardiovascular disease is the tortuosity of the retinal 
veins and their narrowing by the pressure of the retinal arteries wherever 
these vessels cross the veins — the so-called " Hirschberg's vessels" (Fig. 95). 

Because of the fact that the symptoms of chronic contracted kidney are 
so often insidious in their development, the ophthalmologist is often the 
first to recognize the existence of the disease, because a man who considers 
himself in perfect health asks for glasses for failing vision or seeks relief for 



716 DISEASES OF THE KIDNEYS 

blindness in one eye. Not rarely these patients have repeated attacks of rup- 
ture of subconjunctival vessels, as well as hemorrhages into the retina. 

Flexner states that the terminal dysentery of Bright' s disease is often due 
to the Bacillus dy sentence. 

Prognosis. — Here, again, chronic contracted kidney presents a widely differ- 
ent aspect from that of the parenchymatous form, for, while in the latter 
lesion death, as a rule, occurs inside of eighteen months at best, these cases 
often live for many years, if the process is not already far advanced when the 
case is first seen. The points governing prognosis are the state of the heart 
and the vessels, the ability of the kidneys to approximate the normal daily 
task, and the life which the patient can or will lead. It is manifest, from 
what has been said as to its pathology, that the affection is incurable, but 
patients often live as long as ten or fifteen years after undoubted signs of the 
malady are present. The development of signs of uraemia, of feeble heart, 
or of pulmonary congestion, oedema, or pneumonia is, of course, alarming. 

By far the most important factor in determining the probable duration of 
life is the state of the retinal vessels already named. De Schweinitz has 
studied this matter most carefully from the standpoint of the ophthalmologist, 
and we have followed a number of cases together. 

These facts are well emphasized by the following figures, which illus- 
trate the duration of life in chronic interstitial nephritis after the occur- 
rence of retinal changes: Belt collected 419 cases, of which 72 per cent, 
died within one year and 90 per cent, within two years. The cases 
reported from Haab's practice by Possauer showed that none of the men 
applying to the clinic for treatment lived more than two years; of the 
women, 68 per cent, died within the same period of time. Of private 
patients who could live comfortably, only 59 per cent, of the men and 53 per 
cent, of the women had died at the end of two years. Gruening collected 
100 cases, none of which survived more than two years after retinal changes 
began, and Bull found that 69 out of 103 cases died within two years. Of 
the remaining 34, 17 died after a longer period, and 17 were alive at the time 
his paper was published. Harlan analyzed 40 cases with the following 
results: 33 ended fatally at various periods, averaging four months; 3 lived 
a year after the discovery of retinal changes; 3 recovered, and 1 regained his 
eyesight, although the urine was albuminous at the end of two years. Miley 
traced 45 cases, and found the average duration of life to be less than four 
months from the time eye changes were first observed. One of his patients 
lived eighteen months and two fourteen months, but all the others died within 
a year. Webster mentions the case of a clergyman suffering from chronic 
interstitial nephritis, in whom retinal changes had been recognized ten to 
fifteen years before, and " who is still living," and Wert had a woman under 
observation in whom retinal changes had been noticed more than four years 
before he reported the case. Her general condition was much the same as 
when she came under his charge. I have under my care at this time a man 
who has been under observation four years, during which retinal hemor- 
rhages have repeatedly occurred, and whose arterial tension is astonishingly 
high. He is now taking \ a grain of nitroglycerin a day with the iodides, 
to lower his blood pressure and relieve his heart. Such a result is most rare. 



CHRONIC BRIGHT' S DISEASE 717 

Most of these cases with very high tension and retinal changes die from 
apoplexy or an acute myocardial failure soon after retinal changes develop, 
the patient often dropping dead without warning symptoms. These extreme 
instances are interesting, but they are rare in the history of the malady. 

Treatment. — There are few diseases of an incurable character in which the 
patient can be so greatly benefited by treatment. 

The question of diet in cases of chronic contracted kidney is to be decided 
along pretty much the same lines as those which have been drawn in the article 
upon the treatment of chronic parenchymatous nephritis. W. Hale White 
has expressed the belief, in which we coincide, that, as a rule, this disease 
is treated too zealously, and that in the desire to spare the kidneys the patient is 
starved, with the result that the only means by which the degenerative process 
can be retarded, namely, the maintenance of general good health, is impaired. 

As we do not know of any articles of ordinary diet which can be con- 
sidered really harmful in granular kidney, it is best to give the patient 
ordinary plain digestible foods containing the normal proportions of pro- 
teids, fats, carbohydrates, and salts, just as it is necessary to give a person 
in health a similar mixed diet. It need hardly be stated that highly seasoned 
foods, or foods which are difficult of digestion, should be interdicted. Again, 
we are glad to note that Dr. White is in accord with us in believing that the 
limitation of these patients to a diet of chicken and fish without any red meat 
is entirely unnecessary. Not only does such a limitation do no good, but it 
is often harmful in the sense that it makes the patient consider himself 
seriously ill, and also diminishes his appetite. Patients with interstitial 
nephritis, however, should especially eschew all forms of alcohol, since it is 
imperfectly oxidized in these cases, and tends to increase arterial tension. 

It is of vital importance in chronic contracted kidney that arterial tension 
should be kept at a point as near the normal level as possible, since by this 
means danger of rupture of a cerebral vessel is diminished and the work of 
the heart is decreased. A sufficient quantity of nitroglycerin to accomplish 
this result should always be administered. It is not a question of the size of 
the dose, but of the quantity required. It is also to be remembered that 
patients rapidly become accustomed to nitroglycerin, so that ascending doses 
are nearly always necessary. Very large doses may be taken by many of 
these patients without any disagreeable symptoms of the full action of the 
drug. Beginning with yj-g- grain three times a day, I have seen as much 
as J grain a day taken with no other than excellent results. 

Another valuable drug in chronic contracted kidney, both from the stand- 
point of arterial tension and of the fibroid changes in the arteries, is the 
iodide of potassium. There can be no doubt that this salt diminishes arterial 
tension, and if any remedy exercises an influence for good in arresting the 
pathological changes in the kidneys and in the bloodvessels, that remedy is 
certainly one of the iodides. Usually doses of from 10 to 20 grains, three or 
four times a day, are quite sufficient. A useful substitute for the potassium 
salt is the sodium or strontium salts or the syrup of hydriodic acid given in 
ascending doses, beginning with 30 drops three times a day. It goes without 
saying that the iodides have not as powerful an influence in decreasing 
arterial tension as have the nitrites. 



718 DISEASES OF THE KIDNEYS 

Digitalis is rarely needed in chronic interstitial nephritis, as the cardiac 
hypertrophy is usually adequate, and digitalis tends to raise tension in the 
vessels which is undesirable, but in some cases there comes a time when 
the blood pressure falls largely because the advancing myocardial degenera- 
tion and cardiac fatigue prevent the heart from pumping the blood with 
normal energy. In such cases digitalis and strophanthus do good, and 
nitroglycerin may do harm. (See Arteriosclerosis.) 

Urcemia is to be treated by the use of the hot pack, if the patient's heart 
is strong; by the employment of hypodermoclysis, and if the patient is fairly 
full-blooded by venesection as well. (See Ursemia.) Cups may be placed 
over the kidneys, if there is any condition of renal congestion, and three or 
four cups should be placed over the base of each lung, if any signs of pul- 
monary oedema develop. When evidences of pulmonary difficulty arise, full 
hypodermic doses of strychnine are advisable, and if any tendency to urinary 
suppression occurs, J to \ of a grain of cocaine may be given hypodermically 
every four to six hours for several doses. 

Many practitioners have thought it wise to employ full doses of morphine 
hypodermically in the treatment of ursemic convulsions. I have recently 
made a collected investigation in regard to this matter, and have obtained 
the opinion of physicians of experience in both this country and in England. 
This opinion is almost universally adverse to this use of morphine. 

The convulsions should be controlled by nitrite of amyl and by chloroform 
given by inhalation. (See Ursemia.) 

The question of renal decapsulation has already been discussed under 
Chronic Parenchymatous Nephritis. 

If the progress of the disease is slow, it is advisable to send the patient to 
some warm climate during the winter months, if his home is in a northern 
latitude. The object is to avoid rapid changes in temperature in the atmos- 
phere and consequent chilling of the surface, with secondary congestion of 
the kidneys and decrease in the activity of the skin. 

The best climate is to be found in the neighborhood of San Diego, Cali- 
fornia, or in Egypt. 



AMYLOID DISEASE OF THE KIDNEYS. 

Definition. — Amyloid disease of the kidneys is part of a general process 
affecting many organs. The renal manifestation is characterized by the 
deposit of lardacein in the subintimal stratum of the bloodvessels, in the 
glomeruli, and, to a lesser degree, in the connective tissue of the tubules. 

Etiology. — Amyloid disease of the kidney is usually the result of a pro- 
longed suppurative process, such as hip-joint disease, chronic pulmonary 
tuberculosis with cavity, or any cause whereby the system is simultaneously 
sapped by suppuration and poisoned by the absorption of toxic substances. 
It may also be a sequence of one of the prolonged fevers or occur as an 
associated change with chronic diffuse nephritis of the parenchymatous type. 
Syphilis is a common cause, and malaria may be the only demonstrable 
antecedent. 



AMYLOID DISEASE OF THE KIDNEYS 719 

Pathology. — The kidneys are usually enlarged, and when incised the cut 
surface is shining or polished in appearance. When the condition is com- 
bined with interstitial nephritis these organs may be small. The surface of 
the organ is paler than normal, particularly in the cortex, but the pyramids 
are deep red in hue, and the glomeruli are readily seen. 

If an aqueous solution of iodine is painted over the cut surface of such a 
kidney, the areas most affected by the amyloid change stain a deep mahogany 
brown, and if to these areas is applied a dilute aqueous solution of sulphuric 
acid, the brown hue is changed to blue. 

Microscopically the kidney structure when examined reveals the fact that 
the capillary vessels forming the tufts in the capsules are parts of the paren- 
chyma most affected, the tuft being transformed into a waxy mass. The 
disease process also involves the afferent and efferent bloodvessels of the 
tuft and the straight or direct vessels of the kidney. In marked cases the 
connective tissue of the tubules is infiltrated, the interstitial tissue increased, 
and the epithelial cells may be granular or fatty, as in parenchymatous neph- 
ritis. In some instances all these types occur together. 

Symptoms. — There are no symptoms which, taken by themselves, may be 
considered indicative of amyloid disease of the kidneys. It is only when cer- 
tain urinary signs develop in a case which is the subject of those maladies 
which predispose to amyloid change that we can say that a diagnosis is 
assured. The patient is usually pallid, may be well covered by unhealthy 
waxy fat, and the heart is not rarely somewhat enlarged, although no less 
an authority than Dickinson contradicts this view. The urine is passed more 
freely than is normal. It is clear and has a low specific gravity, about 1005 
to 1010. The quantity of albumin which it contains varies, but it is usually 
present in considerable quantity. There is a distinct increase in the quantity 
of serum globulin in the urine. Under the microscope the tube casts are 
found to be hyaline, fatty, or waxy. Occasionally the amyloid reaction 
already named may be demonstrated in the urine. The degree of oedema and 
the state of the bloodvessels and heart depend more upon the presence of 
associated nephritis than upon the amyloid change itself. If nephritis is 
well developed, anasarca and high arterial tension may be present as an 
associated state. 

Prognosis. — The prognosis depends upon the gravity of the causative 
process and the degree to which the secondary change in the kidneys has 
progressed. Then, too, it must be remembered that amyloid disease is not a 
condition limited to the kidneys, but affects such organs as the liver, spleen, 
and even the heart, and, therefore, the patient is peculiarly handicapped in 
his struggle for health. If the casts are fatty or waxy, and are present in 
large numbers, if the albuminuria is copious, and if ansemia is marked, 
the outlook is bad. Indeed, in every case it is anything but good, and 
the longer the suppurative process continues the worse the outlook be- 
comes. 

Treatment. — This consists in the same measures as have been recommended 
for chronic parenchymatous nephritis, such as iron, arsenic, cod-liver oil, 
and fresh air and sunlight to combat the underlying cause. If possible, the 
suppurative process, if such is the cause, should be removed. 



720 DISEASES OF THE KIDNEYS 



URiEMIA. 



Definition. — Uraemia is a condition in which as the result of faulty activity 
of the kidneys a patient develops a series of symptoms of which the most 
notable are stupor, coma, convulsions, or paralysis, or in other instances 
gastrointestinal disorders. 

Etiology and Pathology. — The causes of uraemia are not clearly under- 
stood. It is well known, and universally recognized, that the condition is 
due to perverted renal activity, both as to the elimination of the ordinary 
products of metabolism and the effects of renal disease upon the tissues of 
the body, but beyond this the actual cause is as yet undetermined. 

At one time, under the leadership of Traube, the idea prevailed that the 
symptoms of uraemia were dependent upon changes in the circulation in the 
brain produced by the constriction of its arteries by the vascular changes 
associated with nephritis or by cerebral oedema. In other words, that 
cerebral anaemia due to arterial constriction was the cause of the symptoms. 
This view has been cast aside because it has been shown that ligature of 
the carotid arteries does not cause uraemic symptoms, because it has been 
proved that the high arterial tension of renal disease results in dilatation 
of the cerebral vessels, since they are poorly endowed with muscular fibres, 
and finally because it is impossible to cause active contraction of the cerebral 
vessels by. any drug or measure used for raising arterial tension. 

The theory, that uraemia is due to the retention of the ordinary effete 
materials of the body owing to renal disease, also cannot be accepted as a 
complete explanation of the condition, because it has been found that liga- 
tion of the renal arteries in animals and ligation of the ureters fail to produce 
uraemia, although the function of the kidney is by these means completely 
arrested. Again, suppression of urinary secretion by the presence of stone 
in both kidneys, and even by necrosis of the cortex of both kidneys in man, 
does not cause typical uraemia. Further than this the injection of urea 
and even of healthy urine into the blood does not cause any symptoms 
of true uraemia. Again, in certain cases of renal disease, as in chronic 
contracted kidney of the aged, when the renal excretion is seriously impaired, 
uraemia is rare. All forms of deficient renal activity do not, therefore, 
cause uraemia. 

A third theory is that as a result of the renal disease peculiar poisons are 
made in the body which when they accumulate cause uraemia, or that the 
condition of the system in renal disease permits certain micro-organisms to 
grow and produce a toxic substance. 

A fourth opinion is that the kidney secretes when in health an "internal 
secretion " which governs metabolism and so prevents the formation of cer- 
tain poisons. The last theory falls to the ground because ligation of the 
renal vessels does not result in uraemia, as it would do if these symptoms 
were caused by the lack of some internal secretion. 

We are left, therefore, with the fact that uraemia is due to the presence 
in the body of peculiar poisons arising in Bright's disease, either as the 
result of the growth of micro-organisms or perverted metabolism, and 



URAEMIA 721 

with the knowledge that the kidneys are unable by reason of disease 
to be active in the elimination of any poisons. It would seem probable 
that this combination of extra poisons and deficient renal activity are the 
two factors necessary to the development of uraemia. This is further sup- 
ported by the fact that if the labor of the kidneys is increased by gastro- 
intestinal fermentation or putrefaction, an attack of uraemia is very prone 
to occur. Finally, there is additional proof of the development of extra 
poisons in the body in renal disease. This is found in the marked loss of 
weight in patients suffering from nephritis, the wasting showing that metab- 
olism is seriously impaired and that tissue breakdown is marked. Mani- 
fest loss of weight may not be present because of dropsy, but, if this is removed 
by purging, the wasting is manifest. The toxicity of the urine is increased. 

Symptoms. — Uraemia occurs in several forms. The most common mani- 
festation of uraemia is that in which the patient passes into coma, which 
may be preceded by delirium and drowsiness. In certain cases there is 
associated with the development of the comatose state twitchings and con- 
tractions of widely separated muscles, and particularly the extensors and 
flexors of the forearms. 

The most startling, but by no means the most frequent, form is the 
convulsive type. In this condition the patient, with or without any pre- 
liminary indications of nervous disturbance, is seized with a more or less 
severe epileptoid attack, which usually involves the muscles of the face and 
hands, and then spreads rapidly to the whole body. No sooner is one seizure 
over than another comes on, and with the repetition of the attacks, or it 
may be with the development of the first fit, the patient becomes uncon- 
scious, or has very distinct mental impairment. The body temperature 
usually falls unless the convulsions are so severe as to temporarily cause 
a slight rise. The knee-jerks are usually markedly exaggerated and the 
pupils are contracted. Because these symptoms are so extraordinary, 
the idea has gained ground that convulsive seizures in uraemia are commonly 
met with. This is incorrect, as they are not common except in that pecu- 
liar form of eclamptic convulsion due to toxaemia which is encountered 
in pregnancy. 

A third form is that in which there is marked respiratory disorder of a 
dyspnoeic type. The patient finds it exceedingly difficult to breathe, and 
feels as if suffocated. Not only is the respiration wheezing, as it is in asthma, 
but it is peculiar in that it is accompanied by a hissing sound, the patient 
very frequently ending each expiration with a puffing hiss. Associated 
with these symptoms there may be some duskiness of the skin, but cyanosis 
is not marked. The patient's mind is usually clear, and he not infrequently 
complains of his great difficulty in getting sufficient air. As this condition 
proceeds, the respirations may become "Cheyne-Stokes" in type. Although 
it is generally held that the development of Cheyne-Stokes respirations 
under any circumstances is indicative of a fatal result, it not infrequently 
happens that patients with this symptom arising during the course of uraemia 
recover from that particular attack. Sometimes the Cheyne-Stokes breath- 
ing occurs only during sleep, and it may be the only manifestation of 
uraemia, the mind remaining clear. 
46 



722 DISEASES OF THE KIDNEYS 

There is still a fourth form in which the patient develops mania or acute 
insanity. He is restless, very excited, and may be extremely violent. As a 
rule, after these symptoms have lasted for a short time, the mental excitation 
is followed by gradually increasing drowsiness which finally passes into 
coma. 

In the so-called paralytic form of uraemia, either hemiplegia or mono- 
plegia may come on suddenly, as does hemiplegia in cases of cerebral hemor- 
rhage. But the paralysis is not due to rupture of a bloodvessel, to a forma- 
tion of a thrombus, or the plugging of a vessel by an embolus. So far as is 
known, it depends upon intoxication of the nervous centres controlling the 
parts involved in the paralysis. It is of course possible for cerebral apoplexy 
to complicate uraemia, and for this reason it may be difficult to immediately 
make a differential diagnosis between the hemiplegia of uraemia and the 
complicating hemiplegia of cerebral rupture. 

There is still another form of uraemia which manifests itself in persistent 
insomnia with muscular irritability or cramps and hiccoughs. 

In some cases of uraemia violent gastrointestinal disorders suddenly 
assert themselves, vomiting may be persistent and severe, and nausea intense. 
Not rarely profuse serous purging comes on, which may be an effort on 
the part of the body at elimination. 

In some cases uremic amaurosis develops. This consists in sudden, 
bilateral, and complete blindness. Rarely one eye suffers before the other, 
and in some cases the perception of light may be preserved, although ordinary 
vision is destroyed. In the greater number of these cases the ophthalmo- 
scope reveals no changes in the retina, although it may be found to be cedem- 
atous and there may be an appearance of the optic nerve like that of choked 
disk. This condition develops more commonly in those cases of acute 
nephritis associated with the eruptive fevers, as scarlet fever, than in ordinary 
chronic nephritis. The amaurosis lasts for a few hours to a day or even 
longer than this, and vision often returns as suddenly as it was lost. The 
prognosis is favorable as to vision. 

All of these forms of uraemia differ very materially from that type which 
has been called "latent uraemia" by the late Sir William Roberts, and of 
which mention may be found in connection with the article upon Nephro- 
lithiasis. In these patients life is maintained for periods varying from one 
to two weeks in the presence of total urinary suppression. They remain 
conscious almost to the moment of death, and the uraemic symptoms just 
described in their various forms are never present. There may be some 
headache and nausea and weakness and drowsiness. The temperature is 
subnormal and the pupils are contracted. In some instances vomiting 
is a prominent symptom in this type of uraemia. It is unfortunate that the 
term " latent uraemia" should be applied to this condition, as the condition 
is really not one of latency nor of uraemia as that term is generally under- 
stood. 

A very important symptom of uraemia is the peculiar odor about the 
patient, which is quite characteristic and which may be due in part to urea 
which is being eliminated by the skin or to the presence of some toxic sub- 
stance as yet not isolated. 



URAEMIA 723 

Diagnosis. — The presence of albuminuria with casts of the uriniferous 
tubules, of somewhat thickened bloodvessels, and of an accentuated aortic 
second sound in association with the development of any of the symptoms 
which have just been described, makes the diagnosis of uraemia practically 
certain. If the patient is bled for the purpose of relieving symptoms of 
venous engorgement, it is wise, if opportunity offers, to make a determina- 
tion of the urea in the blood if the physician is sufficiently skilful to perform 
the necessary manipulations. The most difficult differentiation lies between 
ursemic monoplegia and hemiplegia due to rupture of a bloodvessel, or to an 
embolus, or thrombus. In some cases such a differentiation is impossible 
because these vascular lesions may be present as a complication of the 
uraemic state. The presence of the urinary changes just described and 
of the other signs and symptoms mentioned in the article upon Bright's 
Disease will serve to aid in the differentiation to some extent. 

At times, if the uraemic poisoning is not of such a character as to produce 
convulsions, but merely semi-consciousness, the patient may live in a state 
of stupefaction for several days or weeks, and because of the mental condi- 
tion, of the feeble pulse, of the slight fever, of the coated tongue, be con- 
sidered a case of typhoid fever or general tuberculosis. 

Opium poisoning is to be separated from uraemia by the presence of an 
odor of laudanum on the breath if laudanum has been used instead of 
morphine, by the fact that the pupils are contracted to a pinpoint, and by 
the examination of the urine. From alcoholism uraemia is separated by the 
examination of the urine, by the odor of alcohol in the breath, and b} T the 
history of the patient. But it must not be forgotten that many alcoholics 
have chronic renal disease and that the ingestion of considerable quantities 
of alcohol may precipitate an attack of uraemia, and so an alcoholic history 
may be present which will mislead the physician. 

As a rule, sudden fulminating uraemic symptoms develop in patients with 
chronic interstitial nephritis, whereas the types of uraemia with headache, 
vertigo, and other warnings of toxaemia are seen most frequently in the 
parenchymatous form. 

In hot weather, when men are exposed to great heat in rolling mills and 
furnaces, the distinction between heatstroke and uraemia may be difficult, 
since in both conditions violent convulsions with cyanosis may be present. 
In heatstroke, however, the temperature is usually much higher than in 
uraemia and the cyanosis is usually more intense. It is, however, quite 
possible for heatstroke to complicate nephritis. 

Prognosis. — The prognosis is always grave, but not necessarily fatal 
by any means. A professor in one of the medical schools of Philadel- 
phia had a moderate uraemic seizure after nearly every lecture for a 
whole winter course of lectures before a final fatal seizure came on. In 
uraemia due to acute nephritis the prognosis is good if the patient can but 
survive the attacks long enough for the kidneys to regain their function. 
In the cases due to chronic renal disease the outlook depends to some extent 
upon the general state of the patient and particularly the condition of the 
lungs. If any tendency to pulmonary oedema or congestion is present, the 
outlook is much more serious. 



724 DISEASES OF THE KIDNEYS 

Treatment. — The treatment of uraemia depends to some extent upon the 
variety of nephritis which has produced it and the peculiarities of the indi- 
vidual who is suffering from the attack. When ursemia comes on as a com- 
plication of acute nephritis, such as that complicating scarlet fever, the 
patient should have hot compresses placed across the small of the back, 
and, if diarrhoea is not already present, one of the saline purgatives, such 
as the citrate of magnesium or the sulphate of magnesium, should be given 
in sufficiently concentrated form to produce several watery movements. 
After this has been accomplished 5 to 10 grains of the citrate of potassium 
dissolved in Poland water should be given three or four times a day. 

If the symptoms of ursemia persist, it will be necessary to place the patient 
in a warm pack. This may be given in one of two forms, the choice of the 
form depending upon the condition of the patient's skin and the presence 
of an eruption resulting from the disease. The choice also depends to some 
extent upon the temperature of the patient. If the rash has to some extent 
disappeared, the skin is dry and hot, and the temperature high, it is well to 
wrap the patient in a sheet wrung out of water at 70° or 80°, and then to 
immediately surround him with a dry blanket. The primary effect of this 
cold sheet is to aid in the dissipation of heat over the body, but it very rapidly 
becomes warmed by the heat of the body so that the patient at first is under 
the influence of cold, and very shortly afterward is surrounded by a warm 
pack. The primary cold drives the blood from the surface, and the secondary 
heating fills the peripheral capillaries so that the temperature is lowered 
by an improved peripheral circulation, and the skin is thoroughly supplied 
with blood so that it has a better opportunity to eliminate poisons. If no 
fever is present, and the rash has not faded, or if for any reason it is con- 
sidered inadvisable to use cold primarily, the hot pack may be given, the 
patient being quickly wrapped up in a blanket which has been wrung out 
of water as hot as the skin can bear. Outside of this is placed a dry blanket 
and on the patient's head is placed an ice-bag to prevent cerebral congestion. 
Every few moments the patient is given a few sips of cold water to drive 
the blood from the internal portions of the body to the skin, the object 
being to flush the peripheral circulation, and to cause a sweat which will 
relieve internal congestion and eliminate impurities from the body. If the 
arterial tension is high, nitroglycerin may be given in the dose of -g-J-g- of a 
grain to a child, or y^- to a man, every three or four hours; or, in its place 
for a child J drachm to a drachm of the sweet spirit of nitre may be given. 

In the uraemia of chronic parenchymatous nephritis a plan of treatment 
identical with that which has just been described for that of acute nephritis 
may be carried out. As a rule, the patient is already too ansemic to permit 
of bleeding, and his tissues are so oedematous that hypodermoclysis is im- 
possible. 

In the uraemia of chronic contracted kidney with high arterial tension, 
the measures already indicated for the uraemia of acute nephritis may be 
instituted, the nitroglycerin being particularly useful, and being given 
hypodermically in order that it may act promptly. It also has a beneficial 
effect in that it relaxes the spasm of the renal bloodvessels and so produces 
diuresis. If there is much engorgement of the venous system, venesection is 



PYELONEPHRITIS AND PYELITIS 725 

exceedingly useful, particularly if it is accompanied by free hypodermoclysis, 
or, in urgent cases, by an intravenous injection of normal saline solution. 
Sometimes in these cases if the heart seems strong, small doses of pilocar- 
pine, £ of a grain, may be given hypodermically to aid in producing the 
sweat which is caused by the hot pack, and, with the object of preventing 
cardiac depression, it is usually wise to combine with it ^q of a grain of 
strychnine. The lungs and the heart should be carefully watched, and if 
any signs of pulmonary oedema or cardiac failure develop, strychnine should 
be given freely, and 1 or 2 drachms of Hoffmann's anodyne should be admin- 
istered as a rapidly acting diffusible stimulant. In some cases in which 
there is a tendency to suppression of urine, not only nitroglycerin but cocaine 
in the dose of J to J of a grain may be given hypodermically twice or thrice 
a day. Should convulsions occur, they should be controlled by chloroform, 
if they are exceedingly severe, and by the use of a drachm of bromide of 
sodium and 20 grains of chloral by the rectum. Morphine, which has been 
largely used to control ursemic convulsions, is not regarded with favor by 
most practitioners at the present time. If the arterial tension is exceedingly 
high, full doses (5 to 10 minims) of the tincture of veratrum viride, repeated 
every half-hour until some evidences of circulatory depression are produced, 
may be advantageous. 



PYELONEPHRITIS AND PYELITIS. 

Definition. — Pyelonephritis signifies an inflammatory process involving 
both the pelvis of the kidney and the kidney texture itself. The term is 
usually applied to that form in which the condition is suppurative. Some- 
times it is called suppurative pyelonephritis. Pyelitis is an inflammatory 
state of the pelvis of the kidney without involvement of the kidney proper. 
As synonyms to pyelonephritis we may use the terms pyonephritis, pyo- 
nephrosis, and caseative nephritis. 

Etiology. — These conditions are nearly always the result of infection from 
below; that is, they are secondary to infection of the lower urinary tract, 
viz., the bladder or urethra. Very rarely infection of the kidney may take 
place through the blood, but this is only when the vital resistance of all the 
tissues is greatly impaired, or when the infection is very virulent, for the 
healthy kidney quite readily eliminates micro-organisms brought to it by 
the blood stream. It is possible, too, in cases of floating kidney, in which 
the ureter becomes twisted or obstructed so that the vital resistance of the 
pelvis is impaired, that infection through the blood may ensue. Although 
stones in the kidney are now attributed to bacteria, it is conceivable that a 
renal calculus by damaging the pelvic wall may prepare the way for infec- 
tion, so acting as a direct cause of pyelitis. Infected emboli may also produce 
this state. 

The micro-organisms which most frequently cause pyelitis and pyelo- 
nephritis are the Bacillus coli communis, the Streptococcus pyogenes, the 
Staphylococcus pyogenes aureus, the tubercle bacillus, the typhoid bacillus, 
the gonococcus, and the Bacillus proteus vulgaris. Brown has shown that 



726 



DISEASES OF THE KIDNEYS 



the Bacillus coli communis is the most frequent cause in women, probably 
because of the near relationship of the anus and the meatus urinarius. Brown 
also asserts that, whereas some devitalizing cause is usually necessary to 
permit infection, a constantly ammoniacal urine is sufficient cause in many 
cases. 

Pathology and Morbid Anatomy. — Pyelonephritis may be catarrhal, pseudo- 
membranous, gangrenous, or suppurative. The first two forms usually 



Fig. 97 




Brewis' case of pyonephrotic kidney. Girth, forty-eight inches; weight, forty-five pounds. 

depend upon, and are overshadowed by, associated diseases such as typhoid 
fever, and rapidly assume the suppurative type. In pyelonephritis the mucous 
membrane lining the pelvis of the kidney is thickened and coated with pus. 
A fibrinous exudate may also be present. The kidney structure may be 
involved in two ways : either small abscesses are scattered through the paren- 
chyma of the kidney or in long white streaks which project themselves 
along the tubules. The renal tissue in and near these areas is, of course, 



PYELONEPHRITIS AND PYELITIS 727 

necrotic. If the suppurative process proceeds, the calyces of the kidney 
become enlarged, the renal tissues waste and suppurate, and the kidney 
structure is largely replaced by a large single or multiple abscess. Finally, 
if the patient survives so long, the liquid drains off through the ureter, and 
the pus becomes inspissated so that a cheesy mass remains which may 
become infiltrated with lime-salts. This process may extend to the tissues 
surrounding the kidney causing paranephritis. When one kidney is involved 
the cause is nearly always primary disease in the bladder, and to this type 
the term " surgical kidney " is given. 

Symptoms. — The symptoms of pyelitis and pyelonephritis may be in 
many cases so masked by the conditions which produce this disorder 
in the renal pelvis that they are overlooked. Thus the urinary picture 
is commonly obscured by an associated cystitis, which may either pre- 
cede or follow the renal lesion. The most definite symptoms are pain 
and tenderness in the back over the kidneys, w T ith or without frequent 
urination. The pain is increased by jarring the body or by coughing, and 
it is often felt in the testicle or inside of the thigh on the affected side. 
The quantity of urine passed is usually scanty in acute pyelitis but profuse 
in the chronic form. With the development of suppuration septic fever 
develops, vomiting may come on, and occasionally a profuse septic sweat 
follows a chill and fever. The urine is acid and contains pus, blood cells, 
and degenerated epithelium. At times the urine may appear perfectly nor- 
mal, but soon returns to its earlier state. This variation is due to the ureter 
becoming blocked by a plug of putty-like pus, so that for several hours 
only one kidney, and that the healthy one, drains into the bladder. Such 
a variation in the urine therefore proves the difficulty to be unilateral. 
This plugging of a ureter may give rise to attacks of pain, somewhat like 
those due to a renal calculus becoming engaged in the ureter, but the pain 
is rarely so severe. 

Diagnosis. — Pyelonephritis is sometimes taken for malarial fever, as are 
other septic processes, because of the chills, fevers, and sweats. An exami- 
nation of the patient and of his blood and urine readily excludes malaria and 
reveals the renal disease. 

In other cases the dry tongue, loss of weight, diarrhoea, and abdominal 
tympany may mislead one into a diagnosis of typhoid fever. 

From suppurative cystitis the condition is to be differentiated by the 
fact that the pain is felt chiefly in the renal region, by the greater quan- 
tity of pus in the latter state, by the greater alkalinity of the urine in 
vesical disease, and finally by the use of the cystoscope and the ureteral 
catheter. 

Usually there is more albumin in the urine in pyelonephritis than in 
cystitis, and more discomfort in the suprapubic area in the latter condition 
than in the former. 

From perinephric abscess pyelonephritis is separated by the greater ten- 
derness over the kidney in the former condition, by the fact that this area 
is not bulging. Most important of all is the absence of pus in the urine 
in the first condition and its presence in the second. In some cases, how- 
ever, of pyelonephritis very distinct bulging over the kidney is manifested. 



728 DISEASES OF THE KIDNEYS 

A valuable sign in this state is that the swelling occasionally disappears or 
diminishes as the pus and urine escapes through the ureter, when an obstruc- 
tion is removed. A bulging or swelling in the renal area may also be due 
to hydronephrosis, but there is usually no fever in this state. 

The possibility of a painful swelling in the region of the kidney being due 
to an aneurysm must always be excluded before operation is resorted to. 

Prognosis. — Prognosis depends largely upon the cause of the malady and 
the state of the kidney. If the condition is one of simple pyelitis, occurring 
during the course of one of the infectious diseases, the outlook is not neces- 
sarily bad. (See Typhoid Fever.) If the suppuration is marked the prognosis 
is not good, and if the kidney structure is involved to the extent of pyo- 
nephrosis the prognosis is bad, and death may come from the exhaustion of 
prolonged septic fever, from the extension of suppuration to other parts, or 
because of amyloid degeneration in other organs. 

Treatment. — The treatment of pyelitis in its milder phases consists in the 
use of mild diuretics if the urine is concentrated, of counterirritation by 
cups or heat over the loins, and rest in bed. No highly seasoned foods are 
permissible. The reaction of the urine must be determined. If the urine is 
acid, alkaline diuretics and salol are useful. If it is alkaline, then we may 
give 5 grains of uritone or urotropin three or four times a day in a glass of 
sparkling water. The diet should be hearty and easily digested. Bitter 
tonics and iron are useful, but quinine is contraindicated because of the 
state of the bladder, upon which it acts as an irritant. When hectic fever 
is developed and remains persistent the patient should be subjected to 
nephrotomy or nephrectomy before he becomes exhausted by sepsis. Opium 
or morphine may be needed to control the pain. Recently several ob- 
servers have reported cases in which benefit was derived from lavage of 
the renal pelves, by means of ureteral catheterization. 



HYDRONEPHROSIS. 

Definition. — Hydronephrosis is a condition in which because of obstruc- 
tion in the ureter there takes place in the pelvis of the kidney an accumulation 
of fluid which is not purulent. This fluid as it increases in quantity stretches 
and dilates the pelvis and the calyces until very large amounts of fluids are 
retained and a good-sized cyst is formed. 

Etiology and Pathology. — Hydronephrosis may be acquired or congenital, 
constant or intermittent. It arises from permanent or intermittent closure 
of the ureter so that the urine cannot escape into the bladder. When con- 
genital the ureter may never have been patulous or it may have a stricture 
or be abnormally inserted into the bladder wall. When acquired it arises 
from stricture of the ureter, or from plugging by a clot or a fragment of cal- 
culus. It may result from twisting of the ureter in floating kidney, but cal- 
culus is the most common cause of unilateral hydronephrosis. When either 
of these causes are responsible for the retention of fluid, the hydronephrosis 
may be intermittent, because, when the twist is undone, or when the calculus 
slips, the fluid can escape. The patient may remain free from trouble for 



HYDRONEPHROSIS 729 

years unless the obstruction forms again. The obstruction may be at the 
bladder, as in tumor of that organ, or consist in a paracystitis. In the female 
pelvic adhesions, neoplasms, and cysts may press upon the ureter and impede 
the urinary flow. 

The secondary effects of this condition upon the kidney are disastrous if 
it is long continued and severe. The pressure acting upon the renal tissues 
causes atrophy and wasting so that finally the kidney structure largely 
disappears and in its place only a large collection of fluid, surrounded 
by fibrous tissue and remnants of renal tissue, remain. So large may 
the tumor grow that it projects downward into the abdomen, and it has 
even been mistaken for ascites. The other kidney may be similarly affected, 
but often it undergoes hypertrophy to compensate for the inability of its mate. 

Symptoms. — The presence of symptoms depends largely upon the rapidity 
of the accumulation of fluid and the size of the renal pelvis. If it develops 
slowly and if a previous attack has enlarged the pelvic capacity, much fluid 
may be present without the patient presenting any symptoms. If, on the 
other hand, the fluid rapidly accumulates, pain may be very severe. When 
stricture is the cause the accumulation is usually slow, but when a twist or 
a calculus closes the ureter it is speedy and painful. In the slow cases sharp 
pain may be replaced by a sense of weight and dragging. A very charac- 
teristic sign in some cases, when the obstruction is suddenly removed, is a 
profuse flow of urine which fills the bladder rapidly, although it may have 
been emptied but a short time before. The tumor which may have been 
present in such a case disappears with the flow. 

Diagnosis. — Palpation of the abdomen reveals in some cases a mass pro- 
jecting from beneath the floating ribs, in which fluctuation maybe detected. 
When the history of the causes and symptoms is as clear as has just been 
detailed the diagnosis is not difficult, but the history is frequently not clear. 
In children such a mass has been mistaken for an enlarged spleen and for 
a sarcoma of the kidney or of the retroperitoneal glands. (See Tumors of 
the Kidney.) In other cases, if the kidney is floating and hydronephrotic, 
the tumor may be taken for an ovarian cyst, In still other instances the 
tumor may so fill the abdomen as to lead to a diagnosis of ascites. Thus, 
Sutton has recorded a case in which the cyst held no less than thirty gallons ! 
Aspiration of the fluid may reveal that it contains some urea or that it par- 
takes of a urinous odor. 

Prognosis. — The prognosis depends entirely upon the cause of the diffi- 
culty and the state of the other kidney. When the closure is congenital 
and complete, death ensues in a few days. When the closure is due to a 
twist of the ureter or to a calculus, much depends upon whether the flow is 
entirely stopped and how long it is arrested. A single attack followed by 
sudden relief may never be repeated. When the disease is bilateral the 
gradual involvement of the kidneys may result in uraemia, or if infection of 
the kidneys ensues suppuration may develop. 

Treatment. — It is evident that no medicinal treatment can be curative in 
hydronephrosis. Morphine and atropine hypodermically to allay pain and 
relieve spasm may be useful at a time when the obstruction is complete and 
the accumulation of fluid rapid. If the condition is due to a floating kidney 



730 DISEASES OF THE KIDNEYS 

with twisting of the ureter, the replacing of the kidney in its normal position 
may give relief. In other instances the temporary assumption of the knee- 
chest position is curative. If the attacks occur very frequently, it may be 
wise to suture the kidney in place. 

When hydronephrosis occurs in a woman, ureteral catheterization is of 
value: first, because it withdraws the accumulated fluid, and, second, because 
if a stricture is present a catheter may dilate the stricture and so exercise a 
curative influence. But catheterization of the ureter is a much more delicate 
procedure than catheterization of the bladder, and there is greater danger 
of infecting the ureter and kidney, so that the greatest possible caution in 
regard to asepsis must be secured. In certain cases where the accumulation 
of fluid is very rapid, and where the symptoms are urgent, aspiration has 
been practised, but this is not devoid of danger, and gives relief in only about 
50 per cent, of the cases. Morris directs that the needle is best inserted at 
the most bulging point, but that if no such point is manifest it should be 
driven in half-way between the last rib and the crest of the ilium and between 
two and two and a half inches behind the anterior superior spine of the ilium, 
if it is the right kidney which is in trouble. An aspirating needle should be 
used instead of a trocar and cannula. When repeated aspirations are required 
for lelief, nephrotomy is necessary. 



CYSTIC DISEASE OF THE KIDNEY. 

Cysts of the kidney occur as congenital malformations and are acquired 
in late life. There is perhaps no more striking object to be found in a col- 
lection of pathological specimens than a congenital cystic kidney. This 
condition not rarely affects both kidneys, which is an important point to bear 
in mind if any operation on one kidney is thought of. These cystic kidneys 
are not composed of one large cyst, but of a multitude of cysts massed 
together regardless of shape and size, and separated by fibrous bands or by 
strands of atrophied renal tissue. The contents of the cyst is usually a 
clear yellow fluid with an acid reaction and containing urinary salts, but 
occasionally the fluid is opaque and may contain small amounts of blood. 
The causes and processes by which these cysts are developed are not definitely 
known, but it is thought they are formed by extraordinary dilatation of the 
tubules or of Bowman's capsules. Shattock believes they are due to mal- 
development of the mesonephron. Such kidneys often weigh several pounds. 
Although congenital in origin, it is to be remembered that life may be 
continued far into adult years before they give any trouble. 

Congenital cystic kidney (Fig. 98) may project well below the ribs and 
give rise to a diagnosis of sarcoma, hydronephrosis, or of enlarged spleen. 

Cysts of the kidney, single or multiple, may be present in kidneys which 
otherwise show no abnormalities, and these cysts may be smaller than a 
pea or larger than an orange. Their contents may be clear or brown, in 
color, and may be gelatinous in character. 

Attention has already been called to the small cysts which are seen on the 
surface of the kidneys in chronic interstitial nephritis. At times it is difficult 



CYSTIC DISEASE OF THE KIDNEY 



731 



to determine whether the kidney is the site of acquired or congenital 
cysts when these cysts become large and multiple. 

Echinococcus cysts of the kidney also occur. (See article on Para- 
sitism.) 

The symptoms of congenital cystic kidney are in no way peculiar unless 
the kidney be large enough to project in the manner described. Aside from 
this sign the patient presents no signs of renal disease until the cyst, by 
increase in growth and resulting decrease in renal tissue, develops renal 
failure, and the signs of chronic nephritis ensue. In some cases a sudden 

Fig. 98 




Congenital cystic kidney. (Kast and Rumpler.) 



attack of uraemia may be the first symptom of renal difficulty. When the 
condition persists and adult life is reached, there may be a high arterial 
tension and hypertrophy of the heart, as in ordinary chronic nephritis. Often 
they interfere but little with the life of the patient. In the museum of the 
Jefferson Medical College is a cystic kidney weighing seven pounds, diag- 
nosed during life by the late Dr. J. M. Da Costa, and carried by a busy 



732 DISEASES OF THE KIDNEYS 

practitioner of medicine for over two years afterward. The other kidney 
was but slightly affected. 

Beyond the use of pain-relieving drugs, there is nothing that can be done 
for these cases. Operative procedure is contraindicated in the sense of 
nephrectomy, because the other kidney is so often diseased that it is unable 
to carry the burden of elimination if left by itself. 



TUMORS OF THE KIDNEY. 

The kidney is not rarely the seat of morbid growths. They may be benign 
or malignant. The benign growths are the fibromata, which chiefly affect 

the pyramids of the kidney, and less 
commonly the lipomata and angiomata. 
Occasionally papilloma of the mucous 
membrane of the pelvis of the kidney 
develops. The most common malig- 
nant growth in the kidney is sarcoma, 
which is by no means very rare in 
young children, and often grows to a 
very great size. Sarcoma of the kidney 
secondary to sarcoma elsewhere is also 
met with in adults. Endothelioma may 
develop. They are all vascular and 
often bleed, producing hematuria. 
Adenoma of the kidney usually springs 
from the cortical tissues, but it may 
grow to so large a size that it takes the 
place of most of the renal tissue. They 
occur frequently in children and are 
walled off from the rest of the kidney by 
a fibrous sheath. Adenoma is found 
in two forms, the papillary and alveolar. 
Not rarely considerable areas of necrosis 
develop in these tumors. Cancer of the 
kidney as a primary growth is rare. As 
a secondary growth it is more common. 
Of all the tumors affecting the 
kidney those arising from ectopic 
adrenal tissue are probably the most 
frequent. Such tumors, called "hyper- 
nephromata," vary in size from almost 
microscopic masses to growths larger 
than an adult head. In their earlier de- 
velopment such neoplasms are benign, 
but later tend to involve adjacent struc- 

Sarcoma of the right kidney. The dark line mres anc J D V metastasis the lungS. If 
on the abdomen is a blue-pencil outline of the . ^ . ., .. it 

tumor. (Le Conte.) they occur on the right side, the liver 




NEPHROLITHIASIS 733 

is often affected. These tumors are soft, vascular, yellowish, or blood- 
tinged masses developing in the kidney, and often cause hematuria. 

The symptoms of renal tumor, if the growth is benign, are not marked, 
unless it grows large enough to produce pressure. 

When the tumor is malignant, free hoematuria, with clots moulded to the 
shape of the ureter, may be present. Pain develops only when the growth 
presses on neighboring parts or on adjacent nerve trunks, or when the 
weight of the growth is such as to cause a sense of weight in the loin. 
Severe attacks of colicky pain may, however, be present when a clot is being 
forced through the ureter. In some cases marked loss of flesh takes place, 
but children with renal sarcoma often remain remarkedly well nourished. 
The tumor, if large, may project well forward in the belly and give rise to 
the belief that it is an enlarged spleen or liver (Fig. 99). This error 
is frequently made. The colon may give tympany on percussion over 
the growth, showing that it springs from behind that part of the bowel. 
Sarcoma of the kidney must be separated from sarcoma of the retroperi- 
toneal space. Care should be taken that it is not confused with cystic 
kidney, or hydronephrosis, for the malignant growth may be nodular and 
very elastic, or even give a sense of fluctuation on palpation. 

There is, of course, no medical treatment of this state. In some cases 
nephrectomy of the sarcomatous kidney has been performed in young 
children with good results, but there is usually a metastasis elsewhere, 
which ultimately takes life. 



NEPHROLITHIASIS. 

Definition. — This condition is often called " stone in the kidnev/' or 
" renal calculus." It is due to the formation in the tissues of the kidney, 
or in its calyces or pelvis, of concretions composed of solids derived from 
the urine. 

Etiology and Pathology. — The concretions, when in the pelvis of the kidney, 
may be single or multiple, and very great variations in their size may be met 
with. In some instances they are so small as to be scarcely larger than grains 
of sand; in other cases they may be as large as a pea or bean, and in still other 
instances a large calculus may form which completely fills the renal pelvis 
and projects itself into the ureter and into the calyces and infundibula, form- 
ing what is called a "coral calculus." The latter form is, of course, never 
passed from the kidney, but the smaller stones often become engaged in the 
ureter, and in their passage through it to the bladder cause intense pain. 
Not rarely the fine renal sand passes so readily that it attracts no attention 
until it is seen in the urine. 

Not only are concretions found in the calyces and pelvis, but also in the 
tissues of the kidney. Thus, formations of uric acid may take place in the 
tips of the pyramids after birth and cause much pain in the first month of 
life. Again, accumulations of sodium and ammonium urate are not rarely 
found in adults at the tips of the pyramids, particularly in gouty invalids, and 
in very old persons a deposit of lime-salts is found in streaks in the pyramids. 



734 DISEASES OF THE KIDNEYS 

The concretions just spoken of may be formed of a number of urinary 
solids, such as uric acid, calcium oxalate or phosphate, urate or carbonate. 
Cystin and xanthin also are ingredients. The mere existence of these sub- 
stances in the urine is not the cause of the formation of stone, however, 
for if this were true everyone would have calculus. There are at least two 
additional factors present, one of which is the presence of an albuminoid 
substance, which serves to glue together tiny particles of these solids, 
and a condition in which there is an abnormal tendency to crystallization 
of these bodies. The bacterial origin of gallstones and the presence of 
micro-organisms in the nuclei of renal calculi suggest a similar origin for 
both. 

The most common ingredient of stone is uric acid or the urates. Stones 
of this character are met with in people who, because of small quantities of 
fluid ingested, have a scanty urinary flow, or who, by reason of great activity 
of the sweat glands, have little urine. As a consequence of concentration and 
high acidity of the urine, the uric acid and urates are readily separated in 
solid form and held together by the albuminous matrix. Stones of this char- 
acter are quite hard, and their surface is smooth and reddish. 

Phosphatic calculi are of the most common occurrence after those formed 
from uric acid and the urates. They are composed of calcium phosphate, 
ammoniomagnesic phosphate, or both, but they are rarely found in the kid- 
ney, being generally developed in the bladder. They are usually formed 
when the urine is persistently ammoniacal. 

Next to phosphatic calculi, those formed of calcium oxalate are most 
commonly met with. They are peculiar in respect to their great hardness 
and their roughened surface (mulberry calculi). Sometimes when they are 
small they are smooth and rounded, "hemp-seed calculi." They are dark 
in hue and not infrequently, on being split, they are found to be formed about 
a nucleus of uric acid. Oxalate stones are only met with in those who, because 
of digestive or metabolic disorders, pass considerable amounts of oxalates in 
the urine. 

The effects of the presence of stone in the renal pelvis are not always 
marked. Indeed, calculi may be present for years without causing any dis- 
comfort whatever. Sometimes they suddenly cause trouble if the patient 
suffers from a fall which causes the stone to damage the lining membrane of 
the pelvis, and as a result hematuria may ensue, or the stone may be started 
from its nest, and, proceeding to travel down the ureter, cause an attack 
of colic. In still other cases the stone may cause a hydronephrosis by plug- 
ging the orifice of the ureter. Again, the damage done by the sudden move- 
ment of a stone against the tissues may open a path for infection and conse- 
quent pyelitis or even pyelonephritis. 

Frequency. — In certain parts of the world stone is very prevalent, notably 
in some counties in England. This is probably due to certain mineral ingre- 
dients of the water which is taken for drinking purposes. Stone is also very 
commonly met with in China and in India. The late Dr. Kerr, a Chinese 
missionary, removed hundreds of vesical calculi during his residence in 
China. So far as I have been able to discover, stone is not much more preva- 
lent in one part of the United States than in another. 



a i:riiROLiTHiASiS 735 

Prognosis. — The prognosis of nephrolithiasis depends entirely upon the 
question of the state of the kidney tissues about the stone or stones. In many 
cases the stone produces no trouble for years. If, as the result of an injury 
or infection, the surrounding tissues become diseased, the state of the patient 
may become serious from pain or from sepsis. 

Symptoms. — As just stated, stones may be in the kidney for years without 
causing any signs. When they escape into the ureter they cause renal colic, 
which is due to three causes: first, blocking of the ureter results in obstruction 
to urinary flow which causes distention; second, the pressure of the urine on 
the stone forces it forward through the narrow canal, often wounding its 
lining, and, finally, the walls of the ureter are spasmodically contracted 
because of the presence of the stone. The pain is often so severe as to be a 
horrible agony. I have seen a strong and brave man grovel on the floor 
groaning with anguish, and vomiting because of its severity. The pain 
extends into the pelvis and the inner side of the thigh on the affected side, and 
even into the testicle and penis. It also radiates into the back of the chest. 
These symptoms may persist for an hour or for several hours. In the latter 
instances there are often temporary remissions in the pain. Not rarely the 
bladder is exceedingly irritable, and the patient continually passes small quan- 
tities of urine which contains traces of blood from the affected ureter, but 
most of the urine comes from the normal side. 

In cases of suspected renal calculus the urine should be examined micro- 
scopically for blood cells, both during and between attacks. They are 
practically never absent when a calculus is lodged in a ureter. 

When both kidneys are affected, total suppression of urine due to obstruc- 
tion of the ureter or to reflex irritation may ensue, and the resulting toxaemia 
produce death. It is, however, a noteworthy fact that this state is rarely rapid 
in onset or rapidly fatal. The patient often lives for many days, unless there 
has been renal disease present for some time with some degree of toxaemia. 
I have recently seen a case in consultation in which no urine had been passed 
for a week, and the catheter obtained nothing from the bladder, yet the 
patient was conscious and alert when spoken to, appearing drowsy only when 
left alone. This is a state quite separate from ordinary ursemia, and has been 
called "latent uraemia." (See Ursemia.) 

After an attack of renal colic has passed, pain and soreness are felt for some 
hours or days in the affected loin, and tenderness on pressure may be 
elicited. 

Diagnosis. — The pain of renal colic must be separated from that of acute 
appendicitis, that of gallstone colic, and from neuralgia. It must also be 
distinguished from the pain due to hydronephrosis resulting from a twist in 
the ureter. Sometimes a diaphragmatic pleurisy may mislead us. The 
peculiar radiation of the pain into the groin, penis, and inside of the thigh is 
diagnostic. The pain of gallstone is radiated into the back, and is often asso- 
ciated with jaundice. Neuralgia does not cause bloody urine. Twist of the 
ureter can be predicated by finding a floating kidney. Pleurisy is defined by 
the area of the pain, by fixation of the diaphragm, and by a friction sound in 
some cases. A valuable, but by no means absolutely reliable, method of diag- 
nosis is the use of the Roentgen rays, which may or may not reveal a stone, 



736 DISEASES OF THE KIDNEYS 

and which sometimes has caused the surgeon to operate when no stone has 
been found. 

Treatment. — The treatment of nephrolithiasis may be divided into two 
parts : that devoted to the relief of the patient at the time of the attack of renal 
colic, and that devoted to the prevention of the formation of new stones or 
an increase in the size of those already present. For the relief of the attack 
of renal colic, a hypodermic injection of J grain of morphine, with yj-g- grain 
of atropine, should be given at once; or, if atropine is known to be disagree- 
able in its effects upon the patient, nitroglycerin may be used hypodermically, 
for the double purpose of aiding in relaxing the spasm and because it tends 
to prevent the after-disagreeable effects of the opiate. If the heart is in a 
satisfactory condition, chloroform may be given by inhalation, and if the 
patient will lie quietly enough to permit it, hot applications may be made 
over the painful kidney. 

In the intervals between the attacks the patient should be instructed to 
drink large quantities of some pure water like Poland water, or one of the 
Lithia waters, which depend chiefly for their effects upon their purity rather 
than upon their lithia. If the urine is alkaline, lithia waters are contra- 
indicated, and under these circumstances it is well not only to use copious 
draughts of water, but to direct the patient to take uritone, urotropin, or 
benzoate of ammonium, for the purpose of making the urine acid. 

When the urine is excessively acid, it is advisable for the patient not 
only to drink large quantities of water, but also to take 15 or 20 grains of 
bicarbonate of potassium three or four times a day. In other instances the 
citrate of potassium may be given. Sometimes good results follow the use 
of Celestins Vichy water when the urine is acid. If an examination of the 
urine reveals the presence of a large number of urates, it must be borne in 
mind that these have their origin in disordered gastrointestinal functions, 
and the diet must be carefully regulated, and nitromuriatic acid given in full 
doses. Sometimes, too, these cases are benefited by the administration of 
such intestinal antiseptics as salol, or aspirin, in the dose of 5 or 10 grains 
three times a day. 

The patient should be forbidden to drink any sweet wines or beer, and the 
only form of alcoholic stimulant permitted should be rye or Scotch whiskey. 
If the patient can do without any alcohol at all, it is much better for him to 
be content with non-alcoholic drinks. 

If the patient is one who is accustomed to leading a sedentary life, he 
should be instructed that an amount of exercise which is sufficient to pro- 
duce healthy fatigue is absolutely essential; but if he exercises he should 
also drink copiously of water. 

When pain in the kidney is continuous or so frequent in its recurrence that 
the enjoyment of life is impaired, or if there is any evidence of the tissues of 
the pelvis of the kidney or of the kidney itself being irritated or infected, the 
question of operative interference must be carefully considered, and the 
patient advised to seek surgical relief. 



DISORDERS OF URINARY SECRETION 737 



PERINEPHRIC ABSCESS. 

An abscess sometimes forms around the kidney by the extension of infec- 
tion from the pelvis of this organ, because of transmitted lymphatic infection 
from a suppurative appendicitis, from injury to the tissues by a blow or fall, 
by extension of infection from spinal disease, from perforation of the stomach 
or bowel followed by subdiaphragmatic abscess, and rarely after acute 
infectious fevers, as typhoid fever. The pus may cause fain and bulging 
over the kidney; it may burrow upward, and escape into the thorax, or down- 
ward and resemble a psoas abscess. The pus is usually very foul and distinct 
septic symptoms may be present. On the other hand, I have seen at least 
two cases in which there was little pain and no fever. There was nothing 
more than some discomfort, with swelling, over the kidney. Not rarely the 
spine is fixed, and the leg on the affected side is drawn up when the patient 
lies down. 

Treatment.— The treatment is, of course, operative. The patient's vitality 
should be supported by food and stimulants. 



DISORDERS OF URINARY SECRETION. 

Anuria. — Anuria is a condition in which there is a total suppression 
of urine. It arises as the result of thrombosis of the renal vessels, and 
an intense acute nephritis such as that which follows the ingestion and 
elimination of very irritant poisons as cantharides and turpentine. Some- 
times complete anuria also follows the administration of ether when this 
anaesthetic has been given over a long period of time and in too large 
quantities. It is particularly prone to occur if the kidneys are already in 
a state of irritation. In other instances total suppression of urine results, 
reflexly, from the irritation produced by nephrolithiasis. In most instances 
when this occurs both kidneys are affected. Partial or complete anuria also 
sometimes occurs after operations upon the genito-urinary tract. A care- 
ful distinction should be made between anuria when no urine is secreted 
and retention of urine in which no urine is passed, but in which the bladder 
is found to be well filled. 

Treatment. — The treatment of anuria varies somewhat with the cause. 
When the arrest of secretion is due to the presence of stone, an operation 
is theoretically demanded, but usually the diagnosis as to the cause is not 
completed before the patient's condition has become so grave that operative 
interference is of questionable propriety. When the suppression of secre- 
tion is not due to stone, but to reflex irritation or spasm of the renal vessels, 
I have known full doses of nitroglycerin given every three or four hours, 
hypodermically, to relax the bloodvessels and cause free urinary flow. 
This is particularly apt to occur if, simultaneously, the patient receives a 
large injection of cool water by the bowel. If saline solution is used, care 
should be taken that it is not of more than 0.6 per cent, strength, since 
strong saline solutions abstract liquids from the tissues instead of being 

47 



738 DISEASES OF THE KIDNEYS 

absorbed. In these instances our desire is that fluid shall enter the tissues, 
find its way to the bloodvessels and so flush the kidneys. Usually about 
one quart of liquid should be given by gentle hydrostatic pressure. Hot 
compresses, or poultices, may be laid across the loins, and if there is 
any reason to believe that renal congestion is present, three or four dry or 
wet cups may be applied over each kidney. In some instances moderate 
doses of the bromides and the vegetable salts of potash, like the citrate, are 
advisable. If the heart is strong the patient may be subjected to a hot pack 
or may be given a Turkish bath by elevating the bed-clothes and allowing 
hot air to surround his body. Small doses of pilocarpine may be given as 
a diuretic, particularly if the heart is guarded by strychnine. The difficulty 
in using large doses of pilocarpine is that it is prone to produce pulmo- 
nary oedema. 

Hematuria. — Bloody urine, or hematuria, is a condition in which there 
is found in the urine not only the coloring matter of the blood, but red blood 
corpuscles as well. It sometimes occurs with the stage of onset in acute 
fevers and in certain cases of leukaemia. It is also met with in certain forms 
of malarial infection of the sestivo-autumnal type, and in cases of infarction 
of the kidney arising during an attack of endocarditis or from other causes. 
When there is stone in the pelvis of the kidney or any part of the conduct- 
ing tract, and the patient is jarred or jolted, the stone may cause suffi- 
cient local damage to produce bloody urine. Parasites such as the Filaria 
sanguinus hominis and the Bilharzia may produce the same condition. 
Blood also appears in the urine as the result of papilloma, cancer, or other 
neoplasm of the bladder, ureter, renal pelvis, or kidney, ulceration of 
the urethra, and of injuries to the genito-urinary tract by falls or blows. 
Sometimes,, too, it develops in the course of scurvy and purpura hemor- 
rhagica. In acute, and even in chronic parenchymatous, nephritis the urine 
sometimes contains small amounts of blood, but they are visible only under 
the microscope. 

The appearance of the urine when it contains blood is quite charac- 
teristic. It is not only dark red in hue, but it is opaque and contains 
considerable sediment, which is chiefly composed of fibrin and blood cor- 
puscles. In pure renal hematuria the voided urine is more of a smoky hue, 
the red cells are of the shadow or phantom type and clots are rarely if ever 
present. If the urine is very alkaline, the red blood corpuscles may be dis- 
solved rapidly or become colorless and difficult to see. Clots formed before 
the urine is passed nearly always arise from hemorrhage in the bladder, but 
occasionally moulds of the ureters may appear. An examination by means 
of the cystoscope or urethroscope may be necessary to determine the source 
of the hemorrhage, and if the blood comes from the kidney it may be neces- 
sary to catheterize the ureters to determine which kidney is damaged. 

There are occasional instances of hsematuria in which, even at autopsy, no 
sufficient cause can be found. These include the angioneurotic hsematuria 
of Klemperer, the renal haemophilia of Senator, and Gull's "renal epistaxis." 

Treatment. — Treatment of hematuria depends largely upon its cause. 
The patient should be put absolutely at rest. If the blood comes from the 
kidney there is no treatment which can be relied upon as being efficacious. 



DISORDERS OF URINARY SECRETION 739 

Chloride of calcium in the dose of 5 grains three or four times a day may be 
given well diluted with water to increase the coagulability of the blood. 
Gallic acid, tannic acid, and sulphuric acid have been largely used by some 
practitioners, but it is doubtful if they really exercise any definite influence. 
If any one of them does act as a styptic it is probably sulphuric acid. Ten 
drops of the aromatic acid maybe given every three or four hours, well diluted, 
and counterirritation may be applied in the shape of cups or hot compresses 
over the kidneys. Counterirritants like mustard, turpentine, and cantharides 
should be avoided, as they may be absorbed and increase renal irritation. 
The patient should be protected from cold. If the hemorrhage comes from 
the bladder, an injection of a pint of normal salt solution containing J to 1 
ounce of adrenalin chloride solution 1 : 1000 should be injected. 

When the hemorrhage comes from the urethra a similar plan of treatment 
can be resorted to, simply instilling the adrenalin into the portion of the 
urethra which is bleeding. The objection to the use of substances which 
cause a coagulation of the blood is that they produce clots, which may 
become septic or give rise to obstruction. 

Hemoglobinuria. — In all probability hemoglobinuria occurs most fre- 
quently as a complication of malarial infection. There is much doubt as to 
the actual cause of this condition. In some instances it is probably due to 
the destructive action of the malarial parasite on the blood, but it would 
seem probable that in other instances it is due to an associated infection 
or a condition which quinine cannot be expected to remedy. Indeed, a 
large number of cases are now on record in which the administration of 
quinine has been followed by hemoglobinuria or hematuria. This con- 
dition is to be distinctly separated from hematuria, for in this case no 
blood corpuscles are present, but only the hemoglobin or coloring matter 
of the blood. Its presence does not indicate any lesion in the genito-urinary 
tract. Strictly speaking true hemoglobinuria is not present, but methemo- 
globinuria. The urine is clear, but may be quite dark in hue, and deposits 
on standing a heavy, reddish-brown sediment. It usually gives the reaction 
for albumin. 

Hemoglobinuria arises from the ingestion of a large number of poisons, 
such as poisonous mushrooms, chlorate of potash, pyrogallic acid, and some 
of the coal-tar products. Not long since I had under my care a physician 
who suffered from repeated attacks of hemoglobinuria whenever he tinkered 
with his automobile, which was stored in a small, tightly closed shed in which 
the fumes of gasoline were quite concentrated. He never suffered with 
hemoglobinuria before these exposures, and since avoiding them has had 
no return of his trouble. Hemoglobinuria sometimes follows severe burns. 
It may also develop in Raynaud's disease. The discoloration of the urine 
produced by carbolic acid is not due to hemoglobinuria, but to a dark, 
oxidized educt, which is in part hydrochinon. 

Haematinuria. — Under the name of paroxysmal hematinuria, sometimes 
called hcemoglobinurie a f rigor e, a condition rarely occurs in which the 
urine varies in color from a port-wine to a chocolate-brown, or almost black 
hue, the alteration in its appearance lasting, however, for but a few 
hours. Its specific gravity usually ranges from 1.025 to 1.027. The urea 



740 DISEASES OF THE KIDNEYS 

is increased. The quantity of blood which is represented has been estimated 
as equivalent to from seven to twelve parts in one hundred of urine. Blood 
corpuscles are very rarely found in the fluid. The urine not only contains 
haemoglobin, but considerable quantities of albumin and globulin. Not 
infrequently hyaline and granular casts are present. This condition is 
chiefly provoked, apparently, by exposure to cold — that is, by chilling of the 
surface of the body. Aside from exposure to cold and chilling of the surface 
of the body, severe muscular exercise seems to be a causative factor, and not 
infrequently there is also a tendency to vasomotor disorders. Indeed, it is 
probable that a large part of the disorder lies in an abnormal vasomotor 
condition. Gilman Thompson has recently reported two cases and sum- 
marized the literature. It appears that during the past forty years only 206 
cases have been reported, and that most of these have appeared in England, 
Germany, and France, and that very few indeed have been reported as 
occurring in the United States and Canada. The condition affects males 
very much more frequently than females, there being only about 4 per cent, 
of females in the 206 cases so far reported. The period of life at which it 
commonly occurs is between thirty and forty years, but cases have been 
reported as late as the sixty-fourth year. At the time of the attack there is 
usually a sharp rise of temperature, amounting to 102° or 103°, but this 
falls to normal almost as rapidly as it rises, the febrile period lasting only a 
few hours. Chills are often present, and may be the first symptom of the 
attack. Jaundice, which is hematogenous in origin, develops. Some persons 
have thought that the jaundice is hepatogenous, but this is unlikely in view 
of the fact that the urine is not bile-stained and the stools are not lacking 
in bile. 

Paroxysmal hemoglobinuria is to be separated from the hsemoglobin- 
uria met with in some cases of malaria by the fact that the latter is a disease 
of tropical or semi-tropical regions, whereas paroxysmal hsematinuria usually 
occurs in cold climates. In one case the malarial organism is present and 
in the other it is absent. 

Paroxysmal haematinuria is also associated with a neurotic condition, 
with urticaria and with localized areas of cyanosis. 

Treatment. — The treatment consists in avoidance of exposure to cold 
and to causes which produce nervous excitement. Tyson has suggested the 
use of suprarenal gland. Thompson suggests the use of thyroid extract. 
Saundby commends calcium chloride and Chvostek believes that inhala- 
tions of nitrite of amyl may be useful to abort an attack. If the circulation 
is feeble, rapidly acting diffusible stimulants like Hoffmann's anodyne, 
aromatic spirit of ammonia, and small doses of spirit of chloroform are 
advantageous. 

The treatment of hemoglobinuria cannot be direct. Copious draughts 
of water to flush the kidneys, careful attention to the state of the bowels, 
protection from exposure of the surface of the body to cold, and the use of 
foods which are not highly seasoned and irritating to the liver and the kidneys 
are the only measures which the physician can institute. When the cause 
of the condition is malaria the debatable question of administering quinine 
must be discussed and decided. (See Treatment of Malarial Fever.) 



DISORDERS OF URINARY SECRETION 741 

Albuminuria. — Albuminuria is a term applied to a condition of the urine 
in which serum albumin, serum globulin, and, by some writers, other 
urinary proteids, including nucleo-albumin, albumose, peptone, or fibrin 
is found in it. While it is true that delicate chemical tests will frequently 
reveal traces of albumin in the urine, it is also a fact that any quantities 
which can be appreciated by the use of heat and nitric acid or by the 
potassium ferrocyanide or mercuric iodide tests are to be regarded as ab- 
normal. 

As albumin is a colloid substance and therefore does not readily diffuse 
through animal membranes it does not pass through the bloodvessels of the 
kidneys and renal tubules unless these structures have undergone some 
degenerative change, or are subjected to a pressure which they cannot with- 
stand. Sometimes, too, albuminuria may be due to changes in the blood 
itself, whereby its albuminous ingredients are altered or the renal texture is 
secondarily affected. The presence of albumin in the urine when disease 
of the conducting apparatus can be excluded (accidental albuminuria may 
occur through contamination of the urine by vaginal discharges) is there- 
fore indicative in the vast majority of instances of some renal lesion, and 
as chronic parenchymatous nephritis and chronic interstitial nephritis are 
the most common renal diseases, it is usually indicative of one of these 
maladies or of a subacute nephritis complicating one of the acute infectious 
diseases. Twenty years ago albuminuria was considered as pathogno- 
monic of Bright's disease. We now know that albumin often appears in 
the urine when Bright's disease is not present. 

As a general rule it may be stated that the quantity of albumin is in direct 
ratio to the severity of the renal lesion, but there are certain notable excep- 
tions to this, as in the case of chronic contracted kidney, in which disease 
the kidney is seriously affected, yet the albumin is always in small quantity 
and may be absent at times. 

Albuminuria is not rarely met with in cases of congestion of the kidney 
due to cardiac failure. Under these circumstances the quantity of albumin 
present may be very large, almost as great as that which is found in chronic 
parenchymatous nephritis. It is due under these circumstances to a 
structural and probably nutritive alteration brought about by passive 
renal congestion, and the use of cardiac stimulants usually results in 
its disappearance, at least to some degree. So, too, albuminuria may 
develop in certain persons after severe and prolonged exercise, as in 
soldiers after a long march, or in athletes after a long run. One cause of 
this, at least, is feebleness of the heart from exhaustion. 

In still other cases what is known as "Cyclic Albuminuria " comes on, 
which is sometimes due to exposure to cold, and at other times seems 
causeless. Cyclic albuminuria is sometimes called the " albuminuria of 
adolescence," and is, as its name implies, intermittent and is usually not 
present when the patient rises in the morning, but appears as the day 
progresses. The upright posture is in some cases sufficient to induce the 
condition — "orthostatic" albuminuria. Usually the urine is above the 
normal specific gravity and contains no casts. As its name indicates, it 
occurs at puberty, in easily fatigued, overgrown, pallid children. It usually 



742 DISEASES OF THE KIDNEYS 

disappears when puberty is passed and the system is established on an 
adult basis. 

In certain persons the ingestion of excessive quantities of albumin in 
food also produces albuminuria. 

A very high arterial tension due to cardiovascular disease may also cause 
this symptom. While it is true that the cardiovascular disease usually results 
in some impairment of the kidney, it is also a fact that reducing arterial 
pressure in these cases by the use of nitroglycerin often stops the albuminuria. 

Albuminuria may be due, as already stated, to changes in the condition 
of the blood itself, met with in certain cases of anaemia, and in diseases like 
purpura, scurvy, and other conditions which cause marked changes in the 
circulating fluid. 

Tests. — Albumin is best detected in the urine by the general practitioner 
by the use of the so-called heat and nitric acid tests, which may be used sepa- 
rately or in conjunction. A test-tube is two-thirds filled with urine, which if 
cloudy should be filtered, and if alkaline acidified, and the upper part of it is 
held over a lighted alcohol lamp so that the fluid in this portion of the tube 
soon boils. Under these circumstances if albumin is present the upper 
portion of the urine becomes clouded from coagulated albumin, but the 
portion below remains clear until the coagulated albumin is precipitated. 
If earthy phosphates are present some cloudiness of the fluid develops, 
but the addition of a few drops of nitric acid disperses the cloud if it is 
due to the phosphates, but does not do so if it is due to albumin. Many 
physicians use a somewhat less accurate test, which consists in placing one- 
half to one drachm of nitric acid in a test-tube, and allowing an equal quan- 
tity of urine to trickle down the side of the tube so that it overlies the acid. 
If albumin is present a layer of albumin appears at the point of juncture of 
the two fluids. Sometimes, if marked intestinal fermentation is present, a 
reddish-brown, but transparent zone, appears at this level also. 

For the purpose of making a delicate test the potassium ferrocyanide 
method may be employed. The writer has found it most convenient to use 
for this purpose the so-called urinary test tablets which are now placed upon 
the market. Into 30 minims of urine is placed a citric acid tablet for the 
purpose of acidification. To this is then added a tablet of potassium 
ferrocyanide, and the tube is shaken or allowed to stand still until both 
tablets are completely dissolved, when if albumin is present tiny flocculi 
may be seen floating in the fluid, which settle to the bottom of the test-tube 
when it is placed at rest. This is a delicate test for albumin, and has the 
advantage that it does not precipitate mucin, peptones, phosphates, urates, 
or vegetable alkaloids. If the physician does not wish to use these tablets, 
he may add to a test-tube half-full of urine 5 or 6 c.c. of a freshly-pre- 
pared solution of potassium ferrocyanide of the strength of one in twenty, 
adding 10 to 15 drops of acetic acid. In other instances the physician may, 
if he chooses, employ potassiomercuric iodide test tablets in the same 
manner, with equally good results. When the potassium mercuric iodide 
acid test is used, the cloudiness due to albumin does not break up into 
flocculi, as it does when potassium ferrocyanide is employed. 

The following facts in regard to these tests should be remembered. If 



DISORDERS OF URINARY SECRETION 743 

the specimen of urine is very alkaline, more than one citric acid tablet, or 
an extra quantity of acid solution should be added. If cloudiness is pro- 
duced by the acid, it is due to mucin, uric acid, or some oleoresin, as, for 
example, when copaiba or cubebs have been taken internally. If the urine 
is warmed the urates dissolve, but the mucin remains. The precipitate 
produced by the oleoresins clears up by boiling, but returns as soon as the 
urine cools slightly. When the tablet, or solution, of potassium mercuric 
iodide or potassium ferrocyanide is added to the acidulated urine, and 
cloudiness is produced, the urine must be heated. If the reaction is due to 
albumin the precipitate remains undissolved, but if it clears up it may con- 
sist of peptones or derivatives of vegetable alkaloids if the mercury test has 
been employed. When the potassium ferrocyanide test is used peptones 
are not precipitated, and may therefore be excluded. 

For the quantitative estimation of albumin Esbach's method is most 
commonly employed. It consists in using a graduated test-tube which is 
called an albuminometer. This test-tube is marked with the letter "U," 
and higher up with the letter "R." Below the letter "U" are graduate lines 
from 1 to 7. Urine is placed in the tube to the level of the letter "U," 
and the following solution is then added till the fluid in the tube reaches 
the letter "R." The solution used consists of 10 grams of picric acid; 20 
grams of citric acid; 1000 cm. of distilled water. The tube is now corked 
and inverted several times until the test solution and the urine are com- 
pletely mixed. It is then allowed to stand on a rack in a perpendicular 
position for twenty-four hours. At the expiration of the twenty-four hours 
the albumin is found to be at the level of one of the numbers cut on the side 
of the tube, and this represents the number of grams of albumin per litre. 
If it is desired to know the percentage of albumin, a decimal point is placed 
in front of the figure. In cases where the quantity of albumin is so great 
that it cannot be measured by the ordinary Esbach tube, the urine should 
be diluted with water, and the result in grams multiplied by the number 
of times the urine has been diluted. 

There is no excuse for neglecting examination of the urine for albumin. 
In the absence of other apparatus and reagents the urine may be acidified 
with vinegar, boiled in a spoon or cup, and if necessary poured into a glass 
for inspection. 

From what has been said it must be evident that the significance of albu- 
minuria varies. Usually, except in the case of chronic interstitial nephritis, 
its importance from a prognostic standpoint is in direct relation to its quan- 
tity; its cause is also an important factor concerning prognosis. The pres- 
ence of tube casts with the albumin is also of great importance, particularly 
if these tube casts are granular and contain fatty globules. Tube casts 
should always be sought for in the urine, if need be with the aid of the centri- 
fuge, but, on the other hand, it should be remembered that if the centrifuge 
is thoroughly employed, there are few specimens of urine which will not 
reveal an occasional cast. 

No one perhaps has studied more carefully than has Leube this question 
of albuminuria. His view is that while in many cases physiological albu- 
minuria does occur, particularly after severe exercise, we should never- 



744 DISEASES OF THE KIDNEYS 

theless regard all such instances with suspicion. Washburn, in studying 
the records of life insurance cases who were supposed to have physiological 
albuminuria, found that the death rate among them was 17.5 per cent, 
instead of 9 per cent., as it should have been. 

A careful study must be made of the heart, kidney, lungs, and other 
organs before the patient is given a favorable prognosis. 

Wright and Ross have shown that it is sometimes possible to differentiate 
the albuminuria of renal disease and physiological albuminuria by increasing 
the coagulability of the blood through the use of calcium lactate. (For 
dose see article on Purpura.) If the use of this drug arrests the albuminuria 
it does not depend upon actual renal disease. 

While casts may be present in the urine of patients who are thought 
to be healthy, but who have albuminuria, these casts should disappear if 
the patient rests in bed, and they should not be epithelial casts. If they are 
present, then it is not physiological albuminuria. It is perhaps best to say 
that albuminuria ought not to be present, and that its existence at least 
excites suspicion of some renal change. But it does not necessarily mean 
Bright's disease, and I have seen more than one case in which distinct 
albuminuria was present without the association of casts for more than 
fifteen years. 

Pyuria. — Pus in the urine may arise from pyelitis, pyelonephritis, cystitis, 
urethritis, vaginitis, or the rupture of an abscess into the urinary passages 
from contiguous parts. When pus is in urine, it gives it a peculiar opacity, 
and on sedimentation the bottom of the vessel contains a somewhat ropy 
mass, presenting a wavy surface. It is to be distinguished from the phosphatic 
deposits mixed with mucus by the fact that it is not so white, and does not so 
closely resemble white or pinkish powdered chalk. Further than this, the 
phosphates are usually cleared up by boiling or by the addition of acid, but 
urine containing pus is not so altered. 

The treatment of pyuria depends upon the cause of the presence of 
pus. If there is an abscess in the kidney surgical measures are required, 
but if the pus is due to a pyelitis or cystitis the use of substances which 
exercise a mild antiseptic influence is to be resorted to, at least for a time. 
For this purpose the patient may receive 5 grains of uritone or urotropin 
three times a day in sparkling water, or 10 grains of benzoate of ammonium 
three times a day in capsule. For the methods and drugs to be employed 
for irrigating the bladder the reader is referred to works on genito-urinary 
diseases. 

Chyluria. — Chyluria is a condition in which the urine presents a milky 
appearance owing to an admixture of fat. It may occur in some cases of 
pregnancy and during lactation. In other instances it follows injury to the 
lymphatics of the abdominal cavity. The most common form of chyluria 
is that which comes on as a complication or symptom of infection by the 
parasite Filaria sanguinis hominis. This condition, as pointed out else- 
where, is met with most commonly in India, China, and in the Straits 
Settlements, and its cause is the obstruction of the lymphatics produced by 
the presence of the parasites within them. Not rarely urine, when chylous, 
coagulates in the vessel holding it or becomes gelatinous in appearance. 



DISORDERS OF URINARY SECRETION 745 

Phosphaturia. — This term is applied to a condition of the urine in which 
it contains an excess of phosphates and is supposed by some to be associated 
with unusual activity of the nervous system, particularly in connection with 
that degree of excessive nervous strain which is often productive of neuras- 
thenia. Whether this view is correct is debatable. There can, however, 
be no doubt of the fact that in certain of the diseases characterized by great 
loss of flesh, such as tuberculosis, an excess of phosphates is present in the 
urine. Such a condition also arises in acute atrophy of the liver and in cer- 
tain forms of grave anaemia. On the other hand, acute diseases running a 
febrile course, and supposed to be characterized by a great amount of 
tissue breakdown, are not accompanied by this manifestation. In some 
instances in which there is an excess of phosphates present in the urine the 
patient is also diabetic, and in still others the patient, while suffering 
from polyuria and phosphaturia, and who has such diabetic symptoms as 
thirst and loss of flesh, nevertheless does not develop a glycosuria, sugar 
being constantly absent. It has been thought by some that these cases of 
so-called "phosphatic diabetes" represent an early stage of true diabetes, 
for in some of them glycosuria ultimately develops. 

The best remedy for the purpose of cleaning the urine of an excess of 
phosphates is benzoate of ammonium in doses of 10 to 20 grains three 
times a day. 

Oxaluria. — Oxaluria consists in a condition in which urine of high 
specific gravity contains on standing, when decomposition is absent, 
an excess of calcium oxalate crystals. The condition is an important 
one in that it frequently points the way to the correct diagnosis and 
treatment of patients who are suffering from dyspepsia, nervous irritability, 
melancholy, and mental depression with a general condition of wretched- 
ness. It is said to be present in those cases in which there is lack of free 
hydrochloric acid in the secretion of the stomach. It also develops in patients 
who eat pears, cabbage, tomatoes, and, occasionally, in those who take 
coffee to excess. In many patients it is an evidence of faulty metabolism 
due to lack of fresh air and exercise. The condition is of interest from a 
therapeutic standpoint because of the fact that these patients often gain 
great benefit if they receive moderate doses of nitrohydrochloric acid and 
take a fair amount of physical exercise and lead an out-door life. 

Indicanuria. — Traces of indican, or, to speak more correctly, indoxyl 
sulphate of potassium, are present in normal urine, being derived from the 
indol which is formed in the intestine by the decomposition of proteids 
through the action of bacteria. If this indol is absorbed from the intestine 
into the blood, it is oxidized and forms the indoxyl sulphate of potassium just 
named. 

When indicanuria is marked, it is an evidence of an excessive amount of 
intestinal putrefactive change, and the discovery of indicanuria in a patient 
who is suffering from the symptoms of autointoxication is, therefore, of value 
from a diagnostic standpoint. An estimation of this substance in the urine 
is also useful to differentiate intestinal obstruction from ordinary severe 
constipation, for in the former indicanuria is usually marked, and in the 
latter the trace of indican which is present is usually not above the normal. 



746 DISEASES OF THE KIDNEYS 

In rare instances, owing to decomposition of the indoxyl sulphate of potassium 
before it escapes from the body, the urine is blue when it is passed, but in 
the majority of cases in which a blue urine has appeared it has been found 
that the patient has taken methylene blue or some similar aniline dye, 
either as a medicine or in foodstuffs. The presence of indican in the urine is 
determined by heating to the boiling point 5 c.c. of nitric acid in a test-tube 
and adding 5 c.c. of urine. If indican is present in excess, a bluish ring 
develops at the point of contact between the two fluids, and if 2 c.c. of chloro- 
form are added and the liquids mixed by shaking, and the test-tube then set 
aside to stand, it will be found that the layer of chloroform which soon sepa- 
rates has a violet color. 

Lithuria. — Under this heading is mentioned a condition in which an excess 
of uric acid occurs in the urine, chiefly in association with sodium and ammo- 
nium, and sometimes with potassium, lithium, and calcium. An examination 
of the urinary sediment under the microscope may reveal small, reddish grains 
or crystals, looking under the microscope like particles of red pepper. There 
is no condition which is so little understood at the present time as is this one. 
Almost every layman, and a multitude of doctors, continually speak of being 
"full of uric acid," meaning by this that they have muscular stiffness, or that the 
urine shows an excess of urates, or even uric acid crystals. In the majority of 
instances this excessive deposit of urates, or uric acid, depends not upon any 
abnormality in bodily metabolism, but upon conditions of the urine which 
cause the precipitation or deposition of these solids. There is either a condi- 
tion of acidity or a minimum quantity of mineral salts, and as a result pre- 
cipitation takes place. For this so-called "uric acid diathesis," physicians 
prescribe large quantities of lithium and copious draughts of water. There 
can be no doubt that the water is advantageous, but the lithium only does 
good until a certain degree of alkalinity is reached, when it is of little value, 
and if the doses are large it acts as a depressant to the general system. It is 
quite true that persons who eat heartily, drink alcohol, and take no exercise are 
not infrequently overloaded with effete materials representing imperfect meta- 
bolism, which cause disagreeable symptoms. It is also perfectly true that 
exercise, a proper diet, and the use of plenty of drinking water will overcome 
these symptoms, but this does not prove that the patient is a sufferer from the 
" uric acid diathesis." 

Melanuria. — Melanuria is a condition in which the urine at the time it is 
passed, or shortly after its exposure to the air, becomes intensely dark in hue, 
owing to the presence in it of melanin. It is found in certain conditions in 
which this substance is produced in the body by pathological processes, such 
as melanotic growths. If a solution of ferric chloride is added to the urine, it 
becomes inky black. If caustic potash is added, it becomes at first violet and 
then claret colored, and if acetic acid is added to this mixture it may become 
blue. The test most commonly employed is the solution of ferric chloride 
mentioned. 

Myelopathic Albumosuria.— The presence in the urine of the so-called 
Bence-Jones albumose or proteid has by a number of observations been 
shown to be most suggestive of the rather rare tumor of bone known as 
multiple myeloma or medullary osteosarcoma, "Kahler's Disease." The test 



DISORDERS OF URINARY SECRETION 747 

is quite simple. The urine, if not distinctly acid, should be made so with 
acetic acid and then heated. At 50° C, if it contains this albumose, it 
becomes milky; at 60° C. it deposits a thick precipitate which clings to the 
sides of the tube or collects on the surface. Further heating to 100° C. 
causes the almost complete disappearance of the precipitate, which, how- 
ever, re-forms as the urine cools. 



DISEASES OE THE DUCTLESS GLANDS AND 
LYMPHATIC SYSTEM. 



DISEASES OF THE THYROID GLAND. 
GOITRE. 

Definition.— Under the term goitre, bronchocele, thyreocele, or struma is 
included almost all enlargements of the thyroid gland, but the application of 
so general a term is not to be regarded with favor. It is better, therefore, to 
consider the various diseases of the thyroid as inflammatory (traumatic 
strumitis), infectious (tuberculous or syphilitic strumitis), and parasitic 
(echinococcic) strumitis. Of the remaining so-called hypertrophies of the 
gland it may be said that some of them at least are apparently not of the 
nature of neoplasms, and to these the term "simple" or "benign goitre" is 
applied; whereas, in the case of those enlargements which are due to the 
development of tumors within the gland, we apply the term "neoplastic 
goitre," as, for example, endotheliomatous, sarcomatous, and cancerous 
growths (malignant goitre). (See Tumors of the Thyroid.) 

With regard to some of the simple or benign goitres, it is still unsettled as to 
whether they are neoplastic, that is, adenomatous, in every instance. In some 
cases they are undoubtedly adenomatous. In still other cases the greatly 
enlarged gland may, under the microscope, have a histological formation like 
that of the normal organ. To this type of goitre the name "hyperplastic 
goitre" is applied, including those varieties characterized by reproduction 
of the parenchyma of the gland and called by some writers "parenchymatous 
goitre." When the enlarged gland contains cysts developing from its acini, 
the mass is called a "cystic goitre." Cystic goitres result from the distention 
of the gland spaces, with absorption of the intervening walls, thereby giving 
rise to cavities of various sizes. The contents of these cysts may be gelatin- 
ous or colloid. In some instances the enlargement depends upon dilatation 
of bloodvessels, and apparently upon the overgrowth and dilatation of new 
bloodvessels, forming the so-called vascular goitre, and not rarely there is a 
blending of two or more of the types already mentioned. Such conditions 
are known as "mixed goitres." 

In ordinary goitre there takes place an increase in the size of the alveoli 
in the thyroid gland and a simultaneous formation of new glandular tissue. 
Side by side with this increase there is often colloid degeneration, and when 
this degenerative process is marked the state is called colloid struma or 

(749) 



750 DISEASES OF THE THYROID GLAND 

colloid goitre. Not uncommonly still other degenerative changes take place, 
in which the walls of the alveoli break down, and in this way several 
cavities are thrown together, forming cysts, which may hold colloid matter 
and blood derived from the vessels in the alveolar walls. This is called cystic 
goitre. In still other cases the bloodvessels of the gland become dilated, so 
that a telangiectatic state develops. Finally, it sometimes happens that all of 
these changes take place in the same gland, and upon them may be super- 
imposed acute inflammation and even malignant growth. The increase in 
size may be limited to a single part of the gland or be widely diffused. 

Etiology. — The cause of ordinary enlargement of the thyroid gland of the 
fibroid and cystic type is unknown, but there can be no doubt that it depends, 
at least in part, upon the character of the drinking water used. My colleague, 
Professor Keen, has just investigated a very remarkable prevalence of the 
disease in the interior of the State of Pennsylvania, in which the relationship 
of water supply and goitre is extraordinary, a very large number of the people 
on one side of a mountain ridge being affected, and those across the divide 
escaping. The disease is also said to be very common in some parts of 
Michigan and in Switzerland. The suggestion of Grasset that goitre is of 
protozoal origin has not been favorably received. In support of his view he 
calls attention to the fact that, like malaria, goitre is endemic in certain 
areas, and he is inclined to believe that the thyroid enlargement is anal- 
ogous to the splenic tumor of chronic malarial infection. The disease is 
more frequent in women than in men, and in adults than in children, in 
which class it is very rare. 

Symptoms. — The symptoms of goitre are usually of no consequence until 
the growth is large enough to be seen or until, by its pressure on the adjacent 
tissues, it causes difficulty in breathing and interferes with swallowing or with 
the function of the vagus nerves. The goitre may involve all of the gland, 
its isthmus, or either one of the lateral lobes. Rarely aberrant goitres arise 
in ectopic or misplaced thyroid tissues, and they may be intrathoracic or 
occur at the base of the tongue (lingual goitre). In still other instances they 
have been known to develop along the course of the thyroglossal ducts or in 
adjacent areas. The degree to which the cervical tissues are displaced in 
those cases in which the growth is chiefly in one lobe is remarkable. Not 
long since I sent to Dr. Keen for operation a patient whose hyoid bone was 
pushed to one side so that it rested nearly under his right ear. 

Treatment. — There is no medicinal treatment of much value in goitre. 
Painting the part with iodine and the use of various counterirritant ointments 
have been resorted to, but they have no real effect over the growth. If it 
becomes very large, it must be excised if the pressure symptoms are severe. 



SWELLING OF THE THYROID. 

This occurs from two chief causes, namely, from inflammation and from 
hypersemia or congestion. Some writers have described an angioneurotic 
form. When the swelling is due to inflammation it may arise from infection 
of the gland, as in typhoid fever or other acute infectious diseases, and may 



EXOPHTHALMIC GOITRE 751 

follow vaccination or sepsis; or, again, it may be due to tuberculosis of the 
gland, or to syphilis with the formation of gummata. Occasionally marked 
swelling arises from trauma, and this may be acute or chronic. 

It is asserted by Fothergill that there are recorded five cases of enlargement 
of the fetal thyroid due to the administration of potassium chlorate to the 
mother. 

Some years ago I reported the case of a woman who, in stooping in a dark 
room, struck her neck against the edge of a chair and at once felt violent pain 
in the thyroid gland. The gland rapidly became swollen, and the patient 
presented all the symptoms seen in persons to whom large doses of thyroid 
gland have been given, such as headache, a rapid pulse, and a tendency to 
syncope. In still another case, seen by me, an army surgeon on the fight- 
ing line received a severe blow in the thyroid, and developed a chronic 
enlargement of the thyroid gland, with some tachycardia. 

The thyroid gland is also found enlarged by hyperemia in young girls, 
particularly at the menstrual period, and in young women in their first preg- 
nancy. It also occurs in young persons who suffer from cardiac disease. 
Such an enlargement usually passes away when the cause is removed. 

Sometimes thyroiditis occurs in the insane, but its etiology and symp- 
tomatology need further study. 



TUMORS OF THE THYROID GLAND. 

The tumors of this gland are adenoma, in which state the condition is 
practically that of goitre as already described, carcinoma, sarcoma, and 
endothelioma. The sarcomata are usually primary. Morf has been able 
to collect but 39 instances of carcinoma of the thyroid; he himself adds 
1 case. Of the 173 cases of cancer of the thyroid collected by Orcel, 14 
invaded the trachea. 

Carcinomata are also usually primary and undergo metastasis to nearby 
tissues or even to distant structures. The growth may develop in the 
parenchyma or in the connective tissue of the gland. 

An interesting form of tumor of the thyroid is the so-called carcino- 
sarcoma, or mixed tumor of this gland. 

Occasionally old, quiescent goitres may become malignant, undergoing 
either sarcomatous or carcinomatous degeneration. 

An anomalous condition in this group of affections is thyroid metastasis, 
consisting in the growth of typical thyroid tissue at points distant from the 
glands. These growths are quite commonly in bones and are seldom 
malignant. The thyroid itself may show no change. 



EXOPHTHALMIC GOITRE. 

Definition. — Exophthalmic goitre is often called "Basedow's disease," 
"Parry's disease," or "Graves' disease." Parry described it (1825) ten 
years before it was described by Graves (1835) and fifteen years before it 
was described by Basedow (1840). Exophthalmic goitre is an entirely 



752 DISEASES OF THE THYROID GLAND 

different disease from ordinary goitre or simple enlargement of the thyroid 
gland. It is a malady in which, as its name implies, there is protrusion of 
the eyeballs, and, in addition, palpitation of the heart, with a very rapid 
pulse. There are fine tremors in the hands, arms, and head, and disordered 
vascular tone. A tendency to abnormal sweating of the palms of the hands, 
and great mental depression is often present. 

Satterthwaite recognizes acute, subacute, and chronic forms of Graves' dis- 
ease, and says we may speak of acute or temporary and essential or chronic 
forms. A secondary form is that in which an old goitre takes on the symp- 
toms of Graves' disease. 

Frequency. — In 10,603 cases admitted to the Jefferson Hospital, there were 
1 1 cases of exophthalmic goitre, or 1 in 964. In the University Hospital, out 
of 35,076 cases, there were 48 cases of exophthalmic goitre, or 1 in 730. Of 
7270 cases treated at the Dispensary for Nervous Diseases at the Orthopaedic 
Hospital and Infirmary for Nervous Diseases, Eshner found that 30 were 
exophthalmic goitre, or 1 in 242. It is therefore by no means a rare disease. 

Etiology. — The cause of exophthalmic goitre is not known, but, as is the 
case with most diseases of obscure causation, a multitude of factors have been 
named as possible causes for its development, varying all the way from rheu- 
matism and tonsillitis to fright and traumatism. The disease is very much 
more frequent in women than in men. Thus, out of 1839 cases collected from 
various sources, 1553 were females and 286 males, a proportion of about 6 to 1, 
and its average age incidence is between sixteen and forty years. Cases 
are on record in which it has affected children as young as two and a half 
years. In some statistics, collected by me some years ago, it was shown that 
there is a very distinct hereditary influence present in many cases. There 
can be little doubt that the symptoms which are present in exophthalmic 
goitre are dependent upon excessive internal secretion of the thyroid gland, 
or, if not upon excessive secretion, to the entrance into the general system 
of more of the active principle of the thyroid gland than is normal. It has 
been claimed that the cause lies in disorder of the sympathetic ganglia, but 
there is no adequate proof of the correctness of this view. 

Pathology and Morbid Anatomy. — So far as the morbid changes are con- 
cerned, there is an excess of fat in the orbit as compared to the quantity of 
fat in other portions of the body. 

The heart may be normal or dilated. Not rarely there is some undue 
relaxation of the sphincteric fibres around the mitral orifice of the heart. 
The thyroid is enlarged, the veins covering it are dilated and numerous, 
and the arteries supplying its tissues are enlarged and tortuous. On the 
other hand, certain observations have shown that in many instances there is 
no remarkable change in the vascularity of the organ. 

A microscopic examination of the thyroid gland reveals, in many instances, 
however, a very marked increase in the development of its parenchyma, and 
the epithelium lining its vesicles is changed in appearance. The colloid 
substance in the vesicles partly or entirely disappears and is replaced by 
mucoid material which takes a stain badly. The epithelial cells lining 
the vesicles frequently desquamate. Greenfield has shown that additional 
tubules lined by a layer of epithelium are also developed. After the disease 



EXOPHTHALMIC GOITRE 753 

has lasted for a considerable period of time, there is not infrequently an 
overgrowth of connective tissue in the gland. MacCallum finds that, as a 
whole, the changes resemble most closely those found in experimentally 
produced compensatory hypertrophy of the thyroid. 

The thymus gland is enlarged in a very considerable proportion of cases, 
but a microscopic examination of it does not show pathological changes in 
most instances. 

The parathyroids are often found to be atrophied and the thymus gland 
is persistent and often hypertrophic. 

Certain alterations have been described in the sympathetic system and in 
the central nervous system, but it has not been proved that these have any 
close relationship with the disease. 

Symptoms. — The 'protrusion of the eyeballs, even when it is present to a 
moderate degree, is so striking that attention is directed to this symptom 
almost as soon as the patient is seen. It varies greatly in degree. In some 
cases the eyeballs may be so prominent that it is impossible for the lids to 
completely close, whereas in others the exophthalmos may be very slight 
indeed. While it is true that the exophthalmos may not be equally developed 
on both sides, it is nearly always bilateral, although a few instances of uni- 
lateral exophthalmos have been reported. 

Under the name of von Graefe's sign, a condition is found, in which, if 
the patient is directed to look at the floor, the upper eyelid does not follow 
the eyeball in its downward rotation as rapidly as it should. This symptom 
is not always present. Stelwag's sign consists in a widening of the palpebral 
fissure, with retraction of the lids, to such an extent that the sclerotic coat of 
the eye is seen above and below the iris. This very distinctly increases the 
exophthalmic effect. With this symptom there is also diminished reflex 
excitability, so that winking is delayed when a sudden movement is made 
toward the patient. Under the name of Mobiles' sign is described a con- 
dition in which there is a lack of power of convergence, so that if a pencil 
is brought near the patient's face the eyes cannot converge, as they do in a 
normal individual. 

Notwithstanding the exophthalmos, vision, as a rule, is not interfered with, 
but ulceration of the cornea sometimes occurs as the result of the inability of 
the eyelids to protect the eye. (See Fig. 100.) 

The increase in the size of the thyroid gland is usually not very great, and 
it never becomes as large as in many cases of ordinary goitre. 

On inspection the gland may seem to pulsate, and on palpation it often 
transmits a thrill to the finger-tip. If the stethoscope be placed over the 
gland, a distinct humming murmur can be heard. This same murmur is 
also detected, even more clearly, if the stethoscope be placed over the 
carotid arteries. 

The gland is never very hard, but may be soft and fluctuating, and is apt 
to vary in size considerably from week to week or from day to day. Tachy- 
cardia is practically always present in these cases. The pulse varies from 
90 to 100 or even 200 beats a minute, the ordinary rapid pulse being very 
much increased on exertion or excitement. 

If the finger-tips of the patient are rested upon the finger-tips of the physi- 
48 



754 



DISEASES OF THE THYROID GLAND 



cian, there can be felt not infrequently a fine tremor, sometimes called "rail- 
road bridge tremor," owing to its resemblance to the sensation produced in 
one's feet when standing upon a railroad bridge during the time a train is 
passing over it. In other instances the tremor is very marked and coarse in 
character. 

The patient nearly always complains of feebleness and mental depression, 
and in some cases melancholia may be so profound as to result in suicide, as 
in a patient recently under my observation. An irritating nervous cough and 
occasional attacks of dyspnoea may occur, and cases are on record in which 



Fig. 100 




Exophthalmic goitre. The illustration shows the enlarged thyroid gland. The exophthalmos was so 
great that the lids had to be sewed together to protect the eyes. 

the patient has suddenly died from urgent dyspnoea, which has had its origin 
in intense swelling of the thyroid gland, so that it has pressed upon the trachea 
in much the same manner as does the enlarged thymus in status lymphaticus. 
Another symptom which, when it develops, must always be regarded with 
alarm, is excessive and obstinate vomiting. This condition may speedily pass 
by, but in some cases it has persisted until death has ensued. Sudden attacks 
of diarrh&a are not rare. The digestion is fairly good, but the appetite is 
uncertain, and the patient craves abnormal things as she does in hysteria. 
Oftentimes a constant "rifting up" of wind gives great annoyance. The 
nervousness is so intense that in many cases the patient's life is almost unbear- 
able because of the irritation produced by noises and other sources of irrita- 
tion which ordinarily would not be noticed. Nervous chills or tremblings are 
often a source of great annoyance to the patient, and the palms of the hands 



EXOPHTHALMIC GOITRE 755 

are prone to be wet with excessive perspiration. Patches of pigmentation on 
the skin often develop. There is usually distinct loss of weight and 
strength. 

Prognosis. — A certain number of cases of exophthalmic goitre undoubtedly 
recover, but they are always liable to relapse. Rapid loss of flesh and 
strength, marked tachycardia, persistent vomiting, and diarrhoea are all of 
them symptoms which would cause us to give a guarded or unfavorable 
prognosis. Whereas, if the symptoms are mild, we have a right to feel corre- 
spondingly encouraged. Sometimes exophthalmic goitre may last so short 
a time as a few days or weeks. In other instances it may continue for many 
years. 

Treatment. — The treatment of exophthalmic goitre is not very satisfactory. 
When the thyroid gland was first used as a therapeutic agent it w T as given to 
a considerable number of persons suffering from exophthalmic goitre, with 
the idea that it might do good, but from the first it must have been manifest 
that it could not be of value because the patient is suffering from too much 
thyroid secretion, and the addition of more of the thyroid substance must in 
consequence be disadvantageous. 

Le'pine has recommended antithyroid serum in the treatment of Graves' 
disease. This serum is obtained from animals immunized against hyper- 
thyroidism. Under the name of thyroid serum Moebius has given us serum 
derived from sheep from which the thyroid gland had been removed six 
weeks before. The dose is 1 to 5 c.c. three times a day, given by the mouth. 
A similar preparation is prepared in this country by Parke, Davis & Co., 
and is called "Thyroidectin." The dose is 5 to 10 grains t. i. d., in capsules. 

In most instances the patient should receive a carefully carried out rest 
cure, extending over a period of from four to six weeks, with regulation of 
the diet and massage and electricity. Sometimes a course of hydrotherapy 
is advantageous, and change of air and scene is particularly valuable if the 
patient has been subjected to nervous stress. All forms of exercise or gayety 
which tend to exhaust the nervous system should be forbidden. 

The drugs which seem to be of most benefit are those which belong to 
the class of sedatives. WTien the heart's action is very excessive, I have 
known full doses of tincture of veratrum viride to be most advantageous, 
in that they quiet the heart not only by depressing its muscle, but also by 
stimulating the pneumogastric nerve. In other instances the bromides may be 
employed. In still other cases I have seen gelsemium employed to advantage. 

The disadvantage of opium or morphine, for the production of nervous 
quiet, is the danger of establishing the "habit." This is a very real danger 
in these patients, because of their lack of nervous equilibrium. Sometimes 
belladonna may be given with advantage to quiet the circulatory and 
nervous excitement. 

Within the last twenty years a very large number of operations have 
been performed upon patients with exophthalmic goitre, with the object of 
curing the disease. In some instances the thyroid arteries have been tied. 
In others the capsule of the gland has been stripped from it and made fast 
in the wound, so that the tissues will shrivel. In still another class of cases 
the cervical sympathetic has been cut, and Jaboulay has strongly advocated 



756 DISEASES OF THE THYROID GLAND 

this measure. The value of operative procedure is, however, well summed 
up by my colleague, J. Chalmers Da Costa, who says : 

" Treat most cases medically and by rest; if medical treatment fails, 
consider the advisability of surgical treatment. 

" Do not operate if there is great hysteria; if the gland is very large, 
thyroidectomy will fail; if the gland is very small, it will do no good to 
remove it. 

" If the symptoms are urgent, if the goitre is distinct, but not excessively 
large, if it has relapsed under medical treatment, or if the patient refuses to 
submit to the necessary restrictions of medical treatment, perform thyroid- 
ectomy. 

" Take Kocher's advice, and do not promise cure, but realize that the 
patient may die or there may be a partial cure. 

"When thyroidectomy is performed do not remove the entire gland. Remove 
one lobe only, or one lobe and a half or two-thirds of the remaining lobe. 
Even so-called complete thyroidectomies are not often really complete, as a 
remnant of the processus pyramidalis is usually left behind. In addition to 
removing a part of the gland, take Kocher's advice and tie three of the four 
thyroid arteries. 

" Do not give a general anaesthetic, but produce local anaesthesia (Kocher). 
A general anaesthetic is very dangerous in goitre operations." 

In advanced cases with threatened suffocation, it may be necessary to do 
tracheotomy. If the goitre is small, if the symptoms are marked, and do 
not yield to rest and medical treatment, and the patient refuses thyroid- 
ectomy, we can perform bilateral resection of the cervical sympathetic 
ganglia. 

MYXCEDEMA. 

Definition. — Myxcedema is a disease in which extraordinary nutritional 
changes take place in the body as the result of absence, atrophy, removal, 
or inactivity of the thyroid gland. It is characterized by a peculiar swelling 
of the subcutaneous tissues, by falling of the hair, by mental failure, and by 
feebleness of the circulation. Myxcedema is closely related to cretinism in 
children. It is sometimes called "Athyrea" and "Gull's disease." 

Etiology. — The cause of myxcedema is failure of the body to receive the 
normal quantity of secretion from the thyroid gland. In this sense it may 
be considered the antithesis of exophthalmic goitre. The cause of the 
atrophy or inactivity of the gland is unknown. 

Myxcedema occurs more frequently in married than in single women, and 
it appears most commonly after thirty years of age. It affects women and 
men in the proportion of 6 to 1. 

Pathology and Morbid Anatomy. — When the thyroid gland undergoes 
atrophy, when it is removed by surgical operation, and when, as the result of 
a specific infection, as actinomycosis or morbid growth, its function is 
destroyed, myxcedema ensues. In most cases the atrophy of the thyroid 
gland can be readily recognized, but in others the gland may seem larger 
than normal. This increase in size may be due to infiltrations, tumors, cysts, 



MYXCEDEMA 757 

subacute or chronic inflammatory processes leading to an overgrowth of 
the connective tissue of the gland, and is not a sign of any actual increase in 
glandular structure. 

The state of the subcutaneous tissues is very remarkable. They are puffy 
and swollen, and if incised are found infiltrated with a mucoid or jelly-like 
material. This material is present in such excessive quantities that the 
cutaneous glands are pressed upon and their nutrition interfered with, so that 
the skin becomes dry and harsh, and the hair falls out. Nor does this process 
of infiltration cease with the involvement of the subcutaneous tissues, for 
in the liver and in the kidneys the cells are pushed apart and compressed. 
The kidneys are larger than normal, and considerably toughened in texture. 

Frequency. — Myxcedema is a rare disease, particularly in the United States. 
Physicians connected with large hospitals may see a case only once in many 
years. 

Symptoms. — The symptoms of myxoedema are infiltration of the tissues of 
the entire body, so that they appear at first glance to be dropsical, but they 
do not "pit" on pressure and are quite firm and resistant. The skin is dry, 
pallid, and poorly nourished, the hair falls till only a few strands are left, and 
the eyebrows disappear. The expression is altered by the obliteration of the 
facial lines, and by the stupidity from which the patient suffers, for a form of 
mental inertia develops. As the disease advances muscular feebleness often 
arises, so that the patient falls, and there may be difficulty in holding the 
head erect. The temperature is slightly subnormal, the heart is feeble, and 
albuminuria is sometimes present. 

Prognosis. — The prognosis depends entirely upon the treatment. If no 
specific treatment is resorted to death invariably ensues as a result of general 
asthenia or from some intercurrent malady. If specific treatment is adequate 
recovery usually takes place, provided the patient is not seen until after the 
disease is very far advanced. 

Treatment. — Aside from the use of antitoxin in diphtheria, there is no 
therapeutic measure which produces such extraordinary results and acts in 
so specific a manner as the administration of thyroid gland in myxcedema 
and in cretinism. The dried thyroid gland of the sheep should be given the 
patient in gradually ascending doses, beginning with 2 grains in capsule 
twice or thrice a day, and gradually increasing the amount until 10 to 15 
grains are taken daily, provided the patient does well on these doses and 
seems to need large quantities. When the extract of the thyroid gland is 
used, the dose is J grain three times a day to start with. Meltzer states that 
the extract and dried gland prepared by Parke, Davis & Co. have given him 
the best results. When overdoses are taken symptoms of cardiac weakness 
develop. These are dangerous and should be controlled by the use of strych- 
nine and by insisting that the patient remain in bed for several days. Indeed, 
rest in bed is the safer plan whenever ascending doses are being employed, 
After thyroid gland has been given long enough to cause great improvement, 
so that the patient is practically well, it is essential that about one-half the 
dose be continued indefinitely or at certain periods, in order to prevent a 
relapse, for the sheep's thyroid must take the place of the wasted gland in 
the neck. 



758 



DISEASES OF THE THYROID GLAND 



As these patients are very susceptible to cold, they should be carefully 
clothed and sent to a warm climate in the winter months, if possible. 

CRETINISM. 

Definition. — Cretinism is sometimes called congenital myxcedema, or the 
myxcedema of childhood, and depends upon the same causes as does myx- 
cedema, in that the curious systemic changes which develop in the patient are 
the result of an absence of the secretion of the thyroid gland. 

Cretinism occurs in two forms, as endemic cretinism and sporadic cretinism. 

The conditions leading to thyroid absence or inadequacy are not known. 
It is true that in some instances the results of the marriage of near relatives 



Fig. 101 



Fig. 102 




A case of cretinism, showing the improvement produced by the administration of thyroid gland. 

(Davisson's case.) 

or the presence of a tuberculous history has seemed to indicate that there 
might be some connection between these factors and the development of the 
disease, but in most cases these causes are absent. 

Symptoms. — The symptoms of cretinism rarely develop before the end of 
the second year, but the symptoms may be noticeable from the time the child 
is twelve months of age, when the parents usually consider that the child is 
somewhat "backward." At this time it is found" to be stunted and mentally 
dull. The head and the hands and feet may seem unduly large in proportion 



CRETINISM 759 

to the size of the trunk and limbs. The face is stupid and heavy, and the eyes 
dull. The palpebral openings are narrow and elongated, and the nose is broad 
and flat, with heavy nostrils. The lips are coarse, are apt to protrude, are 
usually held apart, and not infrequently there is a good deal of dribbling of 
saliva. The tongue is swollen, and there seems to be some weakness of the 
cervical muscles, so that the head is not well carried on the shoulders. An 
anteroposterior curvature of the spinal column is often present, so that the 
abdomen is very much protruded. The legs are short and bent, as in rickets, 
and the skin is sallow and greasy. The hair is scanty and brittle, and the skin 
is badly nourished. The temperature is subnormal, but there are no important 
changes in either the urine or the blood. The most marked alterations from 
normal in the blood are a diminution in the quantity of haemoglobin. In 
many instances the child has little more intelligence than that which is 
needed to take its food. In other cases it is vicious and dirty. 

An autopsy in a case of cretinism usually reveals an absence of the 
thyroid gland, its place being taken by a few fatty granules, or by a fibro- 
cystic growth. On opening the skull there is found to be an excess of intra- 
ventricular and interarachnoid fluid. 

Diagnosis. — There is no difficulty in diagnosticating cretinism if a typical 
case is presented. Given a patient suffering from rickets and idiocy, some 
resemblance to true cretinism may be present, but the state of the skin and 
hair and the absence of the thyroid gland in true cretinism render a separa- 
tion possible. 

Prognosis. — The prognosis in cretinism is very good, even better than in the 
myxoedema of adults, provided the treatment is instituted while the patient 
is yet a child in years. If the patient has survived till adult years are reached, 
the results are not so satisfactory and extraordinary. 

Treatment. — The treatment consists in the administration of thyroid gland 
or thyroid extract, beginning with J of a grain of the extract three times a 
day and gradually increasing it, or using 1 or 2 grains of the dry gland once, 
twice, or thrice a day, according to the size and age of the child. Under the 
administration of these substances the most remarkable change takes place 
in the patient. The first noticeable alteration is a great decrease in body 
weight, with a similar decrease in the bulkiness of the child. The skin 
becomes more moist and appears better nourished, and the expression 
improves. There is also an improvement in the color of the skin and in the 
quantity of haemoglobin in each blood corpuscle. Still later, after this pri- 
mary decrease in weight, a real improvement in nutrition takes place, and 
the child begins to gain, so that it no longer looks stunted, but appears more 
like a healthy individual. The mental improvement is perhaps the slowest 
part of the cure, and in some instances the mind never fully reaches the 
development of that of a healthy child, although the nutrition of the body may 
be excellent. The effect of the administration of thyroid upon the growth of 
the teeth is equally remarkable with that upon the general nutrition. Before 
thyroid is given the milk teeth are usually badly formed and rapidly decay; 
but if thyroid is administered freely before the permanent tooth appear, they 
are often developed as they would be in the jaws of a healthy child. 



760 DISEASES OF THE SUPRARENAL GLANDS 

DISEASES OF THE SUPKARENAL GLANDS. 

ADDISON'S DISEASE. 

Definition. — The name Addison's disease is applied to a condition in which 
the patient suffers from a characteristic pigmentation of the skin, pallor, and 
loss of strength, and in which the chief microscopic changes are alterations in 
the suprarenal bodies. 

History. — Addison's disease gets its name from Thomas Addison, the 
physician who first clearly described the malady in 1849 at Guy's Hospital, 
London. The condition did not receive attention from the profession in 
general until 1854, when Addison wrote a special monograph on the 
subject. 

Etiology and Pathology. — The cause of Addison's disease is not known in 
the sense that we recognize a cause which is responsible for all cases. In 
about 50 per cent, of the cases so far reported which have come to autopsy, 
tuberculosis of the suprarenal glands has been found. That this lesion is not 
sufficient in all cases to cause the general systemic manifestations of the dis- 
ease is proved by the fact that identical changes have been found in the supra- 
renal bodies when none of these symptoms have been present. In certain 
cases hemorrhages into the suprarenal bodies as the result of injuries have 
caused the symptoms to develop. 

As a matter of fact, the view, as to the relationship of these causes to the 
disease, expressed by Addison fifty years ago is probably correct, namely, 
that any lesion of these bodies which interferes with their function may cause 
the malady. 

In some instances the disease seems to be primarily the result of patholog- 
ical changes in the semilunar ganglia of the abdominal sympathetic nervous 
system. Rolleston has expressed the plausible view that in these cases the 
disease arises in all probability by reason of the fact that the glands are 
cut off in circulation and nerve supply by growths or inflammatory exu- 
dates. 

Morbid Anatomy. — The common lesion in cases of Addison's disease is, 
as already stated, tuberculosis, and next to this in frequency is atrophy. The 
tuberculous change is of the fibrocaseous type, except in rare instances, and 
usually begins in the medulla of the gland. The stage of infiltration is 
followed by caseation and commonly more or less fibrosis; in other words, 
there is an attempt at healing. The fibrocaseous area may be restricted to 
the adrenal or extend beyond it. Calcification is not uncommon, and 
pyogenic infection may cause abscess. The tuberculous process may be 
primary and confined to the adrenal body, as in the two cases reported by 
Symes and Fisher. 

In the form of the disease in which atrophic changes occur in the glands, 
the wasting may be so complete that only a small fibrous mass remains to 
indicate their former existence. In still others an overgrowth of fibrous tissue 
resembling the sclerosis found in the other organs of the body may take place, 



ADDISON'S DISEASE 761 

with secondary atrophy of the parenchyma. Peterson has collected 26 such 
cases. In still other cases the glands have been found to be the seat of hemor- 
rhage (adrenal apoplexy), thrombosis of the vessels, or malignant disease. 
The changes found in the semilunar ganglia and in the plexuses composing 
the abdominal sympathetic system are, as already stated, in all probability, 
indirect causes of the disease, although Hale White has shown that changes 
take place in these tissues in ordinary individuals as the result of advancing 
age. It is difficult to determine, therefore, whether the reports of changes in 
these tissues made by some observers have been really etiological factors in 
the disease. Further, a very large proportion of cases in which Addison's 
disease has been present have failed to show alterations in the semilunar 
ganglia or in the abdominal sympathetic. In some cases a hyperplasia of 
the lymphoid structures in the alimentary canal has been noted. 

Finally, it is not to be forgotten that Addison's disease may be present 
without noticeable lesions in the suprarenal bodies, and it is also a fact that 
these bodies may be almost completely destroyed by a growth or by tuber- 
culosis without any symptoms of this malady developing. 

The pigmentation of the skin is due to the deposition of pigment in the 
cells of the Malpighian stratum, and according to Earkshevitch, who studied 
the skin removed from a living subject, in the subjacent tissues. The pig- 
mented cells are supposed to obtain their pigment from the haemoglobin of 
the blood, but they contain no iron. The discoloration of the mucous mem- 
branes is due also to the deposit of pigment. The pigmentation of the 
mucous membranes is in patches, and Mann asserts that it is deposited only 
where the parts are rubbed or subjected to causes that produce hyperemia. 

That there have been, and are in existence at present, several theories as 
to the lesions which result in Addison's disease must have been evident from 
what has already been said. The only ones that have received general 
recognition have been the "nervous theory," that the disease was due to 
changes in the abdominal nervous apparatus; or the original theory of 
Addison, that it is due to failure of the suprarenal glands to carry out their 
normal function. The nervous theory has now been generally cast aside, 
and we have left Addison's own proposition modified by our extended 
knowledge of internal glandular secretion. Space does not permit a discus- 
sion of the views for and against this opinion. These can be found exhaust- 
ively, and most capably, discussed by Rolleston in Allbutt's System of 
Medicine, vol. iv. Suffice it to say, that the opinion generally held to-day is 
that these symptoms come on because the suprarenal secretion fails to find 
its way into the general economy. Changes in the sympathetic nervous 
system may also be a factor. 

Symptoms. — The symptoms of Addison's disease are chiefly those which 
are represented by the term general asthenia. The patient gives the history 
of being easily tired and, indeed, of a constant sense of fatigue. Even after 
a night's rest he feels as weary in the morning as when he went to bed. The 
sensation of feebleness is associated with profound muscular weakness as 
the disease progresses, but there is little or no true emaciation. The term 
" invincible languor " used by Rolleston well describes the patient's state. An 
examination of the heart shows its muscle is greatly enfeebled, so that the 



762 DISEASES OF THE SUPRARENAL GLANDS 

cardiac sounds are lacking in normal tone. The pulse is soft, and easily 
extinguishable by the pressure of the finger. The extremities are cold and 
the general body temperature may be subnormal. Anaemia is well marked, 
but usually not excessive, the blood cells being decreased to 3,000,000 or a 
little lower. 

No mention as yet has been made among this list of symptoms of the one 
characteristic manifestation of the malady which is practically pathog- 
nomonic, namely, the pigmentation of the skin. While its peculiarities 
would naturally lead one to speak of it first, mention of it has been delayed 
because its appearance is often delayed until the other symptoms are quite 
well developed. In other words, it usually follows and does not precede 
the constitutional manifestations of the disease. There are, however, rare 
exceptions to this, and cases have been recorded in which the pigmentation 
has been present for long periods before any other signs of xAIdison's dis- 
ease developed. The pigmentation may be over the entire body, but as a 
rule it is in patches, and chiefly affects the skin of the face, of the neck, and 
the extensor surfaces of the hands and forearms. If the mucous membrane 
of the mouth is examined the lips at the point of contact are noticeably 
darkened and the edges of the tongue, particularly on its under surface, may 
show discoloration as if ink had been taken into the mouth. 

Diagnosis. — Except in well-defined cases it may require weeks or months 
of watching to determine that a patient has this malady. Pregnancy not 
rarely is associated with the presence of pigmented spots on the skin, but 
the condition of the uterus and its contents prevent a mistake being made 
as to the cause. In some cases of hypertrophic cirrhosis of the liver there 
may be in addition to jaundice very marked pigmentation. I have under 
my care at the time this is written a man who has hypertrophic cirrhosis, 
jaundice, and such deep pigmentation of the skin that he looks as if coated 
with coal-dust. In such a case the state of the liver reveals the cause. 

In the rare malady called diabetes bronze, in which there is hypertrophic 
cirrhosis, jaundice, diabetes, and pigmentation of the skin, the state of the 
liver and urine will aid in the differentiation. In certain cases of advanced 
pulmonary tuberculosis the skin is pigmented a dirty brown, and in patches 
may be considerably discolored, but here the pulmonary state prevents con- 
fusion as to its cause. 

The prolonged use of arsenic may have a similar effect, not only on the 
extremities, but on the skin of the chest and abdomen, which may become 
much darker than normal without any neuritis being present. In syphilitics 
the site of old eruptions may be stained, and in vagabonds who are infested 
with lice, and have been much exposed to the weather, areas of discoloration 
of the skin may be present. It is said that the discoloration of the skin called 
chronic argyria, due to the prolonged use of silver internally, has been con- 
fused with the state of the skin in Addison's disease. This would be scarcely 
possible if the observer had ever seen a case of chronic silver poisoning, 
for the discoloration of argyria is a peculiar lividity rather than a pigmenta- 
tion, and it is uniform on exposed parts of the body. 

As Addison's disease is due in a large proportion of cases to tuberculosis 
of the adrenal bodies, the tuberculin test may be employed to give additional 



ADDISON'S DISEASE 763 

information in the case; but even if this test is positive the possibility of 
tuberculous foci elsewhere giving the reaction, and the fact that syphilitics 
sometimes react, should make us hesitate before resting too heavily upon 
this means of diagnosis. 

Prognosis. — It may be stated that given a patient with Addison's disease 
developed so far that a diagnosis is certain, then death from the malady is 
certain also. Lewin in a collection of 500 cases found that 5 were cured 
and 28 improved. In the 2 cases I have seen, 1 of which is now under 
observation, the disease had, at times, certainly been arrested in its progress 
under the use of full doses of suprarenal gland. Because of the gradual 
development of the malady, its average duration is difficult to determine, 
but its course is not very rapid. Wilks believes it to be about eighteen 
months, but in some cases it lasts for years. Very rapidly fatal cases are 
also on record. 

Treatment. — The question of the proper plan of treatment of Addison's 
disease cannot be answered positively until the pathologist is able to give us 
a clear conception of the morbid processes which produce the chain of 
symptoms already described. The very fact that different pathological 
changes, or diseases, affect the suprarenal bodies, and so produce the symp- 
toms of this malady, indicates that the therapy must vary with the cause. 
Theoretically the use of suprarenal gland of the sheep is indicated in every 
case, but practical experience has shown that only in a small proportion of 
those cases in which it has been used has it done good. It is not, therefore, 
to be compared to the value of thyroid gland in myxcedema or cretinism. 
It has been proved that suprarenal gland has little effect on blood pressure 
if it is taken by the stomach, and that its active principle w T hen in concen- 
trated form often causes abscess when it is given hypodermically. Probably 
the best plan is to give the patient adrenalin chloride in normal salt solution 
by hypodermoclysis every day or every other day, using 1 to 2 drachms of 
the adrenalin chloride (1:1000 solution), as put upon the market, to a half- 
pint or pint of saline fluid. When the desiccated gland is used by the 
mouth, from 2 to 10 grains may be given three times a day in capsule. It 
is unfortunately true that even when the adrenalin gland is freely used, the 
disease is, at the best, only delayed in its progress in most cases. 

Adams has collected 97 cases treated with suprarenal gland. Of these 
7 were made worse, 43 experienced no real benefit, 31 showed marked 
improvement, and 16 were said to be cured. In the successful cases the 
gland was given solely by the mouth. If the patient is at all feeble he should 
be kept in bed, not only because in this manner we conserve his flagging 
energies, but also because a number of cases of syncope and sudden death 
from this disease have occurred in patients who have made a sudden effort. 
An easily digested diet, the avoidance of purgatives which may induce 
dangerous purging, and the use of iron and arsenic as tonics form the rest 
of the treatment. 



764 DISEASES OF THE SPLEEN 



DISEASES OF THE SPLEEN. 

Diseases of the spleen occurring independently of other diseases may be 
said not to exist. In myelogenous leukaemia, in splenic anaemia, in 
malarial fever, and in cases of hepatic cirrhosis or heart disease, the spleen is 
often greatly enlarged, but in no case is this condition primary. So, too, 
in the prolonged infectious fevers, such as typhoid fever, the spleen is 
usually swollen. 

In some cases the surface of the spleen may be traversed by a crevice or 
indentation which almost divides its body into different parts, and in 
others there may be found an accessory spleen or accessory spleens in 
nearby parts of the abdominal cavity. In very old people the spleen is often 
greatly atrophied. 

An infarct of the spleen is due to an embolus which usually has its origin 
in the heart, or which arises from some area of septic infection, or in other 
cases a thrombus forms in the splenic vein and produces a similar effect. 
The latter condition is the cause of the infarct met with in typhoid fever 
and in leukaemia. 

Abscess of the spleen as the result of septic infection is by no means rare, 
and such abscesses always depend upon infected emboli. 

Hydatid cyst of the spleen is rare not only because hydatid cyst is rare in 
this country, but also because it seldom develops in this gland even in those 
parts of the world in which hydatid disease is common. 

Malignant growths in the spleen are among the rarest pathological lesions. 
Primary growths are practically unknown and secondary growths are also 
very rare. From statistics at St. George's Hospital, London, collected by 
Walker, it is found that in 161 cases of carcinoma involving all parts of the 
body secondary growths appeared in the spleen seven times, and in 50 
cases of sarcoma the spleen was affected once. Taylor in 677 cases of 
carcinoma, epithelioma, and sarcoma found secondary growths in the 
spleen in twenty-three instances. Sometimes in cases of cancer of the 
gall-bladder or of the pylorus the growth extends to the spleen by direct 
invasion. 

Movable spleen, like movable kidney, is a condition in which this organ 
wanders away from its normal position so that it may be found far removed 
from its ordinary area, and even so low as the pelvis. Its displacement is 
usually associated with a sense of dragging in the left hypochondrium or 
loin, and if the pedicle becomes twisted great pain may be suffered, with fever, 
collapse, and finally necrosis of the splenic tissues. Osier records a case in 
which this occurred and in which abdominal section resulted in recovery, 
although a considerable part of the spleen was lost by sloughing. 

It is necessary to separate wandering spleen from floating kidney. This 
can be done by the discovery of the splenic notch, by the greater sense of 
resistance in the otherwise normal kidney, and by the presence of reson- 
ance on percussion in the splenic area where splenic dulness is usually 
demonstrable. 

Rupture of the spleen is a rare accident, but occurs occasionally in those 



SPLENIC ANEMIA 765 

who, while suffering from great congestion or enlargement of this organ, 
meet with an accident in which the splenic area is subjected to a severe 
blow. Cases are also on record in which the spleen has ruptured as the 
result of great distention. Rupture of the spleen will be found discussed 
under Malaria. The symptoms are those of internal hemorrhage and 
demand an immediate abdominal section. 

The treatment of wandering spleen consists in the wearing of a bandage 
and pad to retain the organ in its place, and, if need be, we may resort to 
an operation to fix it by causing adhesions to form around it. Extirpation 
of the spleen has been advised in cases in which the symptoms are very dis- 
tressing, but this should be done only when the condition is very urgent; 
for while the spleen has been proved to be not necessary to life, its removal 
jeopardizes existence and the patient passes through a long period of con- 
valescence before recovery occurs. 



SPLENIC ANEMIA. 

Definition. — Among the types of splenomegaly the condition known as 
splenic anaemia is one about which great difference of opinion has existed. 
Its existence has been denied by some physicians and asserted by others. 
At present it is generally considered that a distinct morbid state to which 
this name may be applied really exists. It is essentially a condition of 
anaemia with enlargement of the spleen, and lacks all of the additional 
conditions which are associated with these states in other maladies, as, for 
example, leukaemia, lymphadenoma, or lymphatic leukaemia. 

Etiology. — This is unknown, but some suppose it to be due to intestinal 
infection. 

Pathology and Morbid Anatomy. — An examination of the spleen in this dis- 
ease shows that it is not only greatly enlarged, but that it shows signs of the 
existence of a perisplenitis with localized areas of capsular thickening. In 
some portions of the organ old infarcts may be found which in turn have 
caused puckering of its surface or depressed scars. When the spleen is cut 
it is found to be more resistant to the knife than normal, and it is somewhat 
fibroid. If a section is placed under the microscope it is found that the con- 
nective tissue is increased and the lymphoid elements wasted. The Mal- 
pighian bodies are fibroid. There is also in some cases a marked prolifera- 
tion of the endothelial cells which line the blood sinuses. These cells are 
very large and may be so numerous as to fill these spaces till they resemble 
an endotheliomatous growth. 

Dock and Warthin have called particular attention to hyperplasia of the 
haemolymph nodes and thrombosis of the splenic vein. The association of 
splenic fibrosis with enlargement and cirrhosis of the liver constitute the 
type studied by Banti (Banti's disease), and this is thought to be a later 
stage of the process characterized in its early manifestations by splenic 
enlargement. 

Symptoms. — The symptoms of splenic anaemia are pallor, dyspnwa on 
exertion, and feebleness associated with enlargement of the spleen. An exami- 



766 DISEASES OF THE SPLEEN 

nation of the blood does not throw any great light on the character of the 
case. Indeed, the blood changes are often in no way different from those 
of lymphadenoma or gumma of the spleen. The red cells number about 
3,500,000, and the haemoglobin equals about 50 per cent. When the disease 
is advanced poikilocytes and nucleated red cells are present. The white 
cells are not increased as in leukaemia, but usually are below the normal 
number, amounting to about 4500 per c.mm. 

Diagnosis. — The diagnosis of splenic anaemia is very difficult and should 
not be reached until a careful study of the patient's past and present condi- 
tion has been carefully made and his blood repeatedly examined. A con- 
siderable number of cases of so-called splenic anaemia have proved to be 
other diseases when studied longer or examined postmortem. All possible 
causes for enlargement of the spleen should be excluded before a decision 
is reached. 

Splenic anaemia must be separated from the " anaemia infantum " of von 
Jaksch, in which the spleen is enlarged, but in which the changes in the 
blood and in the liver and spleen in no way correspond to those seen in 
splenic anaemia. This condition must also not be confused with enlargement 
of the spleen due to syphilis with the formation of gummata; nor with sar- 
coma of the spleen ; nor with the anaemia of chronic malarial poisoning, with 
secondary splenic enlargement, nor with amyloid disease. It must also be 
separated from the anaemia associated with enlargement of the spleen sec- 
ondary to cirrhosis of the liver, and from a condition described by Gaucher 
of chronic inflammation of the spleen (epitheliome primitive). Sometimes, 
too, in children suffering from rickets and marasmus with gastrointestinal 
intoxication, there is a considerable degree of anaemia and some enlarge- 
ment of the spleen. Such cases have been thought to represent an infantile 
form of splenic anaemia, but the subsequent history of the patient seems to 
contradict this view. 
Rolleston gives the following as the clinical characteristics of splenic anaemia: 

1. Splenic enlargement which cannot be correlated with any known cause. 

2. Absence of enlargement of the lymphatic glands. 

3. Anaemia of a type midway between secondary anaemia and chlorosis. 

4. Leukopenia, or at most no increase in the number of white blood 
corpuscles. 

5. An extremely prolonged course lasting years. 

6. A tendency to periodic hemorrhages, especially from the gastrointes- 
tinal tract. 

Prognosis. — The prognosis under medical treatment is always unfavorable. 

Treatment. — The treatment consists in the administration of full doses 
of arsenic, but, so far as we know, no method of treatment has yet been 
devised which materially alters the general progress of the disease. 

According to Harris and Herzog, of 19 cases subjected to splenectomy, 
14 recovered. To these series Scott has added 6 cases with 4 recoveries. 
Queen and Duval collected 6 cases and added 1 original case in which 
removal of the spleen was followed by a cure. They state in addition that 
a beginning hepatic cirrhosis may be arrested by splenectomy, although it 
is difficult to understand how this operation can exercise this effect. 



HODGKIN'S DISEASE 767 



BANTI'S DISEASE. 



Under the name of Band's disease a condition characterized by enlarge- 
ment of the spleen, anaemia, cirrhosis of the liver, jaundice, and ascites is 
met with. It is thought by some that Banti's disease is a terminal stage of 
splenic anaemia; but, on the other hand, it is certain that this is not always 
the case. The disease is very rare. 

HODGKIN'S DISEASE. 

Definition. — Hodgkin's disease is a condition in which there is marked 
swelling and overgrowth of the lymphatic glands, both internal and external, 
with a moderate degree of anosmia which is in no way peculiar to this malady. 
The spleen is usually enlarged. The overgrowth of the lymph nodes and 
lymphatic tissues generally is closely allied to malignant lyinphadenoma. 
Another name for the disease is " pseudoleukemia." 

History. — Although a difference between this state and scrofulous enlarge- 
ment of the lymph nodes had been made prior to 1830, it was not until 
Hodgkin in 1832 described cases seen at Guy's Hospital that it was gen- 
erally recognized. In 1856 Wilkes in London and Bonfils in France still 
further illuminated the subject. 

It was not until Virchow completed his work on the histology of the blood 
that Hodgkin's disease became clearly differentiated from leukaemia of the 
lymphatic type. The fact that changes of a peculiar character exist in the 
lymph nodes was not known until 1897, when several investigators, notably 
Fischer, described them. 

Etiology. — The cause of Hodgkin's disease is unknown. Within the last 
few years the view that it was a peculiar condition due to infection by the 
Bacillus tuberculosis gained a number of adherents, and there are without 
doubt certain facts connected with the malady which tend to substantiate 
this view. On the other hand, it may be considered as pretty well settled 
that this view is erroneous, for Dorothy Reed, Longcope and Simmons have 
published careful investigations which seem to prove that Hodgkin's disease 
possesses definite pathological characteristics peculiar to itself. The disease 
is more frequent in males than in females, and in adults than in childhood. 

Pathology and Morbid Anatomy. — The changes which are most marked 
are enlargement of the lymphatic glands at first in limited areas and later 
all over the body. The cervical and inguinal glands are usually the most 
prominent, and the outlines of the neck may be completely obliterated. 
At autopsy the retrobronchial and retroperitoneal glands may be found 
enormously increased in size, forming a mass as large as the arm, and pressing 
on adjoining tissues such as the thoracic duct and the bloodvessels. The 
affected nodes are discrete and regularly enlarged. Their consistency varies. 
Sometimes they are firm and dense, at others so soft as to fluctuate. The 
cut surface of these glands is translucent, gray, or more rarely yellowish, 
and the tissues of the glands bulge forward. An overgrowth of lymphoid 
tissue may take place at the apices of the lungs and lead to a diagnosis of 



768 DISEASES OF THE SPLEEN 

tuberculosis. Death may be due to pressure on the thoracic bloodvessels, 
and perhaps to pulmonary infiltration and exudation. Osier asserts that 
infiltration of the lung does not occur in this disease, and that when such 
an infiltration does take place the disease is true lymphosarcoma. There 
is also enlargement of the spleen with overgrowth of the lymphoid bodies, 
which are grayish-white in appearance, and consist of lymph follicles held 
together by a reticulum of connective tissue. The marrow of the long bones 
may be lymphoid or purulent in appearance, as it is in some cases of 
myelogenous leukaemia. The liver and kidneys may also be enlarged 
and contain lymphoid masses. 

The characteristic lesions of Hodgkin's disease are an early increase in the 
lymphadenoid tissues with a proliferation of endothelial cells, the formation 
of uninuclear and multinuclear giant cells, thickening of the reticulum, and 
lastly an overgrowth of the connective tissue of the lymph nodes to the 
development of which the increased density of these masses is due. Eosino- 
phil cells in most cases are present in very large number in the lymph nodes 
and in the bone-marrow. Not only is the disease characterized by these 
changes in the pre-existing lymph nodes, but there is a constant formation 
of new nodes which soon become similarly affected. 

The blood changes are most variable. In some cases they are moderate, 
in others severe, in that the red cells may be decreased in number, but even 
when the patient is at death's door there may be fully 3,000,000 cells present. 
The red cells are not altered in a manner which is in any way characteristic. 
The changes consist solely in a diminution in number to a moderate degree, 
and in a reduction of the amount of haemoglobin. The leukocytes are not 
increased as in true leukaemia, but are often actually diminished. Pinkus 
thought a relative increase of the lymphocytes constant, but this change was 
present in but 1 of Longcope's 7 cases, although a very large proportion of the 
white cells may be of this variety. Occasionally the increase of white cells 
may rise to the number seen in certain inflammatory states, as from 30,000 
to 40,000. In the later stages the blood picture may assume all the charac- 
teristics of an intense secondary anaemia. 

Symptoms. — The symptoms of pseudoleukemia are those of ordinary 
severe secondary anaemia, with shortness of breath and palpitation of the 
heart on exertion. The enlarged masses of glands in the neck and groins 
may be very characteristic in appearance, associated as they are with pallor 
and pufjiness of the face. When the internal glands are primarily and chiefly 
involved the diagnosis from tuberculosis may be difficult because the pressure 
may cause consolidation with patches of dulness on percussion, and because 
a distinct febrile movement is often present. 

These masses by producing pressure may give rise to paroxysms of cough 
or of pain or constant dyspn&a. When the inguinal glands are affected 
nedema of the lower extremities may develop, and shooting pains may be felt 
in the legs. After the glandular masses become very large, superficial 
sloughing may occur, and therefore the resemblance to a suppurating tuber- 
culous mass may be increased (Fig. 103). I have seen an actinomycosis 
of the neck produce similar symptoms. Bronzing of the skin may occur. 
Moderate fever is often present. It may be low and regular or high and 



HODGKIN'S DISEASE 



769 



irregular in type. Occasionally it has an intermittent character with sharp 
exacerbations, so that it resembles intermittent or remittent malarial fever. 
Jaundice due to pressure on the bile-ducts may appear. 

Additional symptoms met with in some cases are murmurs in the great 
vessels, produced partly by the anaemia but chiefly by the pressure caused 
by the growths. Deafness due to closure of the Eustachian tubes by growths 
in the pharynx and unequal pupils due to pressure on the cervical sym- 
pathetic, may be present. 

Fig. 103 




Hodgkin's disease. 

Diagnosis. — From true leukaemia pseudoleukemia is to be separated 
by the absence of the large excess of leukocytes, and the lack of the leuko- 
cytes peculiar to that disease. From enlargement of the lymph glands due 
to tuberculosis it is to be separated by the test with tuberculin (see Tuber- 
culosis), and by the fact that tuberculosis rarely produces enlargement of 
the cervical glands on both sides and in both groins, and by the absence of 
a tuberculous focus elsewhere. When doubt exists a part or all of an 
enlarged mass of glands may be excised and examined microscopically to 
determine the character of the disease. 
49 



770 DISEASES OF THE SPLEEN 

In many cases the clinical diagnosis is most difficult. I have seen the 
most eminent clinicians mistake this malady for tuberculosis. Very rarely 
a form of multiple lipoma distributed in the lymph-node areas closely 
resembles Hodgkin's disease; the picture may further be confused by the 
presence of glandular and calcific masses in the fatty tumors; such a case 
has been observed in the Jefferson Medical College Hospital; Chantemesse 
and Podwyssotsky figure such a case under the name adenolipomatosis. 

Prognosis. — The prognosis in Hodgkin's disease is absolutely bad. Not 
one recovers. These patients have periods of improvement when courage 
runs high, but after all the inevitable progress is downward. Death comes 
from interference with circulation or respiration or by general asthenia. 

Treatment. — The best treatment is the use of arsenic in full doses. Re- 
cently excellent results have been obtained by Senn, Finch, and others in 
some of these cases by the use of the a--rays, the parts involved being exposed 
to the rays, repeatedly, over a long period of time. 



STATUS LYMPHATICUS. 

Definition. — The term status lymphaticus or " lymphatic constitution," 
sometimes called " constitutio lymphatica," is applied to a state which occurs 
chiefly in children or infants, and which is characterized by %perplasia of 
the lymph nodes, the thymus gland, and the spleen, and by a hypoplasia of 
the heart and arteries. The lymphoid bone-marrow is also affected. The 
fact of particular interest is that patients with this condition sometimes suffer 
sudden death, which, coming on in children who, on superficial examination, 
appear unusually robust and plump, is all the more startling. 

History. — As long ago as 1614 Plater made note of the fact that the thymus 
gland was found enlarged in certain cases of sudden death, and in 1830 Kopp 
described a form of difficult breathing which he called "thymic asthma," 
and which he considered was due to pressure upon the trachea by an enlarged 
thymus gland. This view, which was apparently disproved by Friedleben in 
1858, received no further support until in 1888 it was revived by Grawitz, 
only to be controverted again by Paltauf in 1889. 

Etiology. — The etiology of this state is not known, but it is apparently a 
congenital fault, and is associated with a low decree of vital resistance to 
infection. Hedniga has reported an instance in which out of a family of 
nine children, five died of this malady. 

Blumer has recently put forward certain facts which seem to show that 
this condition is the result of the development in the body of a toxic sub- 
stance, a cytotoxin. To this state the term lymphotoxismus has been applied. 
According to this view, the overgrowth of the lymphatic tissues in the differ- 
ent parts of the body is a sequence of the action of this poison and not the 
cause of its development. 

Pathology and Morbid Anatomy. — An autopsy in a case of this character 
reveals an overgrowth and swelling of the lymph glands in the thorax, abdo- 
men, and cervical and inguinal chains, and enlargement of the tonsils. The 
lymph nodes of the intestinal tract are very markedly swollen and sharply 



STATUS LYMPH ATICUS 771 

defined. The spleen appears larger than normal, and the lymphoid tissue 
of the Malpighian bodies is in a state of overgrowth. The changes in the 
thymus gland are, however, the most important, because it is supposed that 
the sudden congestion, hyperplasia, and swelling of the gland which occurs 
causes death by pressure upon the great vessels of the neck and upon the 
trachea. The thyroid gland may also be enlarged. If the shafts of the long 
bones are opened, yellow marrow is found to be substituted for red marrow. 
The heart and aorta are poorly developed. 

Congestion and oedema of the lungs have been found in some cases at 
autopsy, and in others atelectatic patches have been discovered. In all 
of these cases the pressure upon the air passages was responsible for these 
changes. 

Symptoms. — There are no symptoms in any way characteristic of this state, 
except that the child may, on close examination, be found to suffer from 
rickets, some enlargement of the lymphatics, and a rather feeble heart. The 
recollection of the possible presence of this state should make the physician 
particularly careful when administering an anaesthetic to a child of the 
lymphatic type, especially if the condition to be relieved is overgrowth of the 
lymph tissues, such as the postnasal adenoids and spongy tonsils, as sudden 
death may ensue. Hand has reported a case in which tetany was present. In 
a case recently reported by Musser and Ullom an unusually robust and well- 
developed, but overfat, boy of five years suffered from a little hoarseness on 
one day, and on the next seemed about as w^ell as usual. That same night 
he went to sleep at the usual time, but at 2 a.m. was seen to be somewhat 
pinched and livid. A few hours later he became more cyanosed and pre- 
sented a rapid pulse and labored breathing. His respirations were character- 
ized by loud rales in the bronchial tubes and larynx. His temperature grad- 
ually rose till it reached 105°, at which time convulsions developed, and he 
died shortly afterward. The urine was loaded with albumin. 

Several cases of so-called teething convulsions in infants have been found 
at autopsy to be due to this disease. Sometimes the child is found dead 
in bed. 

Treatment. — We know so little of the cause of this state, and so few cases 
have been subjected to treatment, that no definite plan of treatment can be 
outlined, save that fresh air and sunshine and iron iodide, and arsenic are 
useful. 

If the thymic enlargement be demonstrable, operation might be resorted 
to. Rehn opened the mediastinum, drew the gland forward and stitched it 
in position; recovery followed. Carter operated on a case for tracheal 
obstruction, recognized the thymic enlargement, and introduced a tube which 
gave temporary relief, but the child died. 



772 DISEASES OF THE THYMUS GLAND 



DISEASES OF THE THYMUS GLAND. 

The thymus gland is found well developed in infants up to the second year 
of life, after which time it gradually decreases in size till it reaches a degree 
of degeneration and atrophy in which it may be said to no longer exist. This 
occurs about the time of puberty. In fully developed adults it is represented 
by a small aggregation of lymphoid and fatty cells. Very rarely the thymus 
persists without any change in its tissues, even in adult life. When it remains 
large, or increases in size as the result of disease, as in the status lymphaticus, 
it may cause symptoms by pressing on the trachea and the great vessels of 
the neck and chest. 

Diseases of the thymus gland are very rare. In some cases a state of 
so-called hypertrophy is present, but this is rarely a true hypertrophy, the 
gland being swollen and filled with lymphoid cells. Occasionally minute 
hemorrhages may take place into its tissues or beneath its capsule. Abscess 
has been recorded as having occurred, and growths, benign and malignant, 
have been found in its tissues. It has been found affected by tuberculosis. 

Many years ago enlarged thymus was supposed to be the cause of spas- 
modic croup. That an enlarged gland may cause some interference with 
respiration is conceivable, but we now know that spasmodic croup is usually 
due to rickets or postnasal adenoids. Those interested in this subject should 
read Jacobi's essay published in 1888 in the Transactions oj the Association 
of American Physicians } vol. iii. p. 297. 



DISEASES OF THE BLOOD. 



ANiEMIA. 

Definition. — The word anaemia signifies a state of the blood in which there 
is lacking the normal quantity of red cells or of haemoglobin in these cells. 
When the cause of this state is due to some disorder of the blood-making or 
blood-destroying tissues, it is called essential or primary anaemia. When due 
to some other cause, such as hemorrhage or one of the acute infectious dis- 
eases, it is called secondary anaemia. Fortunately, most cases of anaemia 
belong to this latter class, and they will, therefore, be considered first. 

Secondary Anaemia. 

Secondary anaemia arises from a host of causes and is characterized in most 
cases by a diminution in the number of the red cells, and an even greater 
reduction in the haemoglobin content of each cell. In some cases it comes on 
as a result of breathing vitiated air, as in factory girls and stenographers. 
In other cases it is due to overwork and insufficient or improper food, and in 
still other cases to protracted digestive disturbance or to chronic constipation, 
which, by causing autointoxication, is the active factor in producing the 
condition. The late Sir Andrew Clark was an earnest exponent of this view. 

Hemorrhage is, of course, a very potent cause. When it is profuse the 
change appears so promptly that the cause is evident, but in many cases 
anaemia arises as the result of repeated small losses of blood, as from hemor- 
rhoids when the patient is at stool. Under conditions of hemorrhage, 
nucleated cells and a few poikilocytes may be found. After a single large 
hemorrhage the rapidity of recovery is extraordinary, being more rapid than 
when the loss of blood has been prolonged. Cases are occasionally met with 
in which, by reason of lack of regenerative power in the blood-making organs, 
a sharp hemorrhage is followed by death in a short time. 

Toxic states due to renal disease or to the various infectious maladies, 
particularly malaria and syphilis, often cause anaemia, and prolonged lacta- 
tion, frequent child-bearing, and the growth of tumors of large size also 
produce it. When the tumors are malignant, the anaemia is also partly toxic. 
Not infrequently we meet with cases in which the anaemia is due to chronic 
metallic poisoning, as from arsenic, lead, and mercury. In other instances 
the anaemia is due to intestinal parasites, such as the Ankylostomum duo- 
denote or the tapeworm. 

In all cases of marked and apparently causeless anaemia, the possibility of 
the condition being due to intestinal parasites should be borne in mind, and 

(773) 



774 DISEASES OF THE BLOOD 

the stools examined, not only for the ordinary tapeworm, but for uncinaria 
as well. Further than this, the marked increase in the eosinophiles in the 
blood in nearly all cases of parasitic infection should be recalled. Walker has 
collated the following interesting table in this connection: 









Large 




Eosinophiles. 


Polymorphonuclears. 


mononuclears. 


Normal 


1 to 4 per cent. 


60 to 70 per cent. 


5 to 8 per cent. 


Taenia . 


. 6 to 13 " 






Ankylostoma duodenale 


12.43 " 






Filaria medinensis . 


6 to 36 " 






Filaria loa 


53 " 


23 




Oxyuris vermicularis 


0.4 to 13.7 " 






Bilharzia hsematobia 


16 to 48 " 


44 to 58 


12.5 " 



He makes the interesting statement that a practical application of this has 
been already made. . In the feces obtained from one of the closets in a large 
college the eggs of the Anhylostomum duodenale were found. The pupils 
who had used the receptacle on the specified day were asked to submit them- 
selves to examination, but their feces yielded negative results. An examina- 
tion of the blood of each pupil was made, eosinophilia was observed in 2 
cases, and ova subsequently detected in their feces. 

Symptoms. — The symptoms of secondary anaemia vary greatly in different 
individuals, some patients with marked pallor presenting no other noteworthy 
symptoms, while others whose cheeks have color, nevertheless, suffer from 
'palpitation and dyspnoea on exertion. It is important to bear in mind that 
there are fat anaemics and red-cheeked ansemics, and that many persons who 
look pallid really have a normal number of red cells and a normal percentage 
of haemoglobin. Headache, neuralgia, loss of appetite, constipation, and 
attacks of syncope are sometimes due to anaemia, and in women amenorrhea 
is often due to this cause. 

Diagnosis. — The diagnosis between secondary and primary anaemia is to be 
made by the history of the patient, and chiefly by the fact that the abnormal- 
ities, as to the shape and character of the red cells found in the primary 
anaemias (which see), are far more marked than in the secondary forms. 

Treatment. — In the treatment of secondary anaemia three things are abso- 
lutely essential: the removal of the cause, if possible, the institution of a 
proper diet, and a hygienic mode of life, and the administration of iron and 
arsenic, and often of the bitter tonics, in order that the condition of the blood 
may be directly improved. If the method of life of the patient is unhealthy, 
it must be corrected, and, above all, plenty of fresh air and sunshine must be 
obtained. The sleeping-rooms should be well ventilated, and the patient 
must be dieted in such a way that the bowels are moved regularly and 
adequately every day, at least once, for constipation, as already stated, is 
usually present, and is often the cause. Under these circumstances aloes and 
cascara sagrada are probably the best laxatives to administer, particularly 
if iron is given. When persistent diarrhoea is the cause of the anaemia, I have 
found that Rockbridge Alum Spring water is a useful remedy, and in some 
instances it is advisable to give one of the astringent preparations of iron like 
the dried sulphate in the dose of J to J grain three times a day. If the 



ANEMIA 



775 



Fig. 104 



anaemia is due to a loss of blood by hemorrhoids, this loss must be arrested 
by local treatment. The appetite should be stimulated by the use of drugs 
like nux vomica, quinine, or other bitter tonics like cardamom or gentian. A 
good prescription for many of these cases is a pill composed as follows: 

Be — Ferri redacti . . . . . . . . gr. v. 

Acid, arsenosi . . . . . . . . gr. J. 

Ext. nucis vomicae ....... gr. v. — M. 

Ft. in pil. No. xx. 

Sig. — One t. i. d. after meals. 

The nux vomica may, in some cases, be replaced by 2 grains of quinine. 
If the digestion is impaired, hydrochloric acid and pepsin, or pancreatin and 
bicarbonate of soda, or taka-diastase in 2 to 3 grain doses with meals is 
advisable. 

Primary or Essential Anaemias. 

Chlorosis. Definition. — Chlorosis is a condition of the blood usually met 
with in young girls, and characterized by a marked diminution in the quantity 
of haemoglobin, and by a less marked decrease in the 
red cells. Until recently it was considered a second- 
ary anaemia but haematologists now class it in the 
primary anaemias chiefly because it is believed to be 
due, at least in part, to defective haemogenesis. 

Etiology. — There are still many who believe that 
chlorosis is a secondary anaemia. It is certainly 
associated with many causes of secondary anaemia, 
such as constipation, inanition, and bad air. What- 
ever influence these causes may have, there can be 
no doubt that the processes which take place about 
the age of puberty in the female sex are closely con- 
cerned in its production, for the disease is scarcely 
ever met with except at a period of life near these 
changes. Occasionally, however, it develops in later 
life, and it is then called "chlorosis tarda." Bramwell 
and others have shown that there is also a heredi- 
tary influence. 

The two chief causes are a natural predisposition 
to anaemia and an inability to utilize iron from the 
food. Some believe that the intestinal mucosa is at 
fault, others that the spleen is functionally perverted, but, as Ewing well says, 
there can be no doubt that chlorosis results from a functional insufficiency 
of the bone-marrow, which is prone to occur at puberty. 

Pathology. — The following are the chief changes in the blood : The chief 
alteration is the decrease of the haemoglobin in each corpuscle, so that a low 
color index is one of the points necessary to a diagnosis of the disease. So 
low a percentage of haemoglobin as 10 has been recorded by Bramwell, but 
the average low limit is from 30 to 40 per cent., and the color index about 
0.5 per cent. The second change is a diminution in the number of the red 



47 If 


46 


45 I 


44 




42 / 






39 \ 


38 1 \ 


37 1 


36 [ 


35 1 


34 1 I 


33 ft \ 






w 30 n_ i 


LU 29 


f> 28 i 




°!6 1 ... 






CC 23 f 


m 22 \ 




n 20 J 


2 19 j-\- /I 


18 I M 


17 


16 


15 




13 




11 


10 ft 


9 I ^ 


8 * \ 


7 1 




5 f X 


4 ' 1 r 


3 j V \. 


a / » W 




, ;~ 



Age incidence of chlorosis. 
(Bramwell.) 



776 DISEASES OF THE BLOOD 

cells, but usually this is not so marked. Taking the normal for a woman as 
approximately 4,800,000 to the cubic millimetre, the fall is usually not more 
than from 500,000 to 1,000,000. When a very great fall in the number of red 
cells is present, they may amount to only 2,000,000, but in such a case a sus- 
picion of pernicious anaemia comes forward. 

If the chlorosis is severe, the red cells vary as to size and shape, and a 
number of large red cells, with a full complement of haemoglobin, may 
be present. As a rule, the size of the red cells is reduced. Imperfectly 
formed cells (poikilocytes) are found, but they are present in very small 
numbers. Granular degeneration of the red cells has been particularly 
well studied by the chief of my medical clinic, Dr. J. C. Da Costa, Jr., and 
by Stengel, White, and the younger Pepper. 

The leukocytes in cases of chlorosis do not suffer much change, as a rule, 
but some patients show an increase of the lymphocytes. Dr. Da Costa 
has shown that most of these are large lymphocytes, and that the 
lymphocytes may amount to 40 per cent, of all the white cells. The 
specific gravity of the blood is reduced pari passu with the haemoglobin. 
Although extravascular coagulation is retarded, in some cases there is a 
tendency to thrombosis. 

Aside from the blood changes, a state of hypoplasia of the tissues of the 
heart and larger arteries is often present, but this condition is not peculiar to 
chlorosis, but to the lymphatic constitution. When recovery begins to take 
place the number of undersized red cells decreases and the cells of normal 
size increase their haemoglobin content. 

Symptoms. — The symptoms of chlorosis are a peculiar pallor of the skin, 
which often has a greenish hue, whence the name "green sickness." The 
patient is nearly if not always plump and possessed of a good quantity of 
subcutaneous fat. Occasionally the superficial vessels are well supplied with 
blood, so that the patient is ruddy, thereby misleading the physician who fails 
to study the blood. This type is called chlorosis florida. The subjective 
symptoms are dyspnwa on exertion, palpitation of the heart, vertigo, and 
perhaps attacks of partial syncope. Constipation is nearly always marked. 
Headache is quite constant, and there is usually a most persistent absence of 
appetite. There is also mental depression and apathy. Physical examination 
will reveal a diastolic haemic murmur at the third left costal cartilage, and over 
the right carotid artery a bruit is often heard. 

The complications of chlorosis which are serious are the development of 
thrombi in the veins of the legs and in the cerebral sinuses. From such 
thrombi fragments may arise, which may result in pulmonary embolism. 
Slight fever may occur, but the hands and feet are usually cold. Amenorrhcea 
is a very constant symptom. 

The blood changes, as discovered by the haemoglobinometer and haemato- 
cytometer have already been described. 

Diagnosis. — The well-nourished state of the chlorotic patient is also 
present in pernicious anaemia, but the differentiation is found in the blood 
count (see Pernicious Anaemia), for in that disease the decrease in the white 
cells is usually marked. The irritability of the heart must not be taken for 
a sign of cardiac disease because a murmur is present, nor, in the absence of 



ANEMIA 777 

urinary changes, should the puffy face and ankles be thought to be due to 
renal disease, unless the urine reveals albumin and casts. 

Prognosis. — The ultimate prognosis in cases of chlorosis is usually very 
good, but a long period often passes without much improvement. When the 
number of the red cells is not greatly reduced and they are normal in shape 
and size, recovery under proper treatment is usually rapid. This holds true 
even if the color-index is very low. When the red cells are as low as 3,000,000, 
are badly shaped, and many of them undersized, the prognosis as to rapid 
recovery is bad. So, too, when the lymphocytes are very numerous, a speedy 
cure is rarely seen. Relapses are very frequent. 

Treatment. — The treatment of chlorosis does not differ materially from 
that which was given for the treatment of ordinary secondary anaemia, except 
that chlorotic patients are usually more obstinately constipated, and, 
therefore, particular attention must be given to the state of the bowels. 
Fresh air and sunshine are also very essential in these cases. More important 
than all, it must be remembered that chlorotic patients usually need very 
much larger quantities of iron than do ordinary anaemic cases. W T hether this 
is due to an inability to absorb iron or whether there is an excess of sulphides 
in the bowels, which change a goodly portion of the iron into a sulphide of iron, 
is not known. During the winter months chlorotic patients usually do best 
at seaside resorts or at places like Lakewood, N. J., which are low in altitude. 
In the summer months they should be sent to high altitudes, varying from 
3000 to 5000 feet, unless these high altitudes tend to increase palpitation of 
the heart and dyspnoea. 

Pernicious Anaemia. Definition. — Pernicious anaemia is a disease of 
the blood arising from faulty haemogenesis and excessive haemolysis or 
blood disintegration. It is a fatal malady characterized by three chief 
changes, viz., an extraordinary decrease in the number and alterations 
in the morphology of the red cells and by certain changes in the bone- 
marrow. 

History. — Andral in France, in 1821, reported cases of what was probably 
this disease, and Channing in Boston recognized them in 1832. Pepper and 
Tyson showed the bone-marrow changes in 1875. Sorenson, in 1874, made 
the first observations as to the number of the red cells, reporting cases with 
only 470,000 corpuscles. 

Etiology. — The etiology is still unknown, but it is probable that certain 
of the causes of ordinary secondary anaemia may antedate pernicious anaemia. 
Age has no great influence. Most cases appear between twenty and forty 
years of age, but even young children of less than five years have been seen 
with the malady. In some of the reported cases the Ankylostomum duodenale, 
the Bothriocephalus lotus, or tapeworm, and the Oxyuris vermicularis have 
been found. The first-named parasites can cause grave anaemia, but it is 
doubtful if any of them alone can cause pernicious anaemia. So, too, severe 
hemorrhage, syphilis, and pregnancy have been found associated with the 
development of the disease. They are not the actual cause, but rather 
predisposing causes. The various fevers, as malaria and typhoid fever, only 
exert an indirect effect, and the condition of the gastrointestinal tract, at 
one time thought to be responsible, has been proved to be only a predis- 



778 DISEASES OF THE BLOOD 

posing or secondary condition. Hunter thinks the disease is due to bacterial 
infection of the alimentary canal from a foul mouth. 

Morbid Anatomy. — The most noteworthy pathological changes are the alter- 
ations in the blood and in the bone-marrow. Unlike cases of chlorosis, the 
blood may be difficult to obtain. In marked cases it does not form a rounded 
drop, but flows from the puncture made by the needle or scalpel sometime 
after the wound is inflicted. Coagulation is usually delayed, and even at 
an autopsy made many hours after death the blood may still be fluid. The 
red cells are decreased to 2,000,000, then to 1,000,000, and sometimes to less 
than 500,000 to the cubic millimetre. A great proportion of the remaining 
cells are larger than normal (megalocytes),and some are smaller (microcytes). 
Many of the red cells are misshapen (poikilocytes) , and the amount of 
haemoglobin in most of the red cells is considerably increased, although 
some of them may be poor in haemoglobin. Red cells possessing nuclei 
(erythroblasts) are also present in considerable number. Some of these 
are large (megaloblasts) and others of normal size (normoblasts). Small 
nucleated red cells called microblasts are also present. The presence of 
the megaloblast is an important aid in reaching a positive diagnosis. These 
nucleated cells, both large and small, contain a great amount of haemo- 
globin, and some of them differ from ordinary red cells in one very im- 
portant particular — namely, they possess amoeboid movement — and, further, 
when the blood is examined, they are seen to form rouleaux as do ordinary 
red cells. A granular degeneration which permits basophilic staining also 
occurs in the red cells. 

In mild cases the leukocytes may not be altered in number, although 
usually they are slightly reduced. Rarely they are greatly reduced «in 
number if the case is severe. As a rule, but few myelocytes occur and the 
lymphocytes may be increased. 

The haemoglobin is reduced, the average being 25 to 30 per cent., but not 
in proportion to the red cells, hence a high color index is the rule. 

When the bone-marrow is examined very marked changes are manifest. 
There is an excess of large nucleated red cells, many of which are giganto- 
blasts. The liver, spleen, lymph glands, and particularly the liver, are 
loaded with iron derived from the destroyed red blood cells, and even the 
urine contains pigment from this source; Hunter denies an excess of iron 
in the spleen. Fatty degeneration of the liver, kidneys, and of the heart 
muscle are often present, and because of similar changes in the walls of 
the arteries and of the altered character of the blood, hemorrhages into the 
retina and into other parts may occur. In some cases marked atrophy of 
the gastric tubules is found. A diffuse degenerative change occurs in the 
posterior and lateral columns of the spinal cord. 

Symptoms. — A patient with pernicious anaemia usually first seeks medical 
advice because he is feeling weak and lacks initiative. Often he suffers 
from some dyspnoea on exertion and has a throbbing headache or attacks of 
vertigo. His tissues are well filled with fat and his appearance is plump, 
but he is pallid and cheesy looking. The sclerotic part of the eyes is pecu- 
liarly pearly and the lips, gums, and tongue are prone to be very pale and 
bloodless. There may be slight puffiness of the face on the dependent side 



ANEMIA 779 

if the patient lies on his side in bed. A purring hoomic murmur is often 
heard over the pulmonary artery at the third left costal cartilage, and the 
arteries of the neck pulsate and throb with a peculiar jerking, expansile 
movement. An irregular fever is very constantly present. When the disease 
is far advanced a state of mental torpor with muttering delirium may occur. 

Diagnosis. — The fact that the patient is in middle life, or even older, 
serves to separate this state from chlorosis, which has its greatest fre- 
quency at the eighteenth or nineteenth year. Again, pernicious anaemia is 
more common in men, chlorosis in women. The skin in pernicious anaemia 
is prone to show a cheesy-yellow hue in distinction from the greenish- 
yellow of chlorosis. From the blood of the chlorotic that of pernicious 
anaemia differs so radically that a diagnosis is readily made in typical cases, 
for in the former we have cells poor in haemoglobin and here we have 
cells rich in haemoglobin. In the former the red cells are not greatly 
decreased in number, here they are markedly diminished. In chlorosis the 
size of the red cells is below the normal, in pernicious anaemia the average is 
above the normal. Again, in chlorosis we do not find, to the same degree, 
nucleated red cells or cells with mitotic nuclei, nor red cells with amoe- 
boid movement. The color-index in chlorosis is low and in pernicious 
anaemia high. In cases of gastric cancer there is present ordinary sec- 
ondary anaemia and the presence of gastric symptoms to aid the diagnosis. 
Finally, Ewing states that unless at least 33 per cent, of the red cells are 
oversized, the diagnosis of pernicious anaemia must be made with reserve. 

Prognosis and Treatment. — The prognosis of true pernicious anaemia is 
almost invariably fatal, although there have been a considerable number 
of cases in which recovery has been said to have occurred. Many cases 
have periods of extraordinary improvement in all the symptoms as well 
as in the blood, and then a disheartening relapse takes place. This may 
be repeated several times. Most cases die within a year after they are 
first seen. A great decrease in the number of red cells and a large number 
of megaloblasts are bad signs. 

The prognosis in pernicious anaemia depends not a little upon the quan- 
tities of arsenic which the patient can take without developing disagree- 
able symptoms from its use, for many of these cases are markedly 
benefited if they can take what might be called massive doses of this drug. 
By a process of training with ascending doses I have known patients to take 
as much as 30 minims of Fowler's solution three times a day with no bad 
results except some exfoliation of the skin of the hands after several weeks' 
treatment. Arsenic administered in this manner up to the point of tolerance 
sometimes produces periods of remarkable improvement in this disease, the 
patient's symptoms becoming modified and the number of red blood cells 
becoming markedly increased. 

Of course, all measures which tend to increase the general health of 
the patient are advantageous, such as plenty of sunshine, fresh air, and good 
food. Small quantities of iron may be given from time to time with advan- 
tage. Diarrhoea is to be controlled by the use of sulphuric acid or one of the 
vegetable astringents, such as fluid extract of haematoxylon, kino, or catechu. 
Constipation, if present, is to be relieved by the use of cascara sagrada and 



780 DISEASES OF THE BLOOD 

aloes. In some instances hypodermic injections of arsenic have been 
resorted to with asserted advantage, but this is a method of treatment which 
is rarely if ever justified. If the patient is very anxious to carry out a plan 
of treatment which may possibly be advantageous, inhalations of oxygen 
may be suggested. 

In the treatment of pernicious anaemia it is the universal experience of 
clinicians that iron is by no means as beneficial as is arsenic. Indeed, 
the general proposition may be stated that if anaemia is associated with 
diminution in the number of red blood cells, arsenic is more advan- 
tageous than iron; whereas, in those anaemias which are characterized by 
a low color-index or a diminution in haemoglobin, iron is more useful than 
arsenic. 



LEUKAEMIA. 

Definition. — Leukaemia is a disease in which the blood suffers an extra- 
ordinary increase of leukocytes with associated alterations in the bone- 
marrow, the spleen, and in the lymphatic glands. It is divided into two 
types, that form in which the spleen and bone-marrow are chiefly affected, 
and that in which the lymphatic glands are chiefly involved, the first being 
called splenomedullary leukcemia and the second lymphatic leukaemia. Be- 
cause of the important role played by the bone-marrow in splenomedullary 
type it is sometimes called myelogenous leukcemia. Leukaemia is also some- 
times called leukocythcsmia. 

Although a division of the disease into two types is to some extent justified 
because it renders the study of leukaemia less difficult, and because changes 
in certain tissues preponderate in one instance and in other tissues in other 
instances, it is not to be forgotten that intermediate cases occur in which 
both types of the malady are represented, or at least in which no definite 
dividing line can be drawn. Thus cases are recorded in which the blood 
cells presented the picture of lymphatic leukaemia, but the lymphatic glands 
were not involved but the bone-marrow was altered. Again, it has been 
thought, in times past, that acute and rapidly progressive leukaemia was usu- 
ally of the lymphatic type, and that the subacute or chronic form of the 
disease was commonly of the splenomedullary variety. While this view still 
holds true, we have been forced to recognize the fact that acute cases may 
be of splenomedullary type and that some of the chronic cases may be 
lymphatic. 

History. — As long ago as 1801 Bichat, in France, noted a condition of 
the blood which was probably identical with leukaemia as we know it to-day. 
Thirty years later because of the peculiar appearance of the blood it was 
called "suppurative haematitis," and in 1839 Donne described the blood 
in these cases as consisting largely of " white or mucous globules." Virchow, 
about the middle of the last century, described it as "Weisses Brut," and 
showed that there was no suppurative process present. Bennett made the 
first complete study of the disease in 1851. Since then a host of investiga- 
tors have thrown light upon its characteristics. 



LEUKEMIA 781 

Etiology. — The cause of leukaemia is unknown. It may occur at any 
time of life, but is most frequently met with about the fourth decade. It is 
about twice as common in males as in females. A very large number of condi- 
tions have been brought forward as causes, but none of them have been proved 
to exercise a determining influence. Among these may be named syphilis, 
maaria, and intestinal intoxication. The view has been advanced that 
leukaemia and tuberculosis are nearly related in the sense that the latter 
may act as a cause of the former. This view is incorrect. Gowers tells us 
that the appearances of the lungs in one or two cases have been those of 
tubercle, that extravasations of blood into the lungs are common, and that 
these organs may undergo caseation and a tuberculous process may be simu- 
lated. Cavities may result from lymphoid infiltration. This, however, is not 
phthisis. Susmann has been able to collect only 25 cases from literature 
in which tuberculosis and leukaemia were even associated. Further, when 
the diseases are combined there is a tendency to a decrease in the number 
of leukocytes. A number of observers are strongly inclined to the belief that 
the condition is due to an infection by a parasite, but careful observation 
and experimental studies have afforded no conclusive result. Lowit and 
others have sought to establish a protozoal origin, but their observations are 
inconclusive, and bacteriology, so far, has yielded no promising results. 

Pathology and Morbid Anatomy. — When defining the disease leukaemia 
it was stated that it is a malady which appears in two forms, and that these 
forms may be quite dissimilar in their chief features, or overlap one another, 
according to the degree to which the lymphatic system and the bone-marrow 
are chiefly affected. It is probable that in nearly every instance the bone- 
marrow is involved in the disease process, and almost never are the lesions 
situated only in the lymph nodes and other lymphatic tissues. Further, 
although the lymphocytes of a person in good health are usually derived 
from the lymphatic system, in the patient suffering from lymphatic leu- 
kaemia they are derived, to a large extent, from the bone-marrow as well. 

Having made these preliminary remarks, we can best proceed to the study 
of two forms of leukaemia by considering them separately. 

Splenomedullary Leukaemia. — The color of the blood may be normal in 
some cases, but if the disease is well developed it is much paler in hue because 
of the anaemia and the excess of white cells. The coagulability of the blood is 
greatly decreased or lost. The red corpuscles are not very greatly diminished 
in number until the disease is far advanced, and sometimes not then. They 
rarely fall below 3,000,000 to the cubic millimetre, but they may drop to 
1,000,000. Nucleated red cells, especially normoblasts, are present in varying 
numbers, but megaloblasts are rarely present in any great degree. There 
is a decrease of haemoglobin so that the color-index is about 0.5 to 0.7. 

The white cells show remarkable changes as to number, shape, size, and 
variety. Even in cases which may be called moderate they usually amount 
to 100,000 or 200,000 to the cubic millimetre, and as high as 1,000^,000 have 
been reported, as against a normal of about 6000 to 10,000. Of the varieties 
of white blood cells we find a form which never appears in normal blood, 
and which, if present in considerable numbers, is pathognomonic of the 
disease, namely, large mononuclear leukocytes containing neutrophile 



782 DISEASES OF THE BLOOD 

granules. These cells are called neutrophile myelocytes and appear in 
two forms, viz., the smaller myelocytes, about the size of the polymorpho- 
nuclear leukocyte, possessing a central nucleus which stains quite deeply, 
and a larger cell, which has a pale staining nucleus placed at one side of 
the corpuscle. Eosinophilic and basophilic myelocytes also may be found. 
The relative percentage of polymorphonuclear cells is decreased, although 
the total number of these corpuscles far exceeds the normal. The presence 
of the myelocytes is at the expense of the polymorphonuclear cells. 

The eosinophile cells, leukocytes the granules of which stain intensely 
with eosin, are generally increased in myelsemia, although they are never 
as numerous as are the other forms already named. 

The number of lymphocytes, both large and small, varies within wide 
limits in most cases of splenomedullary leukaemia, and at different times 
in the same case. Relatively they are reduced (as low as 2 per cent.), but 
even in this percentage the blood may contain more mononuclears to the 
cubic millimetre than in health. Very large mononuclear leukocytes with 
faintly staining nuclei are rarely conspicuous by their number. " Mast-cells " 
are usually present, not infrequently reaching 5 or 10 per cent. When 
present in large numbers they are second to myelocytes only in diagnostic 
significance. These mast-cells are polynuclear cells with coarse basophile 
granules. 

The onset of any one of the acute infections may completely change the 
appearance of the blood so that it is no longer characteristic and there may 
be a great increase in polymorphonuclear cells. 

The normal red bone-marrow shows marked hyperplasia and the fatty 
marrow of the long bones undergoes a similar transformation, It con- 
tains nucleated red cells in unusual numbers, and is crowded with leu- 
kocytes which are ancestral to those found in the blood, including all 
forms, but particularly myelocytes. In some cases, however, these changes 
appear in patches rather than all through the bone cavity. At certain points 
the compact portion of the bone may atrophy before the hyperplastic 
marrow, and new subperiosteal nodes may develop. 

The spleen is very much enlarged, sometimes to fifteen times its normal 
size. It is frequently attached to adjacent tissues. Its capsule is usually 
thickened and roughened, and the consistency of the organ increased. On 
section it is seen to be mottled red and gray, or it may be a homogeneous 
red. The trabecule may be thickened and hemorrhagic infarctions may be 
present. The venous system is engorged and purulent-looking clots may 
be found in the heart and vessels. The liver is often enlarged and leukemic 
nodules may be found in it and in the kidneys and thymus gland. 

Lymphatic Leukaemia. — The conspicuous blood changes in this disease 
are confined to the lymphocytes, which are greatly increased in number so 
that they may exceed 80 per cent, of the total number of white cells. For 
this reason the condition is sometimes called lymphaemia. Usually most of 
the cells are small lymphocytes, but the large form may predominate, 
especially in the acute type of the disease. The total increase in leukocytes 
rarely approaches that seen in the splenomedullary form. Nucleated red 
cells are rarely encountered. 



LEUKAEMIA 783 

The lymphatic glands, particularly those which are deeply situated, 
are enlarged, but the spleen and the medulla of the long bones are not 
greatly altered. Cases are on record in which chronic lymphatic leukaemia 
has occurred without any enlargement of the lymph nodes. 

Symptoms. — The symptoms of splenomedullary leukaemia are at first those 
of anaemia, the patient presenting himself because of dyspnoea on exertion, or 
because of lack of energy and poor digestion. Sometimes the swollen spleen 
first calls his attention to his condition. In other cases nose-bleed or gastric 
hemorrhage or renal hemorrhage comes on very early in the disease. In other 
cases there is purpura hemorrhagica. If the hand is placed over the splenic 
area and the abdominal wall moved over the enlarged spleen a creaking 
sensation may sometimes be felt. Not rarely the liver is greatly enlarged, 
and ascites may be present. There is dizziness and vertigo. Occasionally a 
violent diarrhoea develops. The urine is normal, save that it contains uric 
acid in excess. The heart sounds are normal, although the first sound may 
be feeble, and anaemic murmurs can occasionally be heard. Retinal hemor- 
rhages may cause blindness. Hemiplegia with coma, the result of cerebral 
hemorrhage, may occur. A moderate but varying febrile movement is nearly 
always present. Occasionally persistent priapism, probably due to irrita- 
tion of the spinal cells by anaemia, is present. Sudden death may take place. 

In cases of lymphatic leukaemia the symptoms complained of by the 
patient are not different from those just described, but the spleen is not 
much enlarged. The lymph nodes are, however, increased in size, and 
so the appearance of the patient may not be unlike that of Hodgkin's 
disease. 

It is important to recall the fact that in both of these states an 
irregular febrile movement may be present and give rise to the belief 
that some one of the acute or chronic infections characterized by fever 
are present. This is particularly true in certain cases of acute lymphatic 
leuksemia, in which the condition of the patient may be so like that of 
typhoid fever that an examination of the blood is required to determine 
the exact nature of the illness. The condition often runs its course in 
three to four weeks; fever of moderate degree is present, and the general state 
is asthenic. Even an autopsy may not reveal the real cause of the illness, 
because the lymph nodes in the solitary and agminated glands of the intes- 
tine are infiltrated as in typhoid fever. 

Diagnosis. — The pallor, the enlarged spleen, and the state of the blood are 
all part of a picture which cannot be mistaken for any other disease, but in 
doubtful early cases repeated blood examinations may be necessary to deter- 
mine the diagnosis positively. 

Prognosis. — The prognosis of leuksemia, like that of pernicious anaemia, 
is, in the great majority of cases, fatal, but rare instances have been recorded 
in which recovery has taken place. Life may be preserved from a year to 
three years. Unfavorable prognostic signs are marked dyspnoea, an exces- 
sive number of leukocytes, a tendency to exhausting diarrhoea or to hemor- 
rhages, and high fever. The lymphatic type usually runs a more rapidly 
fatal course than the splenomedullary form. When death occurs, the cause 
is usually pulmonary oedema, pneumonia, or exhaustion. 



784 DISEASES OF THE BLOOD 

Treatment. — The treatment of leukaemia in both its forms is identical, but, 
unfortunately, it is by no means successful, for the disease in all instances 
proceeds by a more or less rapid course to a fatal ending. There can, how- 
ever, be no doubt that the administration of arsenic in ascending doses until 
the point of intolerance is reached seems to exercise a favorable influence 
upon the malady, at least in so far that it delays its advance. Cases of 
leukaemia not subjected to treatment not infrequently have periods of remis- 
sion, in which temporary improvement may take place. It is, therefore, 
difficult to determine how much credit should be given to arsenic when the 
remissions occur under its use. Those members of the profession who have 
had the most experience in the treatment of leukaemia, however, regard 
arsenic as being practically the only remedy of any value, and it should 
always be tried, preferably in the form of Fowler's solution. The begin- 
ning doses should be 3 drops three times a day, rapidly increased until the 
patient has some puffiness of the face or some griping of the bowels. 
Recently several clinicians have reported " cures" of this disease by exposing 
the patient to the Roentgen rays. As well shown by Warthin in his ex- 
haustive discussion of this subject the final outcome of most if not all 
of the cases thus treated is relapse and death from the disease. Warthin's 
experimental studies indicate a possible danger from the absorption of sub- 
stances liberated by the destruction of cells brought about by the Roentgen- 
ray exposures. Further investigations will be necessary to place this pro- 
cedure upon a sound therapeutic basis, as it deals with a disease that is 
notoriously resistant to ordinary remedial measures. However, the question 
is one that merits careful study. 



CHLOROMA. 

Under the name chloroma is recognized a condition characterized by the 
formation of greenish lymphoid tumors, especially in the cranial bones and 
periosteum, and the occurrence of a profound anaemia which Dock and 
Warthin regard as, in some if not all cases, a malignant type of leukaemia. 
Exophthalmos and lymphoid infiltration of the cornea and of the conjunc- 
tiva may be present. Later the periosteum of the bones of the spinal 
column become affected. Localized paralyses, from pressure exerted by 
these growths upon nerve trunks, may arise. Another characteristic of 
chloroma is the peculiar green hue of the new-growths ; the cause of this 
coloration is unknown. 

The latest study of this remarkable and rare disease is that made by 
Dock and Warthin. These investigators conclude that the disease consists 
in a neoplastic hyperplasia of the parent cells of the leukocytes which 
develops primarily in the red bone-marrow and secondarily affects the peri- 
osteum. Typical and atypical leukocytes are, therefore, developed, set 
free in the blood, and may appear as large lymphocytes or as neutrophiles 
or eosinophile myelocytes. On the other hand, it is not essential for the 
diagnosis of chloroma that these leukocytic changes be present, for some- 
times they fail to appear. Chloroma may, therefore, be regarded as a 



PURPURA 785 

malady lying midway between leukaemia and lymphosarcoma. The 
essential point of differentiation is the development of the green masses of 
lymphoid tissue which are distinctly neoplastic in character. The prog- 
nosis of chloroma is invariably fatal. 



ANiEMIA INFANTUM. 

Definition. — Under this term von Jaksch has described a form of anaemia 
occurring in children under four vears of age and resembling leukaemia in 
many respects, in that there is great enlargement of the spleen, marked 
leukocytosis, some increase in the size of the liver and of the lymph nodes. 
Yon Jaksch believes that this malady separates itself from a true leukaemia 
of infancy by the fact that the increase in the white cells is never so marked 
as in true leukaemia, that children often recover, and because there is never 
any leukaemic infiltration of the viscera. The cause is not known. 

The red cells are so much decreased that they number only from 3,000,000 
to 1,500,000. There are also present poikilocytes and usually a large number 
of nucleated red cells. The total leukocytosis rarely exceeds 50,000, the chief 
increase being in the mononuclear corpuscles. Myelocytes are absent, or 
not present in sufficient number to justify a diagnosis of leukaemia. The 
liver and spleen are enlarged. The condition is usually met with in rachitic 
or syphilitic children and in those suffering from chronic gastrointestinal 
catarrh. 

Treatment.— The treatment is identical with that of leukaemia. 



PURPURA. 

Under this term is included all those cases in which, as the result of various 
causes, extravasations of small quantities of blood take place into the skin. 
These extravasations are multiple and often very widespread. It must be 
borne in mind that under no condition is purpura a disease in itself. It is a 
symptom or manifestation of some disturbance in the nutrition of the smaller 
bloodvessels or of the blood itself. Thus, it occurs as a manifestation of 
severe infections, such as profound septicaemia, scarlet fever, typhus fever, 
measles, and smallpox, and in infections not so well understood, in which 
micro-organisms, known and unknown, are manifestly the cause of the 
condition. Various investigators have isolated from cases of purpura such 
micro-organisms as the Streptococcus pyogenes, the Staphylococcus pyogenes 
aureus, the pneumococcus , and the Bacillus aerogenes capsulatus. The 
Bacillus coli communis has also been obtained from the blood. Again, cer- 
tain poisons, as snake venom and poisons from the mineral kingdom, may 
cause purpura. A large number of cases of marked purpura have developed 
in persons who have taken iodide of potassium, and after the use of mercury, 
copaiba, and the chlorate of potassium. It may also develop as the result 
of some congenital defect in the blood, as in haemophilia. 

Diseases generally called diathetic, such as scurvy, tuberculosis, Hodgkin's 



786 DISEASES OF THE BLOOD 

disease, and chronic nephritis, may cause this symptom. Purpuric extravasa- 
tions sometimes develop after severe neuralgic seizures in locomotor ataxia 
and along the course of certain nerves in hysterical women. 

Some writers have given the name purpura hemorrhagica to that form of 
purpura in which, in addition to the extravasations into the skin, there are 
also lesions of this character in the mucous membrane of the mouth. 

Under the name " purpura rheumatica, " or " peliosis rheumatica," a form 
of purpura develops in which there is a distribution of the spots chiefly about 
the large joints, particularly about the knees. Associated with this eruption 
there is swelling of the tissues about the joints resembling that seen in rheu- 
matism. There is usually no fever and little pain, although the joints appear 
stiffened at times. It was this arthritic state that gave the name " purpura 
rheumatica " to the condition. In some instances the joint disorder is due 
to acute rheumatism but in the majority it is some other form of infec- 
tion. 

Under the name of " Schonlein's disease" a very much more severe type of 
this condition has been described. Many of the joints are affected, so that 
the patient is bedridden, and the extravasations of blood into the submucous 
tissues and into the skin are so copious that great swelling and even slough- 
ing may result. Some years ago I saw, in consultation with Dr. Wilson, of 
Woodbury, New Jersey, another physician who not only had the joints of 
the extremities greatly affected, but the inferior maxillary joint was also 
involved. The buccal mucous membrane was so infiltrated that we feared 
the development of noma, and the whole face was much distorted by the in- 
filtration. Notwithstanding the severity of the lesions and the intense pros- 
tration of the patient, recovery usually takes place. Care must be taken that 
this form of purpura is not confused with scurvy or scorbutus (which see). 

"Henoch's purpura " is a condition affecting children and characterized by 
lesions in the skin, which may be a combination of purpura and erythema 
multiforma. The joints may or may not be affected, and bleeding from the 
gums may appear. The most distinctive symptom, which is not present in 
all cases, but which may be present when the others are absent, is gastro- 
intestinal crises, in which the child is seized with pain, diarrhoea, and 
vomiting. All these symptoms are prone to recur at irregular intervals. 
Recovery usually occurs, except in those cases in which the hemorrhagic state 
affects the kidneys, when a fatal result may ensue. 

A form of fulminating purpura sometimes develops in young girls and 
causes death in a few days, the patient being apparently overwhelmed by 
some unknown infection. 

There are three hemorrhagic affections of the newborn that occasionally 
occur. 

In children with inherited syphilis, hemorrhage from the mucous mem- 
branes and from the navel, with intense subcutaneous extravasations, may 
occur and cause death. The autopsy shows hemorrhages into the liver and 
kidneys, and signs of inherited syphilis in these parts as well. 

Under the name of WinckePs disease a condition of jaundice develops 
within a week of birth, followed by dyspnoea, hemoglobinuria, and deep 
cyanosis. I saw a case some years ago in which the child was so cyanotic 



HEMOPHILIA 787 

that parts of its body were blue-black. The autopsy in such a case shows 
swelling of the spleen and fatty degeneration of the liver and kidneys. 

A third state called " morbus maculosus neonatorum" develops in new- 
born infants, and consists in hemorrhages from the stomach, intestines, or 
from the navel. It is rarely seen in private practice, and is probably due to 
some infection. 

Hayem and Bensaude have stated that in purpura hemorrhagica the blood , 
when allowed to stand in a vessel for twenty-four hours, slowly clots, but the 
clot does not contract to any extent, and therefore does not squeeze out the 
serum as it does in normal blood. 

Treatment. — The treatment of all forms of purpura is based upon the 
recollection of two facts, viz., first, that the condition is due in most cases to 
an infection or at least to a cause which has impaired the health, and therefore 
every means to aid the vital resistance of the body must be resorted to. The 
food should be easily digested and nutritious; the patient, if able to travel, 
should be removed to some place where he can bask all day in the sunshine. 
Moderate doses of tincture of the chloride of iron should be given each day 
to combat the infection and the anaemia. 

The second point to be recalled is that certain drugs may be employed 
to increase the coagulability of the blood. Of these, the only ones with any 
real claim to power are the lactate and chloride of calcium, which may be 
given in the dose of 20 grains three times a day to an adult, well diluted 
with water. Certain cases seem unable to absorb calcium salts through the 
alimentary canal and these should be treated by hypodermic injection. 
The solution should not be stronger than 1 part in 20 of water and the 
lactate should be used because the chloride is too irritating. The effect of 
one day's dose of 60 grains lasts three or four days, and it should not be too 
frequently repeated, since, if this is done, coagulability is decreased. Turpen- 
tine, oil of erigeron, ergot, and sulphuric acid have all been used. Their 
employment is purely empirical, and there is little reason to rely on them. 
Several ounces of nutritious food, fresh air, and a day in the bright sunlight 
will do more good in this state than all the medicines can accomplish, and 
this, too, without damaging the stomach. The use of these remedies in this 
state is putting " drugs of which we know little into bodies of which we know 
less." 

HAEMOPHILIA. 

Definition. — Haemophilia is a condition of the body in which there is an 
inability to arrest hemorrhage by the normal coagulation of the blood, or in 
which hemorrhage arises apparently without cause and persists without any 
attempt being made by nature to arrest it. The disease is essentially hered- 
itary in most cases, and it is an extraordinary fact that the hemorrhagic 
tendency is transmitted to males only through the female parent, although 
the mother is herself usually not afflicted. 

Etiology. — The cause of this condition is entirely unknown. Virchow 
believed it to be dependent upon an abnormal thinness and narrowness of 
the arteries, but it is probably due to some deficiency in the coagulability of 



788 DISEASES OF THE BLOOD 

the blood as well. Stengel has recorded an instance in which the hemor- 
rhagic tendency was limited to one part of the body, namely, the head, and 
Osier states that the late D. Hayes Agnew described to him a similar case. 

Pathology and Morbid Anatomy. — There are no changes in the blood cells 
that account for this condition; indeed, no peculiar state of the blood is found 
save a diminished coagulability. An examination of the tissues of the 
various organs is also practically negative, save that if the hemorrhage has 
been profuse the changes always met with in marked anaemia are present. 

Symptoms. — An active but oozing capillary hemorrhage is the form in 
which the bleeding usually occurs, and it follows in some instances very slight 
injury. Thus, the mere blowing of the nose may be sufficient to rupture 
the fine vessels of the nasal mucous membrane and cause a dangerous loss 
of blood, and epistaxis is the most common form in which this condition 
manifests itself. Another common source of the blood is from the gum 
after tooth extraction. 

In some cases bloody effusions take place into the large joints. 

Prognosis. — The prognosis depends largely upon the severity of the loss 
of blood and upon the ability of the patient to restore the quantity lost before 
the next bleeding comes on. Fully 50 per cent, of bleeders die before the 
seventh year, but some live to old age. Although girls who reach puberty 
menstruate with their entrance upon adult life, and so are exposed to an 
excessive loss of blood, their mortality rate in this disease is not so high as 
that of boys. 

Treatment. — The treatment consists in the building up of the general 
health by out-door life and exposure to sunshine, and in the use of small tonic 
doses of iron and arsenic if anaemia is present. If a special tendency to 
hemorrhage exists at any particular time, calcium lactate or chloride should 
be given in doses varying from 10 to 20 grains three or four times a day, well 
diluted, to increase the coagulability of the blood, but this must not be used 
for long periods without intermission, as after a certain amount is taken the 
coagulability of the blood is decreased and not increased. The local treatment 
consists in the use of tampons wet with adrenalin chloride, 1 : 1000, or gelatin 
solution of the consistency of thin mucilage may be used for the same pur- 
pose. When adrenalin cannot be obtained, peroxide of hydrogen may be 
applied in the same manner to the bleeding spot. When the hemorrhage 
is from the gum, a compress made of punk may be used, or a compress wet 
with a saturated solution of alum, with MonseFs solution, or with adrenalin 
chloride solution, 1:1000. 



DISEASES OF NUTRITION. 



DIABETES MELLITUS. 



Definition. — Diabetes mellitus is a disease characterized by the appearance 
in the urine of glucose, and the development of polyuria, thirst, and excessive 
appetite, with impairment of nutrition, and in some cases progressive 
emaciation. The mere presence of glucose in the urine does not necessarily 
indicate that diabetes is present. The glycosuria must be associated with 
other morbid processes to present the symptom-complex of the disease. 

History. — Diabetes mellitus has been known since the time of Christ, 
but it was not till the latter part of the seventeenth century that Willis, in 
England, noted that the sweet taste of the urine was probably due to sugar, 
and not until 1775 that Dobson, of England, actually obtained sugar from the 
urine. Since that time a host of experimental investigators and clinicians 
have studied the disease from every aspect and have added much to our 
knowledge of it, but no one has as yet been able to give us a clear conception 
of the causes of the malady. 

Distribution and Frequency. — Diabetes occurs in all parts of the civilized 
world, but is much more common in Europe than in the United States. It 
is frequently met with in France, in Sweden, in Italy, in India, and Ceylon, 
but is comparatively rare in Russia, Holland, and in Brazil. Negroes rarely 
suffer from it, but Hebrews are so frequently affected by it that it may almost 
be said to be the prevalent disease of that race. Kiilz, of Germany, found 
that in 692 cases of diabetes 17.8 per cent, occurred in Jews, which is all the 
more remarkable when we consider that Hebrews constitute only 1.2 per cent, 
of the population of that country. Frerichs found 102 Jews in 400 diabetic 
patients, and von Xoorden 252 Jews in 650 patients suffering from this disease. 

It is a disease of adult life, as a rule, but very young children suffer from 
it occasionally, and even nurslings have from time to time been reported as 
presenting well-developed cases of the malady. To emphasize its rarity in 
children, Stern may be quoted in his assertion that only thirteen deaths have 
been reported from this malady as occurring in children under five years of 
age in the past thirteen years. It is more common in males than in females 
in the proportion of 3 to 2. 

The statement generally made that diabetes is a disease of cities rather 
than of country districts is not altogether true. Some years ago Purdy 
showed that, as a rule, it was much more frequent in the country districts 
than in cities. In the United States the disease is much less frequent in 
the Gulf and South Atlantic States than anywhere else. 

(789) 



790 DISEASES OF NUTRITION 

There can be no doubt that the disease is becoming very much more fre- 
quent than it was several decades ago. I showed this in a paper published 
some years since, based upon statistics gathered from the Jefferson Medical 
College Hospital and other large hospitals here and abroad. Since then 
additional statistics have been collected which indicate the correctness of 
these earlier conclusions. 

According to the mortality statistics of the United States Census Reports 
for six decades, the proportion of deaths from diabetes mellitus in 100,000 
deaths from all known causes has been as follows: 



From 1840 to 1850 . 


. 72 


From 1870 to 1880 . 


. 191 


" 1850 to 1860 . 


. 98 


" 1880 to 1890 . 


. 280 


" 1860 to 1870 . 


. 170 


" 1890 to 1900 . 


. 470 



It seems scarcely credible that so great an increase could have occurred, 
and it is possible that greater care in examining patients and in regard to cor- 
rect death certificates is responsible for part of the increase, yet the records 
of the Massachusetts General Hospital from 1824 to 1898 show that four 
times as many cases of diabetes were admitted to the hospital during the 
last thirteen years of that period as during the first fifteen years. On the 
other hand, it is only fair to state that the statistics of L'Hdtel Dieu, Lyons, 
for seventeen years, which were collected by Alix, for Le*pine, who attempted 
to ascertain if diabetes was increasing in a certain district of France, do not 
show any increase in the disease. 

Etiology. — The causes of diabetes are not known, although it is a well- 
recognized fact that lesions in certain portions of the nervous system are 
followed by glycosuria, and that certain alterations in the islands of Lan- 
gerhans in the pancreas and in the circulation of the liver are also followed 
by the same symptom. (See Pathology.) As somewhat indirect causes 
we recognize severe nervous strain and errorrs in diet, but these alone are 
not sufficient to cause even glycosuria, much less true diabetes, in the vast 
majority of human beings. 

There is some evidence to indicate that the disease is hereditary, for 
sometimes it happens that several members of the same family suffer from 
the malady, but this may be due to their being exposed to the same exciting 
causes, whatever they may be. A more pronounced factor than any so 
far named seems to be excessive indulgence in rich foods and sweet wines, 
but a very small proportion of the persons who commit these dietetic errors 
suffer from diabetes. 

Pathology. — Of the pathology, or morbid physiology, of diabetes we are 
very ignorant, although an immense amount of skilled research has been 
devoted to this subject for years. It is a well-recognized fact that in all 
human beings glycogen is prepared from carbohydrate foods, and even 
from proteids and fats, and deposited in the liver and in the muscles, 
where it lies as in a storehouse as reserve food. It also circulates in the 
healthy blood stream in the proportion of about 1 : 1000, and so is carried 
to various parts of the body for nutritional purposes. 

There are many conditions which produce loss, or leakage, of this sub- 
stance in the form of glucose in the urine. Thus, glycosuria, or the mere 



DIABETES MELLITUS 791 

presence of sugar in the urine, may follow the ingestion of an excess of either 
cane-sugar or grape-sugar or an excess of carbohydrate food. Under these 
circumstances it is simply an overflow of material which the system cannot 
utilize. This being true, it is readily conceivable that in certain states of 
disease the system may be unable to utilize the ordinary amount of glycogen, 
and therefore it escapes from the body. This view receives support from 
the theory advanced by Loewi and Kolisch, who believe that there is in the 
organism a body, or ferment, or agent, which binds the glycogen in the 
tissues in such a form that it does not appear in the blood in excess. If for 
any reason this binding body (Bindekorper) is diminished in power, an 
excess of glucose passes to the kidneys and so escapes from the body. This 
view explains a considerable number of cases of glycosuria, but by no means 
all of them. 

It is a well-known fact that injury or disease of the so-called diabetic 
centre of Claude Bernard in the medulla is followed by glycosuria, and 
that this glycosuria is directly due to a disorder of the blood supply in the 
capillaries of the liver. This may interfere with the "binding" of the gly- 
cogen in that organ. Again, the administration of phloridzin will produce 
glycosuria, but this condition is quite different in its causation from ordinary 
glycosuria, in that the drug acts upon the kidney structure in such a way 
that it permits a leakage of the normal content of glycogen from the blood. 
In other words, in this state the fault does not lie in an inability of the body 
to use its glycogen, but in the inability of the kidneys to prevent its escape 
from the body. 

We find, therefore, that glycosuria and diabetes mellitus are by no means 
identical conditions necessarily, although glycosuria is the predominant 
symptom in this disease. There may be a loss of sugar in the urine for 
many years without any impairment of health, or the glycosuria may not 
be constant, but recurrent and appear only when nutritional processes are 
for any reason jarred or disturbed. In true diabetes mellitus, on the other 
hand, there are associated with the glycosuria more or less profound impair- 
ment of nutrition, with wasting, emaciation, and the development in the 
body of certain poisons which act very deleteriously and may cause death. 

These distinctions, which serve to separate in the mind of the student 
glycosuria from true diabetes mellitus, however, like many other dis- 
tinctions, do not actually hold true in all cases, for we frequently see per- 
sons who begin with the leakage of sugar into the urine and end with true 
diabetes; and we meet intermediate cases in which the degree of emaciation, 
thirst, and polyphagia is so mild that it is difficult to tell whether the patient 
is a sufferer from an inability to deal with carbohydrate food or is really 
diabetic. 

The question of the pathology of this disease, as far as we know it to-day, 
can perhaps be summed up in the following words: In certain individuals 
there exists, as a result of a congenital or acquired defect in the metabolic 
functions of the body, an inability to utilize for the purpose of nutrition all 
the carbohydrate material which is taken as food. Such persons suffer 
from simple glycosuria. If the defect just referred to becomes more marked 
they gradually lose the power to retain and utilize any noteworthy quantity 



792 DISEASES OF NUTRITION 

of the carbohydrates ingested, and when this condition develops they speedily 
emaciate and lose vital resistance. Finally, by reason of some further 
defect in the organs whose functions govern nutrition, such persons actually 
convert their body fat and proteid tissues into sugar and pass it from them 
in the urine, in which cases death soon closes the scene. 

Certain factors tend to produce the chain of disturbances just enumerated, 
and all these agencies may cause changes which may be mild and continue 
so, or, in another case, become severe and rapidly fatal. These may be 
mentioned as follows: 

1. Heredity. It is conceivable that the parent may hand down to the 
offspring certain defects which will interfere with the proper utilization 
of carbohydrates. 

2. Errors in diet, both as to food and drink. It is conceivable that errors 
of this character can so pervert, or overwhelm, the processes of nutrition 
or elimination that primary glycosuria followed by permanent diabetes 
may ensue. Thus, the excessive beer-drinkers of Bavaria often suffer from 
this disease, probably because of the excess of fluid, of alcohol, and of 
carbohydrate which they ingest. These factors pervert the function of the 
liver, of the pancreas, and of the kidney. 

3. Profound nervous worry and mental anxiety are undoubtedly followed 
by diabetes in some persons probably because the nervous mechanism gov- 
erning nutritional processes is perverted in function by the stress and strain. 

4. Certain injuries to the central nervous system may so result, for severe 
trauma of the head or the growth of an intracranial tumor may produce 
diabetes. 

5. Certain infectious diseases may produce temporary glycosuria, which 
disappears with the acute disease or persists and becomes true diabetes, 
probably because the acute infection has damaged beyond repair nervous 
centres or glands whose function is to control glycogenesis and the utiliza- 
tion of glycogen. 

6. Diathetic diseases such as gout undoubtedly cause, or predispose to, 
diabetes in some cases, but whether this influence is direct or simply a sign 
of general perversion of metabolism we do not know. 

Finally, it must be recalled that of all the organs of the body the liver 
and the pancreas are the viscera which show the greatest morbid changes 
in true diabetes. Not only is the liver the organ which is chiefly concerned 
with the manufacture and storing of glycogen, but the pancreas undoubtedly 
exercises a very powerful influence upon the glycogenic processes; for not 
only does it secrete digestive ferments which act in the intestine, but also a 
ferment or factor which enters the blood stream and is intimately concerned 
with the utilization of glycogen. Thus, if the pancreas is extirpated glyco- 
suria is at once developed, and the same condition ensues if the gland is 
totally destroyed by disease. It would appear that the so-called islands of 
Langerhans are the portion of the gland which exercises this influence 
upon the processes connected with the utilization of glycogen, and in 
many cases these islands are found to be distinctly diseased. While dis- 
ease of the pancreas is responsible for the development of diabetes in 
some cases of the malady, it is also a fact that in many cases of very 



DIABETES MELLITUS 793 

severe diabetes the most careful examination of the pancreas after death 
fails to discover any lesion that can be considered in any way responsible for 
the malady. It seems evident, therefore, that many causes may so pervert 
nutritional processes that glycosuria or true diabetes may result, and in this 
sense it may be said that diabetes is not a primary disease, but rather a 
symptom of some primary lesion which we do not at present understand. 

Morbid Anatomy. — The changes found in the islands of Langerhans are 
various. In some cases they manifest capillary engorgement or hemorrhagic 
extravasation. In others there is found a pericapillary or peri-insular scle- 
rosis, an atrophy, a necrobiosis, or hyaline degeneration. The latter is 
probably always primary, and the former conditions usually secondary. 
Aside from changes of the islands of Langerhans in the pancreas, the most 
notable changes presented postmortem in any of the organs of the body are 
found in the liver. This organ is usually markedly hypersemic and darker 
in color than in diseases which do not affect its functions. Microscopically 
it is found that its capillaries are congested, and that the liver cells are 
enlarged and show a tendency to coalesce. These changes are not, how- 
ever, peculiar to the disease, being found in other states; and it is a fact 
worthy of consideration that when death results in cases of severe disease 
of the liver, glycosuria is rather an unusual symptom. 

There is a form of diabetes, associated with hepatic cirrhosis and 
bronzing of the skin, called "bronzed diabetes," owing to the color of the 
skin. 

The structure of the kidneys is diseased in a very large number of diabetics. 
These changes are not in any way a part of the disease itself, but result from 
the increased activity of these organs in excreting water and sugar, and by 
reason of the effect of toxic substances, such as acetone, diacetic acid, and 
oxybutyric acid, which, as they are eliminated, damage the renal tissues. 
The constancy of renal changes in diabetes is proved by the frequency with 
which these organs are found diseased at autopsy when death has occurred 
from this disease. Out of 121 autopsies, reported by Griesinger, Dickinson, 
and Seeger, renal changes in diabetes were found in 77 cases, and Elliott has 
collected statistics from European clinicians which show that albuminuria 
is present in 43.68 per cent, of all cases of diabetes. The renal lesions may 
be divided into two classes: In one class, which is usually met with in 
chronic cases, an ordinary chronic nephritis develops in which parenchy- 
matous and interstitial changes both occur. In the second form, which is 
really toxic in origin, there is a hyaline degeneration of the tubular 
epithelium, the so-called "cellular necrosis of Ebstein." A so-called gly- 
cogen degeneration of Henle's loop and of the straight uriniferous tubules 
(Ehrlich's lesion) is also found, but it cannot be claimed that these changes 
are pathognomonic. 

The changes in the nervous system are usually of little importance. 
Peripheral neuritis is often present. Probably this is purely secondary. 
Distinct changes have, however, been found in the spinal cord in cases 
of diabetes mellitus, notably by Williamson. Using Van Gieson's method 
this clinician found an increase in connective tissue in the columns 
of Goll in the cervical area. There was also a diminution in size 



794 DISEASES OF NUTRITION 

of the nerve fibres in these columns, and the myelin sheaths and axis 
cylinders were also diminished in size, although a few of the myelin 
sheaths were distended. When Marchi's method was employed degen- 
erated fibres were seen in Goll's columns in the cervical, dorsal, and 
lumbar regions, and a few degenerated fibres were present in Burdach's 
columns. So, too, degeneration was found in the intramedullary course of 
the posterior nerve roots, between the posterior surface of the cord and the 
posterior horn of gray matter, and to the median side of the posterior horn. 
These latter changes were most marked in the lumbar and cervical region. 
In a few instances degenerated fibres were seen in the posterior roots just 
outside the pia mater. These changes are probably secondary and due to 
the altered condition of the blood in diabetes. 

The blood is not only unduly rich in glucose, but sometimes contains an 
excess of fat-globules to such an extent that it may form a cream-like layer 
on the clot when it stands after withdrawal. Fraser has recorded a case in 
which an analysis of the blood showed that it contained 16.5 per cent, of 
fat and the pleural fluid 20 per cent. 

The blood in some cases of diabetes mellitus is of a pale salmon color 
which has been thought to be due to the presence of fat, and for this reason 
this condition has been called lipsemia. Futcher, however, has shown that 
this appearance is not entirely due to fat, for it is not possible to remove it 
from drawn blood by the use of ether, and the granules do not stain black 
with osmic acid. He suggests that these granules are in part albuminous. 
More recently Cole, in testing the blood in a case for Hale White, reaches 
the conclusion that true fat is not present, but that the foreign material 
seems to be an ester of cholesterine with one of the higher fatty acids. Heyl 
showed in 1880 that this state of the blood could be demonstrated in the 
retinal vessels, and Hale White has more recently recorded a beautiful case 
of the same character. 

The lungs are often found to contain tuberculous foci, and may show well- 
developed bronchopneumonia or croupous pneumonia, but these are the 
result of terminal infections and not part of the primary disease. Arterio- 
sclerosis and its train of associated lesions are of frequent occurrence in 
diabetes mellitus. 

Symptoms. — The symptoms of diabetes vary very greatly in their severity in 
different cases, so greatly that it is almost impossible to detail any array of 
symptoms which are common to all cases. In many instances the glycosuria 
exists for a considerable period of time before the patient suffers from 
symptoms which lead him to think he is not well. A very well-known 
medical writer in London, some years ago, first discovered he was diabetic 
by observing that flies were unduly attracted to the vessel in which he urin- 
ated, and later by noticing that a few drops of urine which accidentally fell 
on his black trousers left a white stain on drying. Later on, all the diabetic 
manifestations developed, and he died of diabetic gangrene of the foot. 

As a rule, as the disease progresses the patient notices that he passes 
water more frequently and in larger quantity than is normal, he develops 
more or less thirst, and loses sexual desire and power. Later on he begins 
to feel languid and inert; he is usually constipated because of his polyuria, 



DIABETES MELLITUS 795 

and he may develop an inordinate appetite in the endeavor to compensate 
for the loss of nutriment through his urine. The thirst, the polyphagia, and 
the loss of strength and flesh are usually in direct proportion to the polyuria 
and the quantity of sugar excreted. When the polyuria is marked the 
tongue becomes glazed, dry and raw in appearance, and attacks of stomatitis 
or thrush may develop. The skin is also dry and harsh, and the hair lustre- 
less and brittle. The pulse is feeble and the temperature subnormal. 

Although the disease is often characterized by excessive emaciation, this 
symptom is subject to extraordinary variations in different patients. 
Marked loss of flesh is almost constant in all persons under twenty-five years 
of age, but after this time it is by no means uncommon to meet with patients 
who maintain their weight for years. This holds true in direct proportion 
to the years of age and the degree of polyuria and loss of sugar. Where the 
tissues are freely drained of fluid or starved beyond repair the weight of 
course suffers. 

The urine in diabetes mellitus is not only abnormal in that it contains sugar, 
but it not uncommonly contains albumin as well. (See Complications.) 
Its specific gravity is high and ranges from 1.025 to 1.045, and one instance 
of 1.074 is recorded by Trousseau. Such a specific gravity, however, is 
exceedingly rare. Notwithstanding its high specific gravity, however, the 
urine is usually exceedingly limpid and clear, it has a sweet odor, and is acid 
in reaction. 

The quantity of sugar present varies over wide ranges. Sometimes it is 
found in as small an amount as 1 to 3 per cent.; in others it is found to be 
present in the proportion of 10 per cent. The total quantity passed in 
twenty-four hours may be from one ounce, or less, to a pound and a half. 
Very rarely even more escapes. Dickinson reports a case that passed the 
incredible amount of fifty ounces of sugar a day. 

The quantity of urine is also very great in some cases, while in others it 
may not be much above the normal quantity. As much as six to twelve pints 
are often passed in each twenty-four hours, and cases are recorded in which 
as much as thirty pints were passed in this time. 

Complications and Sequelas. — The complications and sequelae of diabetes 
mellitus are important, and so constantly present that they may aid mate- 
rially in the diagnosis of the disease. Many of them are dependent upon 
the fact that the constant loss of sugar lowers nutrition and so decreases 
vital resistance to the various infections, or they result from perverted 
metabolic processes closely associated with the inability of the body to 
properly control the functions governing glycogenesis and the proper 
utilization of glucose in the economy. 

Sweet has demonstrated that for certain organisms the blood loses its 
bactericidal power in diabetes. 

It not infrequently happens that the first symptom presented by a diabetic 
patient is repeated crops of boils or carbuncles. When the urine is examined 
sugar is found, and it becomes evident that the lowered vitality caused by 
diabetes mellitus has permitted infection of the skin to occur. Sometimes the 
carbuncle becomes malignant and speedily destroys the patient. In still other 
instances, which are not as common as has been thought, diabetic gangrene 



796 DISEASES OF NUTRITION 

occurs, the primary lesion being some break in the skin of a finger or toe 
resulting from the blister made by an ill-fitting shoe, or by wounding a corn. 
Through this lesion infection takes place, and vital resistance is so low that 
the micro-organism speedily causes the local death of the part, and almost 
equally rapidly may involve the blood in a diabetic septicaemia. In such 
cases the gangrene is moist. In another class of cases, which depend upon 
secondary vascular changes not due to direct infection, the gangrene is dry 
and of the so-called senile type. 

Elliott's statistics, already quoted, show that albuminuria is present in 
about 43.68 per cent, of diabetics. This albuminuria may at times possess 
grave significance, and is worthy of careful consideration. It may be said to 
arise from three causes, namely, from renal congestion, due to cardiac feeble- 
ness and impairment of the circulation; from degeneration of the kidney, due 
to true nephritis, and, finally, to severe irritation or inflammation of the renal 
tissues by the poisons of the disease. The first type can usually be relieved 
by careful treatment of the heart, and the second type, with casts in the urine, 
is to be regarded as a complicating condition of gravity superimposed upon 
one already exceedingly severe. The third or toxic type is, however, the form 
which presents the most grave and alarming aspect, for its onset is usually 
acute; it comes on when the patient is already profoundly ill, and it often 
betokens the rapid approach of diabetic coma, which in such a case may 
be said to be partly due to the renal lesions. Many clinicians consider 
that coma never comes on without this associated symptom. The kidney 
condition is therefore to be studied carefully in these cases, as it may give 
warning of approaching coma. 

Dyspeptic symptoms are often very annoying. They depend upon 
the excessive eating and drinking, to which many diabetics are forced by 
their thirst and hunger, the feebleness of the digestion arising from the failure 
in vital power, or to perversion of the digestive functions by the toxsemic 
state often developed as the disease advances. Extreme constipation is often 
a very troublesome symptom. 

Pulmonary complications, such as bronchopneumonia or tuberculosis, 
are very frequently met with in diabetics, owing to the lowered vital resist- 
ance which permits infection. Such complications are very often the cause 
of death, particularly tuberculosis. 

Although albuminuria is quite a common symptom, particularly in those 
patients who have arteriosclerosis, general dropsy is rare, notwithstanding 
the enfeeblement of the heart and the impaired state of the kidneys, because 
the urinary flow is so profuse that the body is rapidly drained of fluid. 

Callian has especially studied the influence of diabetes on the female 
genitals; pruritus vulvae is very common; menstrual disturbances are common; 
the atrophy of uterus and ovaries, he thinks, depends on the associated 
sclerosis of their nutritive vessels. 

Diabetes occurs in a certain percentage of cases of acromegaly and 
exophthalmic goitre. 

The nervous complications of diabetes mellitus may be divided into the 
acute and chronic. The acute complications are very serious from a prog- 
nostic point of view, and consist chiefly of diabetic coma. Many theories 



DIABETES MELLITUS 797 

have been advanced as to its direct cause. It is undoubtedly toxic in origin, 
and seems to be chiefly associated with a state of acidiosis, or the presence 
of one or more abnormal acids in the blood, of which one is called /?-oxy- 
butyric acid. The idea that acetone and diacetic acid are the causes has 
been cast aside. In some instances the onset of the coma (sometimes called 
"Kussmaul's coma") is sudden, but it may be gradual, although, even in the 
gradual cases, it is a matter of a few hours at the most, as a rule. 

Diabetic coma may be said to appear in three types: The first, and most 
common, is often met with in young persons, and develops with suddenness 
in many instances; that is to say, its onset lasts but a few hours at the most. 
The early symptoms are those of disorders of digestion, with abdominal pain, 
vomiting, muscular weakness, and drowsiness, which soon ends in coma. The 
breathing in this coma is often slow and deep, very much as it is in the second 
stage of opium poisoning. At other times it is sighing. To the respiratory 
state in this condition Kussmaul applied the descriptive word " Lufthunger." 
The second form often comes on after fatigue, particularly in elderly persons, 
and the symptoms may be those of profound collapse. In the third form the 
early symptoms are those of ataxia and confusion of speech. 

Sometimes the unconsciousness is preceded by great restlessness and 
irritability, while in other instances the onset of the comatose state is gentle. 

Of the ocular complications, cataract, optic nerve atrophy, and diabetic 
retinitis are to be remembered. Sudden blindness due to optic nerve or 
retinal changes occasionally ensues and palsies of the ocular muscles may 
take place. 

Diabetics are also subject to apoplexy. 

Of the subacute nervous symptoms we find painful neuritis, and not infre- 
quently a pseudotabes due to this cause, with loss of knee-jerk, Romberg's 
symptom, and even the Argyll-Robertson pupil. Sometimes a true tabes 
dorsalis seems to develop. 

Diagnosis. — The diagnosis of diabetes mellitus is easily made if the physi- 
cian will carefully examine the urine and will bear in mind the fact that he is 
not justified in deciding that the well-developed disease is present unless some 
symptoms which are characteristic are associated with the glycosuria. It 
may be said that he who has constant glycosuria is in the early stages 
of diabetes mellitus, and this is particularly true if this symptom be 
constant in a young person. On the other hand, it not infrequently hap- 
pens that a person of fifty-five or sixty years develops a mild glycosuria 
which lasts for years, and does not materially impair the health for a long 
period of time. Even these cases, however, often develop into the true 
disease. In other words, we may say that while glycosuria is not diabetes, 
it is a state that indicates a tendency to this disease or the presence of its 
early stages. The separation of the polyuria of diabetes insipidus from that 
of diabetes mellitus is made by the low specific gravity of the urine in the 
former disease, and the fact that sugar is present in the latter malady. 

It not infrequently happens that diabetes mellitus is overlooked because 
the patient does not complain either of thirst or of excessive urination, and the 
physician fails to examine the urine as a matter of routine. But patients often 
present symptoms which, while not distinctly urinary, should at once call 



798 DISEASES OF NUTRITION 

the attention of the physician to the possibility of diabetes being present. 
Thus, any patient who suffers from marked loss of flesh and increasing weak- 
ness should always be suspected of having diabetes, even if signs of tubercu- 
losis are present, for not infrequently the tuberculosis is secondary to the 
diabetes. So, too, women will sometimes complain of pruritus of the vulva 
or eczema of the genitals, or men will state that they are becoming impotent, 
in all of which cases the urine should be examined, since diabetes often pro- 
duces these signs. So, too, defects of vision, due to diabetic cataract, or, more 
rarely, to retinal changes, may be the first symptoms manifest to the patient, 
and still others complain of numbness or tingling in the extremities and 
present the symptoms of locomotor ataxia. On the other hand, as already 
pointed out, physicians not infrequently are so careless as to examine the 
urine only once, and when they discover sugar consider that the case is one 
of diabetes; or they obtain a reaction with Fehling's test, because of the pres- 
ence of some sugar-reducing substance, as when the patient is taking chloral; 
or, again, they mistake physiological glycosuria for true diabetes. It is 
evident that most of these mistakes in the diagnosis of diabetes depend upon 
lack of urinary examination or imperfect methods of testing this secre- 
tion. 

As an illustration of how necessary it is to examine a number of samples 
of urine before determining that the patient has or has not diabetes, it may 
be recalled that urine passed during the night or before breakfast is often 
free from sugar; while that passed after breakfast and during the day may 
contain much of it. 

The condition of diabetic coma is separated from the unconsciousness of 
uraemia by the cider-like odor of the breath, the presence of glycosuria and 
acetonuria, and the absence of the high arterial tension usually met with in 
renal disease, for in this state the pulse is feeble and of low tension. At the 
same time, it is to be recalled that uraemia may complicate diabetes. The 
patient lies in a condition which resembles profound alcoholic intoxication. 
Deeply unconscious, with half-opened eyelids, wandering eyeballs, and 
dilated pupils, he breathes in a panting manner, a deep inspiration being 
followed by a quick expiration. The respiratory rate may not be greatly 
different from the normal, but sometimes it is hurried, and then forms 
"diabetic dyspnoea," with a gradually increasing cyanosis. The tempera- 
ture is usually normal or below normal. This state almost invariably ends 
in from one to two days in death. 

Blood Tests. — In 1896 Williamson, of Manchester, England, introduced a 
modification and improvement upon Bremer's method of distinguishing dia- 
betic from non-diabetic blood, which is of practical clinical value in cases of 
temporary disappearance of sugar from the urine. This test, which is based 
upon the fact that glucose, even in minute quantity, decolorizes warm alka- 
line solutions of methylene blue, is performed as follows: 20 c.mm. of the 
suspected blood are added to 40 c.mm. of distilled water contained in a test- 
tube. Then 1 c.c. of a 1 : 6000 watery solution of methylene blue and 40 c.mm. 
of liquor potassae are added to the mixture. The contents of the tube are then 
well mixed by shaking. A control experiment is made by preparing the 
same quantities of normal blood and reagents in another tube. Both tubes 



DIABETES MELLITUS 799 

are placed in a beaker of water, which is brought to the boiling point over 
a spirit lamp and then allowed to boil for four minutes. By the end of 
this time the fluid containing the diabetic blood will have turned to a 
dirty pale-yellow color. 

In diabetes mellitus the erythrocytes do not stain at all or stain only faintly 
with certain aniline dyes. This has been proposed as a means of diagnosis, 
but as the same phenomenon has been observed in cases of exophthalmic 
goitre, leukaemia, and Hodgkin's disease, it cannot be regarded as of practi- 
cal value. Diabetic blood stains with biebrich-scarlet, while normal blood 
does not. 

Urinary Tests. — For many years the most popular tests for the deter- 
mination of the presence of sugar in the urine have been those which depend 
upon the fact that strongly alkaline solutions of grape-sugar reduce copper 
oxide to lower grades of oxidation. The most frequently employed of these 
tests is that which is made by means of Fehling's solution. This is best 
made in the following manner: 

Copper sulphate, 34.64 gm., with water enough to make 500 c.c. Mix 
and keep in a bottle by itself. Pure Rochelle salts, 173 gm.; solution of 
sodium hydrate, specific gravity 1.330, 100 c.c, and water enough to make 
500 c.c. For use mix equal volumes of these two solutions, thereby forming 
Fehling's solution. About one drachm of this solution is placed in an 
ordinary test-tube and boiled. If the solution does not remain clear, it is 
unsuitable for use. If, on the other hand, it does remain clear on boiling 
the suspected urine is to be added to it a few drops at a time, and the 
boiling continued, when, if sugar is present, the solution becomes opaque 
and yellow in hue, and soon a dense, yellowish-red sediment falls to the 
bottom. Should the quantity of sugar present be exceedingly small, it 
may be necessary to add urine until the volume of urine and the volume 
of Fehling's solution are equal. But the volume of urine must never exceed 
that of the Fehling solution. 

Trommers test is performed in the following manner: 

A drachm of urine is placed in an ordinary test-tube, and is treated with 
sufficient quantity of sulphate of copper solution to render the fluid a light- 
green color. An equal volume of liquor potassse is then added. This results 
in a blue precipitate of hydrated Copper protoxide, which dissolves upon 
shaking the tube, so that a clear-blue solution remains. If the test-tube be 
allowed to stand for some time the copper is gradually reduced, and precipi- 
tation of the yellowish-red suboxide of copper occurs. If the solution is 
heated, the tests act more promptly. Care must be taken that the fluid is 
not boiled actively, as under these circumstances precipitation may take 
place without sugar being present. 

It is hardly necessary to add that in making these tests the greatest possible 
cleanliness in the test-tubes and bottles should be maintained. 

Occasionally the urine in cases of diabetes mellitus contains acetone in 
excess and diacetic and oxybutyric acids. The appearance of acetone in 
amounts greater than normal (0.008 to 0.027) is always to be considered a 
signal of danger of diabetic coma. The test for the presence of acetone 
consists in distilling the urine and adding to several cubic centimetres of the 



gOO DISEASES OF NUTRITION 

distillate a few drops of liquor potassse, to render it alkaline. Several drops 
of Lugol's solution are now added, when, if acetone is present, the fluid 
becomes turbid, and iodoform is precipitated in crystals. If this fluid is 
now heated, the odor of iodoform is noticeable. 

Gerhardt's test consists in adding tincture of chloride of iron to the urine, 
when, if acetone is present in large amount, the fluid becomes a deep red. 

Prognosis. — The prognosis of diabetes is largely influenced by a number 
of factors. In the first place, as a rule, but by no means always, the outlook 
is favorable for long life in direct proportion to the age of the patient. Thus, 
it not infrequently happens that men and women who develop the disease 
after fifty or sixty years of age live the full length of years usually credited 
to human beings of that age. Even in these cases, however, the possibility 
of some intercurrent infection, like pneumonia, is to be borne in mind as a 
constant threat against life. Conversely, the disease is rapidly fatal in pro- 
portion to the youth of the patient. In young persons it runs a rapid course 
and may destroy life in a few weeks. Great emaciation usually develops in 
these cases; whereas, older persons may maintain their weight. The mere 
presence of glycosuria is not justification for as grave a prognosis, even if 
the amount of sugar be marked, as is the presence of glycosuria with associated 
thirst, hunger, and loss of flesh. For the first state is a leakage, while the 
second shows that nutritional changes are marked, and that true complete 
diabetes mellitus is present. 

The prognosis also depends somewhat upon the manner in which the 
patient responds to the regulation of his diet. Thus, if on the gradual with- 
drawal of carbohydrates and the use of proteid and fatty food the sugar is 
no longer found in the urine, and the urine gives no reaction with perchloride 
of iron for acetone, the condition may be considered as a mild form of the 
disease. If, on the other hand, the quantity of sugar diminishes, but does 
not disappear, and the urine gives any reaction with perchloride of iron, the 
case should be considered as one of moderate severity. Again, if the gradual 
decrease in starchy foods, until the patient is taking no carbohydrates, fails to 
diminish the sugar excretion, and if a perchloride of iron test gives a Bur- 
gundy or port-wine coloration, showing the presence of acetone in excess, 
then the disease is to be considered as severe. 

The cause of death in diabetes mellitus is usually one of the acute infec- 
tions, such as pneumonia, tuberculosis, or septicaemia, with or without 
carbuncle. Diabetic coma is another common cause of death. Frerichs 
found that 150 out of 250 deaths in diabetes were caused by coma. 
Of 43 fatal cases observed by Taylor, death resulted from coma in 26. 
Mackenzie found 19 deaths from coma in 87 fatal cases. 

Mandel and Lusk have recently stated the following proposition as to 
prognosis: If a diabetic be put on a meat-fat diet (rich cream, meat, butter, 
and eggs), and the twenty-four-hour urine of the second day be properly 
collected, 1 the discovery of 3.65 grams of dextrose to 1 gram of nitrogen 

1 " The urine should be collected so that an early morning hour (before breakfast) terminates the period 
for one day. This is necessary, because the sugar formed from eaten proteid is eliminated before the 
nitrogen belonging to the same. The long period between the evening meal and breakfast allows for 
the elimination of both constituents." 



DIABETES MELLITUS 801 

signifies a complete intolerance for carbohydrates, and probably a quickly 
fatal outcome. They have called this the fatal ratio. 

It may be laid down as a rule, that true diabetes mellitus never gets well, 
but that temporary glycosuria often does so under proper treatment. Diabetes 
may, however, be controlled and life prolonged very materially by resort to 
suitable diet and remedial agents. 

Treatment. — By treatment much can be done for the control of this dis- 
ease. As already stated, simple glycosuria can usually be entirely relieved 
by proper attention to exercise, the regulation of the diet, so that the patient 
does not overeat or overdrink, and particularly by the limitation of the 
amount of carbohydrate food which he ingests. In these cases the appearance 
of sugar in the urine is to be regarded as evidence of the inability of the patient 
to properly utilize these substances in the body. If there is reason to believe 
that he is too sedentary in Ins habits, it sometimes happens that a moderate 
amount of exercise causes a disappearance of the glucose. Again, if he is a 
thin, spare individual, who naturally worries much about business or pro- 
fessional duties, absolute rest from these causes of stress must be insisted 
upon, in order that the nervous system may recover its equipoise. 

When true diabetes mellitus is present, it is even more essential that these 
etiological factors should be controlled. Indeed, it may be well said that to 
attempt treatment by a diet and drugs is useless in a case of diabetes mellitus, 
unless the patient can be properly controlled in regard to his manner of life. 
provided that manner of life is deleterious. In other words, it is futile, in the 
majority of instances, to regulate the diet and to give drugs if the patient is 
to be continually exposed to causes which are more potent for evil than the 
remedies are for good. 

There can be no doubt that the dietetic treatment of diabetes is far more 
important than that by drugs, and it is essential that this fact be borne in 
mind, since physicians are often careless in regard to the question of dietetics. 
and patients are still more so, even after the importance of a proper diet has 
been conveyed to them. Quite frequently they follow the directions of the 
physician for a short time, and then, wearying of being deprived of favorite 
articles of food, take these articles surreptitiously, or openly declare that 
whether it does them harm or good they do not intend to be deprived of 
things of which they are fond. For these reasons the dietetic treatment of 
diabetes is much the more difficult part of the care of these cases. 

As diabetes is a condition in which the body is unable to properly utilize 
carbohydrates and their educts. it is manifest at once that an excess of carbo- 
hydrates must be forbidden; but what is an excess to one individual may not 
be an excess to another, for an excess is that quantity which is more than the 
body can use. For this reason it is usually wise, when placing a patient 
upon an antidiabetic diet, to diminish the quantity of carbohydrates which 
he receives, by a very gradual process, and to watch the quantity of sugar in 
the urine from day to day, since by this means the quantity of carbohydrate 
material which he can utilize may perhaps be approximated. A second 
reason for carrying out this gradual diminution in the quantity of starchy 
food lies in the important fact that not infrequently cases of diabetes are 
plunged into diabetic coma by the institution of a diet practically free from 
51 



802 DISEASES OF NUTRITION 

carbohydrates, perhaps because the system is in such a condition that no 
sudden variations in the character of the food can be permitted. Not only 
is it a clinical fact that coma may be precipitated in this manner, but we also 
know that the quantity of acetone in the urine is greatly increased by severe 
restrictions of carbohydrates. For this reason the physician, when restrict- 
ing diet, should always examine the urine, not only as to its content of sugar, 
but as to content of acetone as well, and if this latter ingredient is present in 
an amount in excess of that which may be considered normal, for a minute 
trace is sometimes present in non-diabetic persons, it is absolutely essential 
that he shall at once restore the full carbohydrate diet, since by so doing the 
quantity of acetone is diminished and the condition of acidiosis which pro- 
duces coma is diminished. (See Treatment of Coma.) The elimination of 
more than one gram of acetone in twenty-four hours is to be considered an 
excess. 

Thirdly, patients will often resent the total removal of carbohydrates from 
their diet list, and yet yield to their gradual removal. On the other hand, it 
is not to be forgotten that in some diabetics a certain amount of carbo- 
hydrate food seems to be essential, in order that they may not manufacture 
glucose from other articles of food, or from the proteids of their own bodies, 
and in order that acidiosis be not produced. That is to say, the administra- 
tion of starch in moderate quantity may compensate for their loss of glucose. 

Sugars should always be excluded. They are unnecessary articles of diet, 
and, aside from the fact that the body is unable to utilize them, they are apt 
to disturb digestion. 

Because carbohydrate food cannot be utilized, it has come to be well 
recognized that the patient must subsist largely upon the different forms 
of meat, both salt and fresh, excepting liver, which contains glycogen, and 
which, therefore, ought not to be given. So, too, butter, cheese, and the 
various oils and fats may be used. 

It has already been pointed out that diabetic patients whose supply of 
carbohydrate material has been cut down should be provided with an amount 
of fat over and above that usually ingested, provided, of course, that the 
individual can digest and assimilate fats. It is evident, however, from a 
series of investigations made by von Noorden and others, that butter, when 
taken in excess of five ounces a day, may cause an increase in the quantity of 
oxybutyric acid in the blood. Von Noorden has pointed out, however, that 
this deleterious effect of large amounts of butter can be diminished if the 
butter is first washed with cold water in a most thorough manner, since by 
this means we remove the lower fatty acids which are chiefly concerned in the 
production of acidiosis. Under these circumstances, von Noorden tells us 
that as much as seven ounces of butter can be taken daily without difficulty. 

Most of the shell-fish are useful, but contain too much glycogen. 

In the way of fresh vegetables, the patient may receive the various greens, 
such as lettuce, spinach, dandelion, cabbage, cauliflower, Brussels sprouts, 
string-beans, celery, watercress, tomatoes, onions, cucumbers, olives, and 
the various kinds of pickles, and practically all of the nuts which are com- 
monly employed as foods, except chestnuts, which contain too large a pro- 
portion of starch. 



DIABETES MELLITUS 803 

Not rarely the patient does best when he is placed upon a diet which varies 
in carbohydrates from week to week; that is to say, he is given a very small 
quantity of carbohydrate one week, and a fairly large quantity of it the next. 
In those instances in which the acetone reaction persists in the urine, whether 
carbohydrates are removed or allowed, von Noorden has strongly recom- 
mended what he calls "the oatmeal cure. ,, In this cure the patient eats noth- 
ing but oatmeal gruel for from one to two weeks, save that in addition to the 
eight ounces of oatmeal he is given a similar quantity of butter and some 
vegetable albumin. Often this mixture is administered as frequently as every 
two hours. Von Noorden asserts that on this diet the excretion of sugar falls 
to a point far below that excreted on a mixed diet from which all carbo- 
hydrate has been removed. At the end of a week or two it is always neces- 
sary to return to other foods temporarily, as otherwise the patient rebels 
against the pursuance of a pure oatmeal diet; but even with these frequent 
returns to an ordinary diet, excellent results are said to be reached. 

Tea, coffee, and cocoa may be employed, provided they are not sweetened by 
cane-sugar, but by saccharin. Dry wines which contain little sugar may be 
given to those who are accustomed to alcoholic drinks, although Scotch 
whiskey, rye whiskey, and dry gin are better than most wines. The various 
simple mineral waters may also be given, and of these both the natural and 
artificial Vichy waters are excellent, because of the quantity of bicarbonate 
of sodium which they contain. The old idea that because the patient urinates 
in excess he should be deprived of water is no longer followed. These patients 
should be allowed water freely, in order that the system may be flushed 
of toxic materials. When constipation is present, the mild saline purgative 
waters may be given, varying from Apenta, Carlsbad, and Hathorn water, 
to the more powerful saline purges. 

Theoretically, gluten provides a source of nourishment for diabetic 
patients, but practically it is almost impossible to obtain a satisfactory gluten 
bread which does not contain a very considerable quantity of starch. There 
are upon the market a few samples of biscuits made from gluten flour which 
probably contain a very small percentage of starch, and these may be freely 
given to these patients. The difficulty in the majority of instances is that 
patients get exceedingly tired of a diet from which all forms of bread are 
excluded, and for this reason it may be impossible to entirely exclude bread 
from the diet list. Most of the biscuits which are made from substitutes for 
wheat flour, such as that of the soya bean, are so oily that patients find it 
difficult to digest them. Almond meal, which also contains a very large 
percentage of oil and no starch, may be given. But here, again, the difficulty 
in digesting the fats it contains is often marked. Perhaps the most satisfac- 
tory bread is that which is known as aleuronat, and which has been highly 
recommended by von Noorden. Williamson gives the following formula for 
its preparation: Mix two ounces (62 gm.) of desiccated cocoanut powder 
with a little water containing a small quantity of German yeast. Make the 
mass into a sort of paste, and put in a warm place for half an hour or longer. 
The small amount of sugar contained in the cocoanut is almost entirely 
decomposed by the fermentation produced by the yeast, and the cocoanut 
paste becomes spongy. Add two ounces (62 gm.) of aleuronat, one beaten 



804 DISEASES OF NUTRITION 

egg, and a small quantity of water, in which a little saccharin has been dis- 
solved, and mix well until a dough is formed. Divide into cakes and bake in 
a moderate oven for twenty or thirty minutes. The great difficulty is to 
obtain cocoanut fibres sufficiently desiccated and powdered. 

Among the articles which are to be carefully avoided are all the sweet fruits, 
such as melons, grapes, peaches, and those vegetables which contain a very 
large amount of starch and sugar, such as rice, sweet potatoes, beets, beans, 
peas, and carrots. 

Although potatoes are eminently a starchy food, recent investigations 
indicate that it is perhaps the best form of starch which can be taken by the 
diabetic. 

The medicinal treatment of diabetes mellitus has narrow limits. It is 
true that a host of drugs have been recommended by various clinicians at 
various times, the statement being made that they were capable of materially 
decreasing the quantity of sugar which was lost in the urine, but further 
experience has almost universally proved that they possess little power. 
Furthermore, very few of them have been shown to possess any influence 
upon the symptoms associated with the glycosuria. In other words, at 
the best they affect only the one symptom of loss of sugar, and in no way 
correct the underlying cause of the malady. 

Without doubt opium is the most valuable drug in the treatment of 
diabetes mellitus in the majority of cases, for it exercises a more potent 
influence in diminishing the elimination of sugar in the urine than any 
other drug. Its alkaloids, morphine and codeine, are also exceedingly 
valuable, and may be employed when they prove capable of controlling the 
glycosuria and when the opium increases the constipation, but neither of 
these alkaloids is the equal of the crude drug. 

There are several important points in regard to the employment of opium, 
or its derivatives, in diabetes: First, patients of all ages seem to be able to 
take large quantities of opium in this disease without developing the evil 
manifestations of the opium habit. Second, these patients usually have 
to take ascending doses of the drug until they reach a dose which controls 
the glycosuria more or less completely. Third, opiates possess the advan- 
tage that they diminish to a large extent nervous irritation and stress. Not 
only do they protect the nervous system from external causes of irritation, 
but by producing mental quiet and diminishing worry they indirectly cause 
good results. An endeavor should be made from time to time to diminish, 
at least temporarily, the quantity of the drug which is taken. Ordinary 
deodorized opium is the best preparation. Patients may start on J grain 
once, twice, or thrice a day, and gradually increase it, if necessary. Or, 
| to J grain of morphine may be given at these intervals. In other instances 
J to 1 grain of codeine may be used as a beginning dose. Some patients 
get so much comfort and such a diminution of glycosuria under moderate 
doses of these drugs that the size of the dose does not have to be increased. 
Thus, I have bad under my care for nearly twelve years a woman who has 
taken but 3 grains of codeine a day during all that time. She has never had 
any desire to increase the dose beyond this amount, and it has kept her 
glycosuria within bounds, besides giving her a great deal of comfort. 



DIABETES MELLITUS 805 

In cases which do not possess marked nervous symptoms, but which are 
rather phlegmatic in type, and have a gouty tendency, the salicylate of 
sodium or salicylate of strontium may be given in full doses varying from 
10 to 20 grains three or four times a day; or, in their place, we may employ 
some of the new coal-tar products, such as antipyrin, acetanilid, and phena- 
cetin. These drugs, however, must be given in full doses to have any effect, 
and they so greatly increase the susceptibility of the patient to cold that they 
must be used with great caution. In cases which have a syphilitic history, or 
which seem to be gouty, the iodide of potassium, in the dose of 10 to 30 grains 
or more three or four times a day, often does good. When the patient can 
digest it, cod-liver oil is an exceedingly valuable alterative and nutrient. 

With the idea that the alkalies aid oxidation processes in the body and so 
help to burn up sugar, various alkalies, as the potassium and sodium salts, 
have been largely employed. Thus, potassium or sodium bicarbonate may 
be given in 10, 15, or 20 grain doses three or four times a day. 

Another remedy which is of value in some cases, particularly if ancemia 
is present, is Fowler's solution in doses varying from 1 to 3 minims three 
times a day. With some clinicians it has a great reputation in this disease. 

In the treatment of the various complications of diabetes we must first 
consider diabetic coma. After coma is once established, we have no method 
of treatment which promises permanent recovery. I have several times 
seen a temporary return to consciousness follow the intravenous injection 
of one quart of normal saline solution, and Continental clinicians have 
employed and strongly recommended the injection of carbonate of sodium 
in solution. (See page £06.) 

When the presence of acetone in the urine or of the early symptoms of 
intoxication indicate that diabetic coma is not far distant, two plans of 
treatment should be promptly instituted. One of these is directed to the 
prevention of the further formation of acidiosis, due to acetone-producing 
substances, and the oxidation of those already found. The other is designed 
to deprive these substances of their poisonous properties. As already pointed 
out, the addition of moderate amounts of starchy foods to the diet results in 
the decrease or disappearance of acetone from the urine — acetone being the 
symbol of intoxication. If this cannot be done by the use of remedies by 
the mouth, because the stomach is unfit to deal with food, then one of the 
monosaccharids, such as levulose or dextrose, should be dissolved in sterile 
salt solution and injected subcutaneously or into a vein. Ordinary sugars 
(disaccharids) cannot be used in this way, because they require the action of 
the digestive juices to be disintegrated. The quantity of fluid used should 
be a quart with 10 per cent, of dextrose. Not less than 50 to 100 grams 
of levulose should be given a day by the mouth. If neither of these can be 
had, glycerin may be given by the mouth. Another point of importance is to 
cut down the fats given to these patients, who before the onset of these symp- 
toms have been subsisting largely upon fats and proteids, because the 
poisons of coma are derived from fats and fatty acids. 

For the diminution of the poisonous properties of the toxic substances 
already formed everyone is in accord that alkalies should be freely admin- 
istered. Vichy water should be taken in large quantities, and 20 or 30 



806 DISEASES OF NUTRITION 

grains of bicarbonate of sodium may be given every two or three hours dis- 
solved in Vichy water, thereby fortifying it. Stadelmann has advised the 
intravenous injection of carbonate of sodium in order that it may combine 
with the acids in the blood, diminish acidiosis, and aid in their elimination. 
For this reason the quantity of acetone in the urine may be temporarily 
increased by this plan of treatment. Naunyn uses 35 to 40 grams of car- 
bonate of sodium (not bicarbonate) dissolved in a quart of water. This must 
be given very slowly by intravenous injection. Even this plan, if instituted 
after coma is present, rarely does more than restore consciousness temporarily. 
If the bowels are confined they should be opened by some saline purge, but 
active purgation should not be resorted to, since by this means concentration 
of the poison may take place if the bowel is not active in the process of 
eliminating poisons from the blood. 



DIABETES INSIPIDUS. 

Definition. — Diabetes insipidus is a condition in which a person passes 
excessive quantities of urine containing no abnormal constituents and of 
a low specific gravity. This term is sometimes applied erroneously to a 
fleeting attack of polyuria due to nervousness or fright and to profuse diu- 
resis following the ingestion of excessive amounts of water. It is also to be 
separated from the constant polyuria sometimes seen in hysterical women. 

Etiology. — Diabetes insipidus is most commonly met with in persons 
under thirty years of age and may occur in early childhood. It is more 
common in males than in females. Very rarely it is definitely hereditary, 
and occasionally there is in the history of the patient a statement that it 
developed after some severe injury, as a railroad accident or fall. In some 
instances this may be due to damage of the central nervous system, in 
others to local nervous lesions. It has also followed sunstroke and pro- 
longed fevers of an infectious type, and it has been met with as a symptom 
in cases of brain tumor. 

The cause is unknown, but it is probably due to some condition of relaxa- 
tion of the bloodvessels supplying the Malpighian tufts, with the result that 
an excessive quantity of fluid passes downward from these tufts through 
the tubules. 

Morbid Anatomy. — No distinct lesions have been found constantly in 
cases of this character at autopsy, and nothing has been learned of the 
pathology of the malady by dead-room investigation. Sometimes the kid- 
neys are found to be swollen and congested, but no real renal lesion explain- 
ing the polyuria has as yet been described. 

Symptoms. — The dominant symptom of diabetes insipidus is, of course, 
a profuse urinary flow. Next to this symptom is the constant thirst suffered 
by the patient, who no sooner provides his system with fluid by drink- 
ing than it escapes from the kidneys. The third symptom of importance 
is the annoyance caused by the necessity of emptying the bladder many 
times a day and the loss of rest at night by reason of the same condition. 
Closely related to these symptoms in its causation is dryness of the mouth 



DIABETES INSIPIDUS 807 

and excessive dryness of the skin. Partly because of the fact that the condi- 
tion develops usually in nervous patients, or in those whose nerves have 
been shattered by accident, persons suffering from diabetes insipidus are 
often very irritable and peevish, an irritability which is maintained by the 
necessity of frequent micturition. The body temperature may be normal 
or subnormal. Tyson states that some cases can take inordinate quantities 
of alcohol without intoxication, but that others are unduly susceptible to 
the cerebral effects of this drug. 

The quantity of urine passed by some cases of diabetes insipidus quite 
equals that passed by well-advanced cases of diabetes mellitus with free 
polyuria. As much as eighty and ninety pints a day have been excreted 
but the usual quantity is rarely above ten or twelve pints. The specific 
gravity is almost as low as ordinary water, and rarely exceeds 1.003 or 1.005, 
owing to the fact that the normal urinary solids are dissolved in such an 
exceedingly large quantity of fluid; but a high specific gravity alone does 
not indicate glycosuria, since diabetic urine may not be over 1.012 or 
1.015. At times the total urea is greatly in excess of that normally 
excreted. Albumin is never present except in very small amount. 

Diagnosis. — Before deciding that a patient has true diabetes insipidus 
it must be determined that the condition is not a fleeting polyuria, but a 
constant state. Tests as to specific gravity of the urine and for sugar will 
reveal diabetes mellitus. The state of the cardiovascular system and the 
eye-grounds may reveal chronic contracted kidney. 

Prognosis. — Prognosis so far as life is concerned is good. Recovery is 
by no means rare, and even if it does not take place death from the malady 
rarely, if ever, occurs. The celebrated case of Willis lived fifty years with 
this condition present. It is only when the diabetes insipidus depends upon 
a serious nervous lesion that the prognosis is bad, and then because of the 
lesion and not because of the polyuria. 

Treatment. — No treatment for diabetes insipidus which has yet been 
instituted has proved satisfactory. It is quite true that a large number of 
remedies have been spoken of in terms of praise by various practitioners, 
but the very number of them indicates that no one of them gives results 
which are definitely curative. The use of vegetable astringents, such as gallic 
acid, with the idea that by this means a diminution in the secretion of urine 
may be brought about, sometimes produces favorable results. The dose 
must be large, from 5 to 20 grains three or four times a day; but even when 
such large doses are used as to disorder the stomach, it not infrequently 
happens that no decrease in the quantity of urine is brought about. In 
other instances good results are said to accrue from the employment of an 
active fluid extract of ergot given in the dose of 20 to 30 minims three or 
four times a day, alone or with the bromide of sodium in the dose 
of 20 grains. The ergot is supposed to act by contracting the capillaries 
in the Malpighian tufts. When the polyuria causes much restlessness 
and insomnia, the remedies already named may be aided by the simul- 
taneous administration of codeine, which will probably not decrease the 
quantity of urine, but which usually acts as a nervous sedative with suffi- 
cient power to prevent the bladder from waking the patient more fre- 



808 DISEASES OF NUTRITION 

quently than is absolutely necessary. The bromides may also be used for 
this purpose. In those cases which are associated with neurasthenia or which 
follow prolonged nervous strain, the "Rest Cure "ora vacation where the 
patient is not annoyed by business or family cares will probably give better 
results than will drugs. 

GOUT. 

Definition. — Gout is a disease which depends for its existence upon a 
disorder of metabolism, as a result of which deposits of biurate of sodium 
take place in the joints and in the fibrous tissues surrounding them. It is 
characterized by associated changes of a fibroid and calcareous character 
in other parts of the body in many instances, and in its acute exacerbations 
it frequently causes severe inflammation and pain in one or more joints. 
The joint of the big toe is very commonly the chief seat of the articular dis- 
order. Gout is sometimes called " podagra." 

Etiology. — The precise cause of gout is unknown, but certain etiological 
factors in its development are universally recognized as being active. The 
first of these is undoubtedly heredity, but while it is true that the tendency 
to the disease is often inherited it is also true that the descendants of gouty 
persons often fail to develop the disease, and that other persons who have 
no gout in their family history suffer from the malady. It is interesting in 
this connection to note that younger children of gouty persons more fre- 
quently fall victims to gout than the children of their earlier years, probably 
because the gouty diathesis is better developed in advanced years in the 
parents than in youth. 

A second factor in the production of gout is mode of life as to exercise 
and mental labor. There is universal accord that great mental and nervous 
stress with little physical exercise frequently produces a gouty diathesis 
and often precipitates an acute attack of the malady in those already gouty. 
Duckworth states that political life in England is notoriously conducive to 
gout, and that lawyers are very prone to it. In the case of the country squire 
who is so often gouty, high living and drinking, with a long heritage of 
dietetic indiscretion, probably overcomes all the good effects of an active 
out-door existence. In those who live chiefly out-of-doors, as farmers, 
soldiers, and sailors, the disease is rare. 

A third factor of some importance is age. While cases of well-developed 
gout are met with in young children and, very rarely, even in infancy, the 
malady commonly does not develop till after the thirtieth year, but rarely 
waits till the fifth decade of life before at least beginning its early manifesta- 
tions. 

A fourth factor is the abuse of alcohol, not in the sense of going on sprees, 
but in such a manner that the system is all the time engaged in oxidizing or 
destroying this drug. Ales and beers — that is, malt liquors — are more prone 
to cause gout than are whiskies and other distilled liquors. Sweet and sour 
wines are also provocative of this disorder, particularly champagne. 

A fifth factor is overeating. There is an increasing number of persons 
in America who do not eat to live, but live to eat, and who stimulate the 



GOUT 809 

digestive organs to greater activity by the use of highly seasoned dishes, 
with the result that they ingest and absorb more food than the system can 
use, stifling oxidation and clogging elimination. 

Finally, a very powerful factor in producing gout, in those who are exposed 
to the metal, is lead poisoning of the chronic type. 

We find, then, that the chief causes of gout are heredity, lack of exercise, 
nervous stress, and the ingestion of more food or drink than the body can 
properly deal with. 

Frequency. — True gout in its frank forms is far less common in England 
than it was in the early part of the last century or in the eighteenth century. 
In America it is certainly very rare. On the other hand, both in England 
and in this country "lurking," "lateral," or masked gout is certainly greatly 
on the increase. The disease is more common in men than in women. 

Pathology. — When we come to a study of this disease from the standpoint 
of perverted physiology or pathology, we encounter a task over which the 
profession has toiled unceasingly year after year with little advance in our 
understanding of gout, but great advance in our knowledge of the meta- 
bolic changes in the body. When Sydenham wrote, after being a sufferer 
from gout for years, that it is due to "the impaired concoction of matters 
both in the parts and juices of the body," he expressed himself as clearly 
and correctly as do many modern writers on this subject. 

The pages of a text-book are not suitable for a discourse in which a multi- 
tude of researches are analyzed and judged, yet it is proper to take note of 
several theories as to the cause of gout that have been strongly advocated by 
one or more investigators, with some basis for their views. 

One theory is that when the blood and lymph are saturated with uric acid 
the urates are precipitated by a slight lowering of the temperature, such as 
is apt to occur in an exposed joint. This theory is not adequate to explain 
the disease, because it has been proved that the fluids are not saturated with 
uric acid or urates in cases of gout, and the disease affects parts which are 
not chilled. 

Again, Kolisch advanced the view that the so-called xanthin bases are the 
cause of gout. This investigator believes that the nucleinic bodies are broken 
up into xanthin and hypoxanthin, and that in the healthy kidneys these are 
in turn changed into uric acid. In gout he thinks that the kidneys fail to per- 
form their function properly, that the xanthins are not transformed into uric 
acid, and that this results in the retention of xanthins, which straightway 
proceed to cause gout. This view has been impaired by the fact that his 
methods of research were faulty and by the fact that other investigators, 
using more accurate methods, get different results. 

His believes that the uric acid of the gouty is a product of the disease, and 
that it is capable of causing evil effects in the body. It is not the prime 
factor, in other words, but a secondary factor, just as the bacillus of diph- 
theria is the prime factor, and the toxins which it produces cause wide- 
spread lesions as secondary factors. In the normal body uric acid is in 
large part destroyed; whereas, in gout it is permitted to exist and induce 
secondary evil effects. Any cause which prevents the destruction of 
uric acid predisposes the patient to its deleterious influences, and these 



810 DISEASES OF NUTRITION 

causes may be inherited, acquired, or due to poisons, such as lead. Here, 
again, we are met by the contradictory fact that in a number of dis- 
eases an excess of uric acid develops without any signs of gout appearing. 
Thus, in leukaemia, pneumonia, and chronic kidney disease this acid cir- 
culates in the blood in excess, but no gout is produced. 

The view of Ebstein is that there is a primary nutritional disturbance in 
the affected joints, and in other tissues, which results in tissue death within 
those parts, and that in these devitalized areas urates are deposited. Finally, 
von Noorden believes that a special ferment acts to produce these local 
nutritional changes and that the deposit of urates then ensues. 

The most popular theory as to the cause of the symptoms has been that 
there is present in the body an excess of uric acid. This is the theory of 
Garrod, and in more recent times has had its most enthusiastic advocate in 
Haig. Garrod's theory that the decrease of uric acid in the urine at the time 
of an attack is due to its retention in the body, and that this retention causes 
an outbreak, is now held to be erroneous, or at least is regarded with grave 
doubt, as is also his view that a decreased alkalinity of the blood causes a 
precipitation of the urates, for Magnus-Levy, Luff, and W. His, Jr., have 
all proved that the quantity of uric acid in the blood is not increased during 
or before an attack, nor is the alkalinity of the blood decreased. Still others 
have shown that the decrease in the excretion of uric acid just before an 
attack of gout is due, in part at least, to a decreased ingestion of food. These 
researches do not prove, however, that uric acid producing substances are 
not present in excess, and it is entirely possible that the scanty elimination 
of uric acid in many of these patients in the interval between attacks is due 
to the failure of the body to change them into uric acid, with the result that 
they cause an attack, at which time the percentage of uric acid excreted 
often temporarily rises. I confess that this view seems the more attractive. 
When we consider that the injection of uric acid into the blood does not cause 
gout, that it is present in leuksemia, pneumonia, and nephritis without causing 
gout, and that no excess of uric acid is found in the blood in gout, it is hard 
to believe that uric acid causes gout. While Kolisch's theory may be imper- 
fect in detail, and while the kidney may not transform xanthin into uric acid, 
it is entirely possible that an excess of xanthin may be present in gout. This 
view is supported by several facts, which indicate that uric acid is an end- 
product derived from nuclein breakdown, and that it is not this healthy end- 
product, but by-products which are morbid in effect. From nuclein we can 
obtain albumin and nucleinic acid; from nucleinic acid we can obtain phos- 
phoric acid and a substance which in turn may be split up into xanthin bases 
and uric acid. If oxidation is complete, uric acid is the chief end-product, 
if it is incomplete, then xanthin is the chief product. Bain and Futcher have 
both shown that when there is an increase in uric acid excretion there is an 
increase in phosphoric acid secretion, and they believe that this throws a side 
light upon the relation of uric acid and xanthin to gout. Thus, in one of 
Futcher's cases there was a marked fall in both phosphoric acid and uric 
acid immediately before an attack, followed by a very great increase at the 
time of the attack, and this again by a fall. The phosphoric acid curve was 
far greater than the uric acid curve. 



GOUT 811 

It would seem, therefore, that the destruction of nucleinic bodies may be 
perverted in gout, and this is all that Futcher's study proves, namely, that 
as phosphoric acid and uric acid are both derived from nuclein, and as they 
are greatly disturbed in amount in relation to the attack, it is fair to assume 
that some relation exists between nucleinic bodies, their derivatives, and 

s out - 

At the present time it would seem probable that we may divide this ques- 
tion of the pathology of gout into two sub-questions, viz. : 

1. Is there present in the body at the time of an attack of gout an excess 
of uric acid, or, rather, of material capable of producing uric acid? The 
answer is "Yes." 

2. What is the reason that this condition develops ? The answer is that we 
do not know, but that it is dependent upon a perversion of metabolism not 
yet understood, whereby in health uric acid, a primarily harmless body, is 
produced, and in disease a by-product is found, which causes an attack dur- 
ing, or before, which urate of sodium is deposited in the tissues. 

Morbid Anatomy. — Gout may produce morbid changes in every tissue of 
the body, even to the hair and nails, but the parts which are most frequently 
impaired by its existence are the heart and the bloodvessels, the kidneys 
and the joints. From the standpoint of outward manifestations and early 
discomfort, the joint changes are, of course, the most important, but from 
the standpoint of the physician, whose duty it is to prolong life, the cardio- 
vascular and renal changes are the factors which deserve most attention. 
Because of the wide distribution of gout in the body, Sydenham wrote: 
"Totum corpus est podagra.*' 

The lesions in the joints are characteristic; the ligaments, tendons, and 
bursse all become affected, and even the articular cartilages are involved. 
In all these tissues deposits of biurate of sodium take place, and they may be 
so copious that the parts are deformed and incapacitated by roughening of 
the cartilaginous surfaces, or by thickening of the sheaths of the tendons and 
joints. In typical cases the disease first attacks the joint of the big toe, then 
the finger joints, after this the metacarpal and metatarsal joints, and still later, 
but much more rarely, the large joints. When these are affected, the wrist, 
elbow, and knee are the parts usually involved. The ball-and-socket joints 
(hip and shoulder) are very rarely involved in gout, and the upper extremities 
are much less frequently affected than the lower ones. Wlien the disease is 
well advanced there is so great a deposit of biurate of sodium that it lies 
under the skin in a white knob, or pea-shaped mass, which looks white and 
chalky. If the skin covering such a deposit is injured, it not rarely undergoes 
necrosis, and biurate of sodium exudes from the part, looking like wet chalk. 
Sometimes on the fingers, near the base of the finger-nails, or about the first 
phalangeal joint, there develop small, hard, uratic masses called "crabs' eyes." 
It is a remarkable fact that these deposits often take place without any other 
manifestation of gout being present and without any pain, so that attention 
may be called to them only by reason of the disfiguration produced. Gouty 
deposits about the base of the finger or at the second joint are, however, 
usually part of a general gouty outbreak. 

When the articulating cartilages are affected two conditions may be pre- 



812 



DISEASES OF NUTRITION 



sented. If no injury has occurred, and if no cause of irritation has existed 
other than the gout, the articulating surface is seen to be smeared or plas- 
tered, to use Duckworth's expression, with a uratic deposit looking as white 
and smooth as fresh white lead (Fig. 105). When irritation has been present 
the articular cartilage may be eroded. In this latter form there is often 
overgrowth of connective or fibrous tissue in the surrounding parts along with 
the deposit of urates, as already described, and stiffening or distortion of the 
joint. The changes in the bursa are often noteworthy. I have a case now under 
treatment in which there is a bursa swollen to the size of a bantam's egg on 
the heel at the insertion of the tendo Achillis. It is a very dusky red and is 
exquisitely sensitive, but contains nothing but fluid. It has often developed 
before, and under active treatment for gout has always disappeared and left 
no trace behind it. 

Fig. 105 




Showing urate of sodium deposited on an articulating surface. (Graupner and Zimmerman.) 

The cardiovascular changes caused by gout do not result from the deposition 
of biurate of sodium in the heart-valves or in the bloodvessel walls. Indeed, 
it is rare for such deposits to be found, although cases are recorded in which 
the cardiac valves and the intima of the aorta have contained the biurate of 
sodium. But while it is true that biurate of sodium is not deposited in the 
vascular system, as it is in the joints, it is also true that gout causes first 
arterial spasm, then arteriocapillary fibrosis, and, finally, advanced calcare- 
ous changes in the vessels. The result of this is cardiac hypertrophy on the 
left side of the heart in particular. The endocardium is never the seat of 
acute endocarditis as a result of true gout. The only endocardial changes 
are those common to ordinary cases of general atheromatous degeneration, 
in that sclerotic changes take place in the valves, particularly those guard- 



GOUT 813 

ing the aortic and mitral orifices. The chorda tendinea are also shortened 
by a similar process and rendered inelastic. 

The pericardium is very rarely affected. 

The venous system is prone to varicosities and calcareous plates may be 
present in the walls of the veins. These in turn may result in thrombosis 
and phlebitis. 

Gout, cardiovascular disease, and angina pectoris are a wicked trio that 
bring many a noble man to death. 

Whatever the gouty poison may be which causes changes in the general 
vascular system, that poison also damages the renal tissues as well. The 
bloodvessels of the kidneys are, of course, involved in the general vascular 
fibrosis, and we have the small, contracted kidney often called a " gouty kidney," 
because it is often the result of gout. Many years ago Ord and Greenfield 
showed that in two-thirds of all cases examined at autopsy in which there was 
gout in the great toe there was chronic granular kidney, and in the remaining 
one-third a condition allied to it. While it is quite true that deposits of 
biurate of sodium are sometimes found in the kidney structure in the region 
of the papillae, and extending outward along the pyramids toward the 
periphery of the organ in whitish streaks, such cases are very rare when 
we consider the number of cases of gout and the number of cases of renal 
disease complicating its existence. 

Symptoms. — These are best studied in three divisions: the acute, the 
chronic, and the aberrant types. 

Acute Gout. — In this form the fully developed symptoms are often pre- 
ceded by several hours or days of nervous irritability, of insomnia, or of general 
wretchedness not easily described. In some cases pruritus ani is present, or 
itching elsewhere may annoy the patient and keep him restless at night. 
The urinary secretion is often scanty and the bladder may be irritable. In 
other cases these symptoms are entirely absent and the patient will recall, 
during his hours of suffering, that he has seldom felt as well as he felt for a 
day or two before the attack came on. 

The attack itself usually consists in the sudden onset of sharp pain and 
inflammation in the ball of the great toe. The pain is very severe and stab- 
bing in character, often extending upward into the foot. A swelling develops 
with surprising rapidity and the skin over it is red, hot, and burnished. In 
addition, the part affected is exquisitely sensitive, so that the pressure of the 
bed-clothes, much less that of a shoe, is insupportable. Not rarely a distinct 
febrile condition is present, the temperature reaching 102° or more. After 
a few hours the agony diminishes, the swelling decreases, and the patient 
is more comfortable, but within the next twenty-four hours the malady may 
return with fresh severity. This may persist for several days, but at the end 
of that time the patient is not only soon on the road to recovery, but feels 
better than for a considerable time before the attack, although the ball of 
the toe may be swollen and inflamed for some days longer. 

There are three noteworthy peculiarities about these seizures, namely, 
that they usually develop after midnight, waking the patient from sleep; 
that although the inflammatory process in and about the joint seems furious 
in its severity, the part never goes on to suppuration, and the onset and 



814 DISEASES OF NUTRITION 

disappearance of the attack is followed by little if any disability in the 
affected part. Only when repeated attacks take place is there developed 
much deformity of the area involved in the gouty manifestation. 

Acute gout is nearly always recurrent. Sometimes it attacks the patient 
every few weeks, in other cases every few months, and in others every few 
years. 

This form of gout is very rare in the United States, but frequent in 
England, although less so than it was many years ago. 

Chronic Gout. — Chronic gout as a distinct condition from acute gout 
does not really exist; that is to say, no sharp line separates this type from 
the acute form. Two types of it may be recognized. In one, repeated 
attacks of acute gout are connected with one another by modified gouty 
manifestations, such as stiffness and soreness in various parts, as in the wrists 
and elbows, or the maintenance of a certain degree of low-grade inflamma- 
tion in the joint of the big toe. In the other form there are no acute out- 
breaks such as have just been described, but a gradual process of gouty 
thickening of fibrous tissues and an equally gradual deposition of biurate of 
sodium about the tendons, the joints, and in the articular cartilages. Similar 
deposits called tophi are found in the edges of the ears, and the "crab's eye" 
formations in the fingers already referred to are found. 

The urine is scanty, the arterial tension is usually high, and the aortic 
second sound accentuated. (See Morbid Anatomy.) 

In some instances sudden inflammatory attacks of moderate severity, 
as compared to the acute attacks in the big toe, develop in one or several 
of the large joints, as the elbow and knee, and may give rise to the belief 
that acute articular rheumatism is present, particularly as a rise of two or 
three degrees of fever may take place. I have seen a patient with severe 
nodular gout of the hands develop an attack of universal articular gout 
after having his hands baked in a hot-air apparatus, probably because the 
treatment caused the distribution of a mass of gouty material in his body. 
The alterations in the appearance of the joints in these attacks has already 
been described when writing of the morbid anatomy of this disease. They 
may resemble very closely that malady called arthritis deformans. 

After this type of gout continues for years the patient comes to his death 
as a result of renal or cardiovascular disease, or by some acute infection, such 
as pneumonia, which finds a ready victim in one whose vital organs are 
already impaired. In other words, death is due to a terminal infection. 

Not rarely patients with this type of gout are intellectually brilliant up to 
the moment of their final illness. The presence of the disease seems to be 
a spur to mental activity. 

Irregular Gout. — Without this division of gout some modern physicians 
would be sadly at sea in diagnosis. It affords a loophole of escape when a 
patient insists on a diagnosis, and Haig deserves the gratitude of many prac- 
titioners for having popularized the idea of "uric acid as a factor in dis- 
ease." There can be no doubt that many patients do present symptoms of 
aberrant or modified gout, but they are by no means as numerous as they 
are thought to be. The gouty poison is capable of producing almost as 
many symptoms and ailments as is hysteria, but not all the symptoms which 



GOUT 815 

are credited to it, and it is unfortunate that "uric acid" is so often a cloak 
to ignorance which so pacifies the physician and patient that a search 
for a true cause is discontinued. Uric acid is, as already stated, in all 
probability not the cause even in the true gouty cases of many of the symp- 
toms presented, but rather the result of the metabolic disorders underlying 
the illness. 

There can be no doubt, on the other hand, that gout really is responsible 
in many cases for the presence of a very large number of disorders in widely 
different organs of the body, such as eczema and other forms of inflamma- 
tory or irritative changes in the skin, notably pruritus. Duckworth speaks 
of a painful induration of the ala of the nose in some gouty persons. In 
the circulatory system the changes caused by gout, even in those who have 
no outward manifestation of the disease, may be very notable, as already 
pointed out. 

In the article on gonorrhoeal infection it has already been stated that a 
suppurative urethritis may be due to gout, and irritability of the bladder 
and renal stone may arise from this cause. So, too, it is not infrequent for 
diabetes mellitus to develop in gouty persons and to be modified in its course 
by anti-gout remedies. 

Albuminuria is also frequently present as a result of the high arterial 
tension or of the nephritis produced by the gouty poison. 

Gouty persons often suffer from sudden and severe attacks of acute pharyn- 
gitis or laryngitis, and from acid dyspepsia, and ophthalmologists con- 
stantly meet with iritis, conjunctivitis, and other inflammatory processes 
in the eye due to this cause. So, too, it often happens that a thickening of 
the tympanic membrane, which causes deafness, has its origin in this malady. 

Finally, and by no means least important, gout or gouty tendencies often 
cause furious attacks of neuralgia and of migraine. Not rarely after such a 
seizure of pain the patient feels unusually well, just as he does after a frank 
attack of gout. 

Retrocedent gout is a condition in which the gouty process suddenly leaves 
the toe or other joint and attacks some one of the internal viscera, pro- 
ducing, it may be, violent purging and vomiting or precipitating an attack 
of angina pectoris. In other cases the patient suffers from an asthmatic 
seizure. Sometimes a sudden uraemia makes it appear that a retrocedent 
gout has gone to the brain. As a matter of fact retrocedent gout is not often 
seen. A letter of inquiry sent by me to several eminent English physicians 
brought replies that they had rarely seen this accident occur, although they 
have frequently met with cases, as we all have, in which a man subject to 
acute gout of the toe has had a gouty angina pectoris after prolonged free- 
dom from trouble in the toe. 

Diagnosis. — The diagnosis of gout when it affects the big toe is a simple 
matter. When present in the form of dermal, ocular, otic, or muscular gout, 
the history of the patient and the character of the attack render a diagnosis 
possible; but when the polyarticular form of gout with fever develops, only 
careful study and the absence of heart changes will enable us to separate 
the conditions if we can find no gouty history and no gouty signs, as in tophi 
in the ears, Again, there may be some hesitancy in separating gout from 



816 DISEASES OF NUTRITION 

chalky deposits and fixation of joints of arthritis deformans in which the 
articular process is somewhat inflammatory and painful, and in which 
fibroid changes in the connective tissue about a joint are present. Arthritis 
deformans is, however, a more surely progressive malady; it causes greater 
crippling of the patient; it is not characterized by chalky crab's eyes and 
tophi in the ears, nor by inflammatory attacks in the eyes or the great toe, 
nor in the tendons and bursse. 

Many of the cases of masked gout can only be diagnosticated by the 
improvement which is produced by proper dietetic measures and the use 
of therapeutic measures known to be beneficial to gouty persons. 

As stated at the beginning of the discussion of irregular gout, remarkably 
various symptoms can be caused by this malady, but all curious symptoms 
should not be credited to it. As Duckworth well says: "Without doubt 
many morbid states have often been flippantly or erroneously set down to 
irregular gout which owned no such designation, and thus a cloak for igno- 
rance has always been at hand to throw over careless observation, ignorance, 
or wilful misinterpretation of symptoms. As a consequence of such errors, 
some have come to regard even truly gouty manifestations, when not articu- 
lar, as actually non-existent, and to deny the dependence of such upon a 
gouty habit. The latter error is no more to be condoned than the former, 
and it may be fraught with mischief to the sufferer." 

Prognosis. — The prognosis of gout is better when it develops after forty 
than if it appears after thirty years of age. In many cases of frank gout 
the prognosis as to life is better than in the insidious form, for the latter often 
attacks the circulatory and renal tissues. Much depends upon the vascu- 
lar system. If it is fibroid the outlook is bad, and if it is not the mere 
existence of gout need not shorten life unless alcohol is abused. Gouty 
persons, however, are not good " risks" in life insurance, as has been proved 
by several sets of statistics. 

Treatment. — The treatment of gout is hygienic, dietetic, and medicinal. 
A further subdivision of the subject may be made into that which is devoted 
to the treatment of an acute attack and into those measures which are taken 
for the relief of the more subacute or irregular manifestations. The hygienic 
measures which are to be employed in the treatment of a person suffering 
from either gout with acute exacerbations, or suppressed gout, consist in 
such exercise as can be taken in the open air without at any time producing 
more than healthy fatigue. Exercise taken to the point of exhaustion is of 
course always deleterious, and particularly in those who are gouty, as it is 
prone to produce an acute attack or reduce vital resistance to such a degree 
that intercurrent maladies may develop. Golf, horseback exercise, and 
similar out-door pursuits are therefore exceedingly advantageous, but are 
not to be carried to an excess. These patients should also be directed to 
drink water in as large a quantity as may be taken without overloading the 
stomach at any one time. Many persons can take half a glass of water 
every hour without producing gastric discomfort or interfering with diges- 
tion; whereas, if they are content to drink only at meal times, but small quan- 
tities of liquid may be ingested. Water aids in producing a profuse urinary 
flow, and so helps to eliminate impurities from the body. If the heart is not 



GOUT 817 

feeble, hot baths or hot Turkish baths may be taken two or three times a 
week with advantage. Often such patients are greatly benefited by going 
to some of the health resorts where hot springs exist. 

The dietetic treatment of gout consists in the exclusion of all sweet wines 
and of fatty or rich foods, and in the ingestion of meals which are sufficiently 
varied in character to maintain the appetite and adequate to maintain 
nutrition. The patient should, however, be particularly warned against 
an excessive quantity of food. In many instances gouty persons will be 
found to take quantities of food which are far in excess of those which are 
required to provide the patient with the 2500 to 3000 calories per day which 
he requires for healthy existence. All wines and beers are also disadvan- 
tageous for this class of patients, but sweet and sour wines and champagnes 
are peculiarly so. In regard to individual articles of food, it has been held 
in the past that red meats were distinctly more harmful than white meats; 
but, as has been pointed out in discussing the dietetics of Bright's disease, 
this view of the relative harmfulness of red and white meat is becoming 
obsolete. Chemical analysis fails to reveal any material difference between 
them. The point of importance is that the patient shall not eat an excessive 
quantity of meat, or meats, which is prepared in such a way that it is diffi- 
cult of digestion, as, for example, larded game birds or larded beef. Of 
the various beverages cocoa is perhaps the best, but rich chocolates are 
harmful. Coffee is usually considered much better than tea. Indeed, Dr. 
Haig is quite confident that tea is an abomination for the gouty. 

In the way of treatment by drugs, there are only three which can be con- 
sidered as exercising an approximately specific influence, namely, colchicum, 
iodine in its various forms, and the salicylates. Of these the iodides and 
salicylates are most useful for the subacute or irregular forms of gout, while 
the colchicum is of most value for the purpose of combating an acute par- 
oxysm. Most patients with constant, irregular, gouty manifestations do 
well if they take continuously, over a long period of time, 10 to 15 grains 
of salicylate of strontium three or four times a day, or 5 or 10 grains of 
iodide of potash or iodide of sodium at similar intervals. By this means 
gouty sore throat, gouty iritis and conjunctivitis, gouty stiffness of the various 
muscles, and gouty neuralgia and migraine may be modified or entirely 
relieved. If there is any tendency to acidity of the urine full doses of citrate 
or acetate of potash, 10 or 15 grains three times a day, should be given, 
well diluted with water. In some instances the urine is alkaline, and when 
it is so the patient feels heavy and depressed. These symptoms can often 
be modified by the use of 10 to 20 grains of benzoate of sodium in capsule 
three or four times a day. 

Acute paroxysms of gout are to be treated by the administration of full 
doses of the wine of colchicum root, repeated in from six to twelve hours, 
the dose varying from 20 to 40 minims according to the irritability of the 
stomach and the idiosyncrasies of the patient to the drug. Not infre- 
quently much better results will be obtained if before the colchicum a 
moderate dose of the compound extract of colocynth, such as 10 to 20 
grains with 1 or 2 grains of extract of hyoscyamus, is given to unload the 
bowels. Colocynth is chosen because experience has shown that it seems 
52 



818 DISEASES OF NUTRITION 

to exercise a more beneficial influence in gout than any other purgative, 
and the hyoscyarnus is used because it prevents the colocynth from pro- 
ducing griping pain. Not infrequently some relief may be obtained if the 
inflamed joint is wrapped with lint laden with a 50 per cent, ichthyol oint- 
ment. Luff has strongly recommended the following application for the 
same purpose: The entire foot is surrounded by a warm pack consisting 
of cotton-wool saturated with the soothing lotion, and then lightly covered 
with oiled silk. The following lotion may be employed: 

& — Sodium bicarbonate . . . . . . %iv. 

Linimentum belladonna? . . . . . . f J iv. 

Tincture of opium . . = . . . . f % iss. 

Water ...... . . . f ^ vii j 

Equal portions of this lotion and hot water should be used to saturate 
the wool which has been rolled around the joint, and the dressing should 
be changed every four hours. 

It is important to remember that no local depleting measures are to be 
instituted under any circumstances. Blisters, leeches, and other forms of 
bloodletting are not only valueless, but dangerous, as they afford oppor- 
tunities for infection. 

Many cases of acute and chronic gout are also benefited if from time to 
time they receive moderate doses of calomel or blue pill, such as 3 or 4 
grains of blue pill or a grain of calomel in broken doses. Many physicians 
at the present time also prefer the active principle of colchicum, colchicine, 
to the wine of colchicum root. It may be given in the dose of y^- to gV of 
a grain every two or three hours in a case of acute gout, or four or five times 
a day in the subacute varieties. 

Although the various salts of lithium are largely employed by some 
practitioners for the purposes of combating the various aberrant forms of 
gout, it is to be remembered that the popularity of these salts depends more 
upon the skilful advertising of tablet manufacturers than upon the actual 
experience of the profession. Those who know most about these salts have 
found that the lithium preparations do not act as well in gout as do the 
salicylates of sodium or potassium, and the idea that lithium has a peculiar 
affinity for the uric acid is, to a large extent, blasted by the knowledge that 
lithium has a greater affinity for the acid sodium phosphate in the blood 
than it has for uric acid; beautiful test-tube experiments to the contrary 
notwithstanding. 

ARTHRITIS DEFORMANS. 

Definition. — Arthritis deformans is a chronic disease affecting the joints, 
and characterized by trophic disturbances in their cartilages, in the ends of 
the bones, and in the synovial membranes. It is to be distinctly separated 
from acute rheumatism and from true gout, although in some cases it appears 
to be a sequel of acute rheumatic infection. Sometimes arthritis deformans 
is called " rheumatoid arthritis," or " osteoarthritis." 



ARTHRITIS DEFORMANS 819 

Etiology. — Much discussion has arisen as to the cause of this malady, 
some adhering to the view that it is due to nervous lesions which result in 
changes in the joints, and others asserting that it is the result of an infection. 
Within recent years the former view has lost in popularity and the latter 
opinion is now in the ascendant, although as yet no one has succeeded in 
isolating the responsible micro-organism. 

In support of the nervous theory we find that trophic changes take place 
not alone in the joints, but in the muscles and skin near the joints affected; 
that pain is often present in the nerve trunks, as in neuritis, and that dis- 
eases of the central nervous system not rarely produce lesions in the joints 
which resemble those found in arthritis deformans. Certain French clin- 
icians have claimed that definite lesions are demonstrable in the spinal cord, 
in the columns of Goll in the cervical level, and in the posterior nerve roots 
as well. The difficulty in accepting the neural theory is that there is no 
proof that these changes are primary and not secondary, for it is well known 
that many joint affections are followed by similar lesions, at least in the 
nerves, skin, and muscles. 

Those who argue in favor of the infectious nature of the malady point to 
the fact that the nearby lymph nodes are often enlarged, as if combating 
infection ; that infection of the joints by various micro-organisms is the usual 
cause of arthritis, and that a considerable portion of the cases of arthritis 
deformans have had at some previous time gonorrhoea or other disease which 
is prone to cause secondary arthritic lesions. Ballantyne, Wohlmann, and 
Bloxall have isolated a bacillus, of dumb-bell shape, which stains with 
fuchsin or methylene blue, but not by Gram's method. Other investigators 
have failed to find it; Chauffard and Ramond have isolated a diplobacillus 
that they think is the cause. Organisms have also been found by Charrin, 
Le Roux, and Bouchard. Poynton and Payne have isolated a diplococcus 
from the synovial membranes in chronic arthritis, and by inoculation have 
produced the joint lesions of rheumatoid arthritis in animals. 

Most clinicians divide the cases of this disease into two classes : the primary, 
in which the arthritic state develops without any preceding joint affection, 
and the secondary, in which there is a history of such an infection. The 
primary cases are those in which the disease develops after a prolonged 
nervous stress or severe physical strain, as in frequent childbearing. The 
secondary form follows acute articular rheumatism and occasionally develops 
after injury to a single joint, although in this case the relationship of cause 
and effect is very doubtful. Even in the cases in which acute rheumatism 
has preceded the malady this relationship is in doubt, and there is nothing 
to prove that there exists any closer tie between them than sequence by 
coincidence. To sum up our knowledge of the etiology of arthritis defor- 
mans, we may say that we really know but little of it. 

Statistics as to the frequency of arthritis deformans in the two sexes differ 
greatly. In Garrod's statistics the disease affected 411 women out of 500 
cases. Stewart has recorded 40 cases, of which 20 were in women; and 
more recently McCrae has reported 110 cases, of which 55 were women and 
55 were men. My own experience at the Jefferson Medical College Hospital 
has been that nearly all are women. 



820 DISEASES OF NUTRITION 

The greatest prevalence of the disease is between twenty and fifty years 
of age, but Moncorvo has collected 48 cases of polyarthritis deformans in 
patients under fourteen years. 

The disease is very rare in the negro race. In a clinic rich in negroes 
McCrae only met with this disease in negroes four times in 110 cases, which 
is all the more noteworthy because negroes are peculiarly subject to other 
arthritic changes. 

Morbid Anatomy. — What the changes are in the early stages of this malady 
is not known, because patients rarely come to autopsy until after the dis- 
ease has existed for a long period. What little information we have indi- 
cates that the process is primarily inflammatory, in that the synovial 
membranes are injected and hypersemic. This is followed by the develop- 
ment of fibrous tissue, and this again by the absorption of the cartilaginous 
coverings of the ends of the bones. By these means cartilages become 
eroded and the ends of the bones become eburnated. Finally, there develops 
from the periosteum covering the ends of the bones, bony growths or knobs 
which lock the joints and because of the thickened membranes and rough- 
ened cartilages increase the tendency to immobility already present. These 
osteophytes are called "Haygarth's nodosities." Associated with these 
changes there is marked wasting of the muscles which govern the move- 
ments of the joint, a wasting not rarely met with in all serious joint affec- 
tions, a glossiness of the skin covering the affected joints due to atrophy of 
the glands in its deeper layers and to changes in the epiderm, and not infre- 
quently trophic changes in the nails which may be greatly thinned, ridged, 
or very brittle. 

The changes in the vertebras consist in overgrowth of the articular car- 
tilages, followed by ossification. The ligaments also become thickened 
or atrophied. Bony formations may appear on the edges of the vertebra?, 
particularly on their anterior surfaces, and finally in this way the whole 
vertebral column becomes an inflexible pillar composed of vertebral bodies 
welded together. 

Symptoms. — The symptoms vary considerably in the manner of their 
onset and in the course of the disease in different cases. The mode of onset 
may take two forms: the slow progressive or gradual type and that type 
in which a series of attacks of articular distress occur which leave behind 
them more and more chronic change in the joints. In some patients the first 
complaint consists in a sensation of roughness in the knee-joint; the part 
feels stiff after it has been in one position for any length of time, and " cracks " 
when it is moved. Not rarely this is first noticed in going up or down stairs 
or in rising from a chair. If the joint is flexed by the physician who holds 
the limb, the cracking can be felt by him. The sensation is one of distress 
more than of pain. 

The tissues about the joint are often swollen, but rarely if ever reddened. 
Usually after one joint is affected another becomes involved, and, as the 
process gradually develops, the patient becomes more and more incapaci- 
tated owing to the advancing changes in the joints and the new areas affected. 

The atrophy of the muscles also increases the inability to move about with 
ease. 



ARTHRITIS DEFORMANS 821 

Finally, the disease involves all the articulations, large and small, even 
the vertebral joints being affected, and the patient is as completely par- 
alyzed from fixation as if suffering from a widespread multiple neuritis. 
Such a result, however, does not occur in most instances, the malady being 
less widely distributed. 

It is a noteworthy fact, for which patients with this disease have cause 
to be devoutly thankful, that in the cases with greatest fixation of the 
large joints the small joints of the hand often escape, and when the 
hands are severely affected it often happens that the large joints are not 
involved. In still other cases the disease after incapacitating one part 
ceases to be progressive. The frequency with which pain occurs in these 
cases is very variable. In some there is none, in others it appears only when 
the parts are used, as in piano-playing, and in others the pain is severe and 
like that of neuritis. 

Free sweating of the palms of the hands and finger-tips often is present. 

Because of the fact that the manifestations of the disease are often limited 
to one part of the body or to one kind of joints, it has been customary to 
divide the cases into those with only one joint affected, the monoarticular 
form; those in which several joints are chiefly affected, the polyarticular 
type; and those in which the spinal column is the chief seat of the disease, 
the so-called spondylitis type. When the joints of the fingers are chiefly 
affected, so that they are locked by the growth of small, bony knobs on the 
sides, these growths are called "Heberden's nodes." An important differ- 
ence between these nodes and those due to the deposit of urates, as in cases 
of gout, is that they are true bony growths, and not due to the deposition of 
urate of sodium in the fibrous tissues. It is easy to see that this classifica- 
tion is purely one of convenience, and has no real pathological reason for its 
existence. 

When the large joints are involved, with associated fixation of spine, 
the patient lies in bed helpless, with the knees flexed and the back so stiff 
that it has been called "poker back." 

Under the name of spondylitis deformans von Bechterew has described 
a state of spinal fixation in which there is pain, compression of the spinal 
nerve roots, and muscular atrophy. Ascending spinal-cord degeneration 
is also present. It is questionable if this can be considered a part of true 
arthritis deformans. So, too, under the name spondylitis rhizomelique, 
otherwise known as the Strumpell-Marie type of spinal fixation, the muscles 
of the shoulder and hip joints are involved, but severe nervous lesions such 
as those just detailed do not develop. Osier believes that both of these 
affections are forms of arthritis deformans. This may be a correct view, 
but, if so, they do not present any symptoms common to arthritis deformans 
as it is generally met with. 

A form of general arthritis without exostosis, but with considerable swell- 
ing of the joints, is sometimes met with in children. The lymphatic glands 
are distinctly enlarged, the mobility of the joints greatly impaired, and the 
atrophy of the muscles well marked. Not only the lymph nodes nearest 
the joints, but all the lymphatics may be swollen. Ansemia is marked. 
To this condition the name "Still's disease" has been applied, because it 



822 DISEASES OF NUTRITION 

has been carefully studied by Dr. Still. Children may also have the poly- 
articular form of arthritis deformans as it occurs in adults. 

Attention must be called to that type of arthritis deformans in which 
the vertebrae suffer alone. In such instances the spine is fixed and immov- 
able, the ankylosis producing so much rigidity that the patient in stooping 
can only bend at the hips. When in addition to fixation deformity takes 
place, the spinal column may be deflected laterally or posteriorly, and the 
arching of the back may be so great that the head is bowed till the chin 
nearly touches the chest and the patient can only see a short distance ahead 
by rotating the eyes upward. Lateral rotation of the head in such a case 
is often impossible. Associated with this form of vertebral arthritis there 
is often a good deal of pain, which may be felt not only in the back, but in 
the hips and even down the course of the sciatic nerves. In those cases in 
which the disease is limited to a small portion of the spinal column the case 
may be considered as one of tuberculous disease, and the only means by 
which a positive diagnosis can be reached is by the use of tuberculin, if no 
changes in other joints point to the malady now under consideration. 

Diagnosis. — When a well-developed, bedridden case of arthritis deformans 
is met with, the patient being " fixed," and the bony knobs locking the joints, 
the diagnosis is not difficult. The difficulty lies in the cases which are in 
the early stages of the malady. This is particularly true of the cases which 
are of the subacute type, and which are ushered in by a somewhat abrupt 
onset, with soreness, stiffness, and pain in the affected parts. The differ- 
entiation of such cases in the first attack from a subacute form of true artic- 
ular rheumatism may be practically impossible. If an endocarditis develops, 
the disease is probably rheumatism, for the endocardium usually escapes 
in rheumatoid arthritis. Another point of differentiation lies in the fact 
that acute articular rheumatism passes from joint to joint, often diminishing 
in the first joints as the others are involved. This is also true of arthritis 
deformans, save that the joints first affected do not get well. The pain of 
rheumatism is greater and the parts affected are more tender to touch. 
Finally, if the articular difficulty persists week after week, in the face of the 
salicylates freely given, if the temperature creeps along at about 99°, and 
if there is crackling in the joints on flexion, the diagnosis of arthritis defor- 
mans is probably correct. 

Rheumatoid arthritis also must be differentiated from the arthritic changes 
due to gonorrhceal infection and those of locomotor ataxia. 

Prognosis. — A well-developed case of arthritis deformans is absolutely 
incurable, and the outlook is gloomy as to freedom of movement. The fact 
that the disease is often characterized by very slow progress and by periods 
of arrest is the most encouraging feature of these cases. 

Treatment. — From the stage of onset the treatment consists in the use of 
gentle massage of the joints with 50 per cent, ichthyol ointment, this oint- 
ment being also thickly smeared over the part between the times at which 
the rubbing occurs. If pain is present acetanilid or antipyrin may be used. 
If much stiffness is present the joint should be baked in a hot-air apparatus 
every day or two. 

It is a vital mistake to give these joints rest as a part of treatment. Barring 



CHRONIC RHEUMATISM 823 

use to the point of fatigue the patient should be told to move the affected 
parts as frequently as possible. 

Fresh air and sunshine are essential factors in controlling the anaemia 
often present. A valuable remedy, probably the best we have, is syrup of 
the iodide of iron in 30 or 60 drop doses three or four times a day well 
diluted with water and taken two hours after meals. 

When deformity which interferes with movement is present it may be wise 
to cut contracted tendons, but this does not increase mobility of the joint, for 
obvious reasons. 

Many patients resort to hot springs and hydrotherapeutic institutes for 
relief from this disease. Such a plan of treatment is good for the general 
health and may seem to arrest the process, but it cannot cause a cure, and 
if the patient's means are limited it is useless to let him waste them in a 
futile search for health. 



CHRONIC RHEUMATISM. 

Definition. — Chronic rheumatism is a condition characterized by a chronic 
low-grade inflammatory process in the synovial membranes and fibrous 
tissues about the larger joints which results in stiffness, soreness, and dis- 
ability. It may or may not be a sequence of acute articular rheumatism. 

Etiology. — The causes of this state are unknown. In many cases it seems 
to be part of the general fibrous change which occurs in other parts of the 
body due to old age. Exposure to cold and wet, as in the case of soldiers, 
firemen, and policemen, seems to be productive of the affection. The 
malady is very common among old negroes. It often causes great crippling. 

Morbid Anatomy. — The chief change consists in thickening of the fibrous 
tissues about the joints, but there is little effusion, as a rule, and no deformity 
aside from inmobility or fixation in an awkward position until secondary 
muscular atrophy ensues, as it usually does in all chronic joint affections. 
Occasionally the articular cartilages undergo changes and some crepitus 
can be felt on motion. 

Symptoms. — Stiffness and inability to move readily are the chief symp- 
toms complained of. These are worse when there is a threatened change 
of weather. If sudden movement is attempted pain is caused. Rest increases 
the stiffness and exercise greatly decreases it, but, on the other hand, suffi- 
cient exercise to limber the joints is often very painful, either at once or 
because of the exaggerated degree of stiffness that may develop. Occasionally 
these patients, particularly if they be women, become exceedingly obese. 

Treatment. — Unlike arthritis deformans, this malady gives us the best 
therapeutic results, in many cases, if the patient can be subjected to the 
salutary influence of the Hot Springs of Arkansas, Virginia, South Dakota, 
Banff, in Canada, or at Bath, in England. The various sulphur springs 
are useful in many cases. WTien these springs cannot be resorted to the 
patient should have the affected joints baked in a hot-air apparatus, or should 
take a Turkish bath several times weekly. A well-constructed Turkish bath 
cabinet, such as is widely sold at present, may be used at home. A 50 per 



824 DISEASES OF NUTRITION 

cent, ichthyol ointment should be well rubbed into the joints twice a day. 
This may be alternated with chloroform liniment containing 4 drachms of 
tincture of belladonna and 2 drachms of tincture of aconite in 8 ounces. 
In other instances iodine ointment diluted one-half with lanolin may be 
used. 

The use of drugs internally is not very satisfactory as to results. Pain 
may be decreased by acetanilid or antipyrin. The salicylates are rarely 
useful, but the iodides often cause great improvement. There is little use 
in dieting these patients. If they eat and drink sensible things the ordi- 
nary diet of health is the best. Alcohol should of course be used but little, 
if at all. 

Warm flannel should be kept next the skin, and cold winds avoided if 
possible by residence in a balmy climate in the winter months. 



MUSCULAR RHEUMATISM. 

Under the name of muscular rheumatism there exists a condition in which 
a patient experiences pain and stiffness when attempting to move certain 
muscles. This condition is most frequently met with in patients who become 
chilled after severe exercise. It sometimes develops when certain portions 
of the body have been exposed to cold and wet, as, for example, the stiff 
neck which follows sitting in a draught of cool air or the lumbago which 
follows exposure to a storm. 

The exact cause of muscular rheumatism is not well understood. It has 
been claimed by some persons that the liquids of the body contain so large 
a quantity of toxic materials, produced by perverted metabolism, that when 
a part is exposed to cold precipitation of these toxic materials takes place, 
either in crystalline or amorphous form, and this causes stiffness and pain. 

Treatment. — The treatment of muscular rheumatism depends somewhat 
upon the condition which has produced it. If it has followed exposure to 
cold, a very hot bath, a Turkish bath, or a hot pack will often serve to dis- 
sipate the pain and stiffness, particularly if after the bath active massage of 
the part affected is practised. In still other instances, particularly if the 
onset of the condition has been very acute, relief is obtained by acupuncture. 
This consists in introducing into the substance of the affected muscle a long 
needle, which does good, it may be, by relieving tension in the sheath of the 
muscle, and allowing some of the serum to escape. In many cases relief is 
obtained by rubbing the affected part with chloroform liniment, to which 
may be added tincture of aconite, tincture of belladonna, and tincture of 
opium. Equal parts of chloral and camphor, which deliquesce when they 
are mixed, may be rubbed over the painful area. Before giving medicines 
internally, the urine should be examined. If it is distinctly acid, the 
patient should receive from 10 to 20 grains of bicarbonate of potassium 
in water three or four times a day. In other instances similar doses of 
bicarbonate of sodium will prove equally efficacious. In still others it 
may be necessary to administer one of the salicylates. Thus, much 
benefit will often follow the use of 10 or 15 grains of strontium salicylate 



RICKETS 825 

given three times a day. Often it is advantageous to combine with this 
4 grains of acetanilid or the same quantity of phenacetin or antipyrin. 
In obstinate cases, or in those in which the symptoms frequently occur, 
the use of iodide of potassium or iodide of strontium in the dose of 5 or 10 
grains three times a day is advantageous, and sometimes the patient requires 
the additional use of y^-g of a grain of colchicine three or four times daily. 
It is not to be forgotten that some of these patients, particularly those that 
suffer from lumbago, owe their condition to autointoxication from the ali- 
mentary canal, which is due to constipation, and in such patients permanent 
relief will not be obtained until the bowels are thoroughly moved each day. 
In some cases the use of one of the saline purgatives is all that is necessary. 



RICKETS. 

Definition. — Rickets, or rachitis, is a nutritional disease of childhood, 
consisting in a general perversion of the processes by which normal growth 
takes place. It is chiefly characterized by imperfect osteogenesis. The ends 
of the bones are often larger than normal, and there is faulty growth in the 
cartilages, muscles, and tendons. 

Etiology. — Two factors are chiefly concerned in the production of rickets, 
namely, dietetic faults and bad hygienic surroundings. Of these the most 
important are errors in diet. On the other hand, it would seem that in some 
cases at least the diet may be correct, yet the faults in nutrition exist because 
the system cannot utilize the materials which are ordinarily employed in 
the production of normal tissues The majority of children suffering from 
rickets improve as soon as their food is properly adjusted. 

In the article on Scurvy attention has been called to the fact that while 
rickets affects both rich and poor, it is chiefly seen in the latter class, whereas 
scurvy in infancy is frequently a disease of the well-to-do. In many cases, 
however, scurvy and rickets exist simultaneously. 

The most common fault with the diet consists in the use of proprietary 
foods for infants, in the use of condensed milk, and in the carrying on of 
lactation until the period is past when the child can obtain sufficient nutri- 
ment from a breast which is secreting a poor quality of milk. 

It is interesting to note in this connection that valuable observations have 
been made upon young animals as to the effect of depriving them of ordinary 
diet and providing them with one not suited to their needs. Thus, Bland 
Sutton fed lion cubs with raw meat and rickets developed. ^Yhen a diet of 
milk, cod-liver oil, and powdered bones was given them they speedily got 
well. Experiments made upon other animals have given like results. 

Edlessen holds that the disease is of infective origin. Mendel thinks it 
depends on some change (atrophy) in the thymus and has formulated a 
system of treatment based on the thymic origin of the malady. Spillman 
rejects the chemical theory and holds that the deficiency in lime-salts is a 
result and not the cause of rickets. There has been much unprofitable dis- 
cussion as to the congenital origin of the disease. Fede and Finizio found, 
among 975 newborn, 4 that might have been called cases of fetal rickets; 



826 



DISEASES OF NUTRITION 



but most of the cases of so-called fetal rickets are instances of achondro- 
plasia. 

Age and nationality are factors of some importance in the causation of 
the disease. Holt states that it is very common in the children of the poorer 
class of Italians found in all our large cities, and it is certainly very common 
in negro children. In both of these classes the race has not so much 
influence as poor food and poor surroundings. 

The disease is rarely met with in children over three years of age, but the 
signs of its existence often persist in the shape of bony deformities all through 
life. Cases of rickets have been reported in children at the time of birth 
and as old as twelve years. Both sexes suffer equally severely from it. 

Diseases which impair nutrition may predispose the child to the devel- 
opment of rickets, but they do not produce it. Thus, congenital syphilis 
may act as a cause, but is not directly responsible. 



Fie. 106 



Fig. 107 





Rachitic epiphysitis, showing proliferated cells in the 
epiphysis. (Graupner and Zimmerman.) 



Syphilitic epiphysitis. 



Morbid Anatomy.— While it is true that we know little of the underlying 
cause of rickets, we have very clear and definite knowledge of its morbid 
anatomy. In healthy children the bones grow longitudinally by the devel- 
opment of bony materials at the space between the diaphysis and the 
epiphysis, and in breadth by the deposition of bony materials by the inner 
layers of the periosteum. The medullary canal is increased in diameter 
by the gradual absorption of the adjacent bone. In rickets the process 
is abnormal in that although the development of cells at the points of 
growth may be carried on to excess, the deposition of mineral matter to form 
bone is inadequate. The resulting structure is softer in texture and more 
vascular than normal, that is the osteoid tissue is perverted (Fig. 106). ^ It 
happens, therefore, that while the length and breadth of the bone is being 
abnormally developed, the lemallse adjacent to the medullary cavity are 
being absorbed, thus leading to structural weakness. Under these condi- 



RICKETS 827 

tions it is not difficult to understand why it is that the bones are unable to 
bear the normal stress and rapidly become deformed if any strain is placed 
upon them. 

Again, the process of development may be so abnormal that areas of bone 
are found in the midst of cartilage and far in advance of the edge of the 
normal bone growth, or the reverse holds true, and in the midst of bone 
there may be a cartilaginous mass with little mineral matter in it. 

Histologically there is excessive proliferation of the cartilages preliminary 
to ossification with irregular distribution of the columns of cells, excessive 
vascularity, and imperfect calcification. These enlargements seem particu- 
larly marked at the ends of the long bones and at the costal ends of the ribs 
and consist of this bone-like (osteoid) tissue, which later solidifies and 
perpetuates deformities of which it was originally the cause. 

In addition to the deformity of the long bones produced in this manner 
we find similar changes occurring in the bones of the head and pelvis. Not 
only do the fontanelles remain open for a longer time than is normal, but 
in addition the surfaces of the bones are found to be soft and porous and 
unduly vascular. In some places the occipital bone may be irregularly 
developed and spaces exist which are closed by membrane alone. This 
condition is called " craniotabes." The frontal bones are often large and 
bulging, forming the so-called " bossy frontals" described by the English 
clinicians. 

The actual deformities which result are bending of the long bones, par- 
ticularly in the legs; the development of pigeon-breast, with an increase in 
the anteroposterior depth of the chest, and the production of spinal curva- 
ture. A very constant state is the presence of swellings or enlargements of 
the ends of the ribs where they join the cartilages, producing the knobs or 
the so-called " rachitic" rosary. The spleen and liver are increased in size 
and Mendel thinks this is compensatory for the loss of thymic function. 
Mettenheimer and Friedleben describe atrophy of the thymus in rickets. 

Symptoms. — The symptoms of rickets, when the condition is well devel- 
oped, are very characteristic and can scarcely be overlooked even by the most 
careless observer. In the earlier stages, however, the manifestations of the 
disease are not so evident, and yet they are important in that they should 
place the physician in a position in which he can prevent further advance 
of the malady. These early symptoms consist in sweating of the head, so 
that the child's pillow is wet with the perspiration, and restless sleep, with 
grinding of the teeth. Partly because of the wet pillow and partly because 
of lowered vitality, rachitic children are very prone to colds and often suffer 
from constant catarrh of various mucous surfaces. Constipation is usually 
a marked symptom. 

In addition to these symptoms a physical examination of the patient will 
reveal in some cases in the early stages beading of the ribs, that is, enlarge- 
ment of the junctures of the costal cartilages and ribs, the so-called "rachitic 
rosary." The forehead may be full and large from the bulging of the frontal 
bones, the so-called "bossy frontals," already referred to, and the belly is 
bulging and tumid. 

If the condition is far advanced all these signs are more marked, and in 



828 DISEASES OF NUTRITION 

addition there may be found wide-open fontanelles and soft spots in the 
skull due to craniotabes. This state of craniotabes is much more marked 
in those cases which suffer from syphilis, and some observers have asserted 
that it only occurs in children who have inherited this malady. Auscultation 
over the open fontanelles may reveal a humming murmur synchronous 
with cardiac systole. Ansemia may or may not be a marked symptom. 

The nervous symptoms consist in laryngeal spasm (spasmodic croup) and 
great irritability. Epileptoid fits or tetany may develop. 

The shape of the thorax is also modified so that the lateral diameter is 
decreased and the anteroposterior diameter increased. This gives it a 
somewhat bulging or " chicken-breast" appearance. In the neighborhood 
of the ensiform cartilage there is seen, in some cases, a shallow depres- 
sion of the costal cartilages and ribs, which extends outward and upward 
toward the axilla on both sides. This depression covers the space of from 
one to three ribs and is called "Harrison's groove." It is chiefly due to 
protrusion of the lower ribs, which are pushed outward by the bulging of 
the abdominal wall. This deformity is most marked in children who suffer 
from spasmodic croup and obstruction of the upper respiratory passages. 
Palpation of the chest wall may reveal the fact that it is abnormally pliable 
or yielding. 

If the child is old enough to walk the long bones become deformed because 
they bend under the weight of the body. For this reason the bones of the 
.legs may be bent and badly curved anteriorly or laterally. There may be 
posterior curvature of the spine. 

Dentition in rachitic children is usually considerably delayed, and is 
accompanied by gastrointestinal disorders, chiefly because a tendency to 
catarrh of these parts is always present. The teeth when cut are usually 
fairly well developed and do not readily decay. This is in contrast to the 
history of syphilitic infants, who often cut their teeth abnormally early and 
then promptly suffer dental decay. 

Several of the symptoms described, while often found when rickets is 
present, are by no means characteristic of this disease, and occur frequently 
in other conditions. These are the craniotabes of syphilis, the laryngeal 
spasms, the systolic cranial murmur, restless sleep, and grinding of the 
teeth. 

Diagnosis. — Rickets should be separated from scurvy, with which disease 
it is very nearly related, and which may be present simultaneously. In 
scurvy the nutrition of the mucous membranes and of the bloodvessels 
seems to be chiefly involved, hematoma and purpuric rashes often develop, 
and bleeding gums are seen. These lesions are practically never seen in 
rickets. There is great muscular soreness on moving the child, and para- 
plegia is more commonly met with in scurvy, although in both states this 
palsy may be present. Again, the scorbutic child rapidly improves when 
given fresh orange- juice and beef-juice. Palsy may be due to acute anterior 
poliomyelitis, but if a careful study of the case is made it will be found in 
rickets that the muscular weakness is universal, whereas in poliomyelitis it 
is limited to certain groups of muscles and the associated rachitic symp- 
toms are absent. 



RICKETS 829 

Prognosis. — The prognosis as to life is good so far as the rickets itself is 
concerned. That is to say, death is never due to rickets. On the other 
hand, a child with rickets is a fair mark for every infection to which it may 
be exposed, and so the mortality of these cases from intercurrent maladies 
is high. If marked deformities exist they of course persist through life, 
except they be in the extremities, when they can be corrected by surgical 
procedures. 

Treatment. — From what has been said it is evident that the first thing to 
be done in a case of rachitis is to regulate the diet, and to see to it that the 
patient receives foodstuffs which contain all the ingredients which are neces- 
sary for the maintenance of normal nutrition. It not infrequently happens 
that the milk which is given to the child is lacking in mineral ingredients 
or contains such an excess of casein that the child's digestion is disordered 
and assimilation is disturbed. The mere fact that the child does not sub- 
sist upon market milk, but upon milk which is obtained by keeping a cow 
for the special purpose of providing sustenance for the infant, is more indic- 
ative of a dietetic cause for the rickets than if the child is obtaining milk 
which is given by a number of cows, for it not infrequently happens that 
the milk of a single cow disagrees with the child or does not contain all the 
materials which are necessary for its proper growth. If the child has been 
largely fed upon proprietary foods, these should be eliminated from the 
diet list and fresh milk and cereals used in their place. In some instances, 
as already stated, the rickets does not depend upon a lack of normal ingre- 
dients in the food, but upon the inability of the child to utilize these 
ingredients. This may depend upon digestive disorder, or upon a disturb- 
ance of trophic function. Under these circumstances it is not only neces- 
sary to investigate the diet, but to administer tonics which will improve 
digestion, such as small doses of quinine, J to J grain, twice or thrice a 
day; minute doses of nux vomica, or small quantities of the hypophosphites 
or the more modern elixir of the glycerophosphates. Of the latter 10 to 25 
minims may be given twice or thrice a day. In other instances tj-J-j- grain 
of phosphorus given in a sugar-coated pill may be used twice or thrice a 
day; or in its place we may administer drachm doses of cod-liver oil, or 
cod-liver oil in the form of a well-made emulsion. 

If ansemia is present 5 drops of the syrup of the iodide of iron may be 
given to a child of two or three years of age two or three times a day. As 
constipation is often a troublesome symptom in rickets, careful attention 
must be paid to the state of the bowels. They may be moved either by the 
use of a little calcined magnesia and followed by a few teaspoonfuls of 
orange-juice, or by one of the non-bitter preparations of cascara sagrada, 
such as aromatic cascara or cascara cordial. 

It is important that a child suffering from rickets should be allowed to 
have exercise without bearing weight upon its long bones. Such a child 
should not be encouraged to walk, but should be placed upon a rug on the 
floor, where it can crawl and roll about. An endeavor on the part of the 
parents to teach such a child to walk when its bones are unable to bear its 
weight results in deformities which may be so severe as to require operative 
measures for their relief. 



830 DISEASES OF NUTRITION 

It is hardly necessary to add that fresh air and sunshine are essential in 
the care of such children. A few weeks at the seashore will often cause a 
remarkable change in nutrition ; whereas the most skilful dietetic and medi- 
cinal treatment, if carried out with unfavorable hygienic surroundings, may 
produce no results whatever. 

In families in which rickets is prone to occur it is often wise to administer 
to the mother during the later months of pregnancy the hypophosphites 
or the glycerophosphates, and other nerve and bone tonics, as by this means 
the antenatal nutrition of the child can be materially influenced. In a well- 
known case in Philadelphia the first three pregnancies resulted in the destruc- 
tion of the mother's teeth and in the birth of children which speedily showed 
rickets; whereas, the last three pregnancies, during which a diet rich in 
mineral ingredients was provided, resulted in the birth of children which 
remained perfectly healthy. 

SCURVY. 

Definition. — Scurvy, or scorbutus, is a disease characterized by more or 
less profound nutritional changes in the body which are largely dependent 
upon the use of certain forms of unsuitable food. There may be extrava- 
sations of blood into the subcutaneous tissues, under the mucous mem- 
branes, and about the joints, and there is often great spinal tenderness when 
the disease occurs in infants. 

Etiology. — There can be no doubt that scurvy is due entirely to the use 
of food which fails to provide all the substances needed for the perfect nutri- 
tion of the body. Not only does it follow the continued use of food which 
is bad in the sense that it is unwholesome, but it arises in those who are 
subjected to a very limited diet of certain kind for long periods of time. 
Prior to the introduction of steamships it was a prevalent disease upon 
vessels in both the navy and in the mercantile marine, often disabling the 
crews and rendering impossible commercial and exploring expeditions. The 
use of steam now causes short voyages, and the better method of preserv- 
ing foodstuffs provides a change of diet almost daily, if it be needed. 

In certain parts of Russia scurvy still occurs in epidemics and is thought 
to be infectious. If this be true it is probably only because lowered vital 
resistance permits an infection to take place. 

Some investigators have believed that the disease arises from a lack of 
vegetable acids found in fruits and vegetables, others that the condition is 
due to an excess of sodium chloride in the blood, and still others that it is 
due to the presence of certain toxic substances developed in the food. Alber- 
toni has recently shown that in scurvy there is a complete absence of free 
hydrochloric acid in the gastric juice and that intestinal putrefaction is 
marked, and that the absorption of fats and carbohydrates is impaired. 

Pathology and Morbid Anatomy. — Anatomically there is nothing charac- 
teristic. The condition of the blood in scurvy resembles that of the blood in 
ordinary secondary anaemia with a decrease in the color index which is quite 
marked. If the case is studied at autopsy hemorrhages into the internal 
organs and upon the serous surfaces of the abdominal and thoracic viscera 



SCURVY 831 

are found and ulceration of the small and large bowel may be present. 
Swelling of the gums, loosening of the teeth, enlargement of the spleen, and 
degenerative changes in the heart, liver, and kidneys are found. Subperi- 
osteal hemorrhages may detach the periosteum over the shafts of the long 
bones and hemorrhage into the joints may also occur. 

Symptoms. — The symptoms of scurvy in adults begin with a sense of gen- 
eral wretchedness, pallor, and feebleness. These are followed by swelling and 
sponginess of the gums, which may bleed if pressed upon and which may 
partly cover the teeth by a process of granulation. The teeth become loosened, 
the mouth becomes foul, the salivary glands swell, and petechia? appear over 
the surface of the body. The skin is dry and badly nourished, and extrava- 
sations of blood may take place into the sheaths of the muscles and joints 
or beneath the periosteum of the long bones. These lesions at times cause 
patches of hardness or induration in the muscles of the thighs or calves. I 
saw this well developed in a case which I had in the wards of St. Agnes' 
Hospital some years ago. 

Infantile scurvy, sometimes called "Barlow's disease," is an interesting 
result of modern life. As seamen have escaped the disease by a better 
diet, babies have fallen victims to it as a result of feeding them with artificial 
foods, and these babies are not, as a rule, the children of the poor, but the 
offspring of the rich. 

It is only within the last decade that the possibility of scurvy occurring in 
young children has been generally recognized by the profession. During 
this period, however, evidence has been presented which shows very clearly 
that scurvy is by no means a very rare affection in early life, and that it 
often manifests itself in such a way as to lead the physician to make a 
very erroneous diagnosis when the patient is first brought to him. 

Perhaps the most frequent error in diagnosis under these circumstances 
is that the child is suffering from muscular or articular rheumatism; this 
decision being reached by reason of the fact that the child seems to suffer 
great pain upon movement, and sometimes has a moderate degree of fever. 

The characteristic symptoms of scurvy in a young child, when they are 
well developed, are so pathognomonic that it is difficult to see how an error 
in diagnosis can be made if the physician is acquainted with the possibility 
of the occurrence of this disease. Like all diseases, however, instances are 
met with in which many of the characteristic symptoms are entirely absent, 
and it is not uncommon for the painful manifestations spoken of to be the 
only evidence of the malady. In still others, we find a peculiar spongy state 
of the gums, which tend to bleed when lightly touched, and which are fre- 
quently so swollen that teeth which have recently broken through the gum 
are speedily covered in by the overgrowth of the mucous membrane, the 
edges of which, about the teeth, frequently look as if they were composed 
of tiny blebs of blood of a dark color. Another symptom of scurvy, which is 
by no means as constant, and yet which is equally characteristic, when it 
occurs, is the development of petechia? in different portions of the body, very 
frequently about the ankles and feet. In still other cases subperiosteal hema- 
toma develops with surprising rapidity, and as pain on movement and the 
development of great swelling are frequently first noticed after a fall or a 



832 DISEASES OF NUTRITION 

blow, it not rarely occurs that the physician is led into the belief that trauma- 
tism is the cause of the illness, without recognizing the fact that it has played 
but a small part in causing the sudden development of a state which really 
indicates grave systemic conditions. It is true that these subperiosteal 
haematomata have been chiefly reported by French clinicians, and have 
been rarely seen in this country; whereas, on the other hand, considerable 
extravasations of bloody serum have been met with in the loose tissues 
after exposure to injuries which in the healthy infant would produce no 
symptoms whatever. Paraplegia may also be present. 

The peculiar characteristics of scurvy in infants are the very grave appear- 
ance of the child when suffering from the disease in its severe forms, the 
rapidity with which it improves under proper treatment, and the rarity 
with which death occurs as the direct result of the malady, since a fatality 
is usually produced by some intercurrent disease. Reinert has, however, 
recorded a fatal case with red cells at 976,000 and haemoglobin at 17 per 
cent. 

Scorbutus in infancy is distinctly a disease of the children of the well-to-do 
in distinction from rickets which, on the other hand, seems to be a disease 
of the poor. Clinical experience, I think, indicates that scorbutic cases are 
rarely brought to hospital dispensaries while rachitic cases are constantly 
seen. On the other hand, scorbutic cases are not uncommonly met with in 
private practice. This clinical fact seems to carry out certain theories which 
have been advanced in regard to rickets in a way which is interesting. It is 
not many years since everyone believed that rickets was due to a deficient 
quantity of bone-forming material in the food of a child, but since that 
time other clinicians have stated their belief that more commonly it depends 
upon inability of the child to assimilate and utilize the ingredients in its food 
which it needs for proper bone growth. Or, in other words, the fault lies not 
with the food, but with the child. Among the poor this inability is probably 
due to unhealthy surroundings and a general lack of sanitation which inter- 
feres with development. On the other hand, such influences are not at work 
among the children of the well-to-do, but these children often receive, for 
long periods of time, the various artificial foods which, in many instances, 
they are incapable of digesting; and not only this, but no change is made in 
their diet for months, either in the quantity of the various ingredients which 
it contains, or in their quality. These children, therefore, suffer from the 
nutritive changes which come on as a result of a limited and fixed diet with 
no variation; whereas, the children of the poor, who often have too great 
a variation in their diet, rarely present scorbutic symptoms and often do 
manifest distinct rachitic symptoms. 

Physicians, in the presence of obscure illness occurring in early childhood, 
should remember the possibility of either one of these affections being the 
underlying cause for the manifestations of disease, and thoroughly investigate 
the question of diet before administering remedies, such as the salicylates 
for rheumatism, iron for the blood, or bromides for nervous irritation. 

Treatment. — The treatment of scurvy in adults consists in providing good 
and varied food, with plenty of oranges or lemons and green vegetables. Sun- 
shine and fresh air are also essentials. Arsenic and iron may be given as 



OBESITY 833 

hsematics. If digestion is impaired it should be aided by hydrochloric acid 
and pepsin or lime-juice and pepsin. For the lesions in the mouth a chlorate 
of potash and myrrh mouth-wash (see Stomatitis) may be used. 

If the disease occurs in a child it is to be treated by changing the food 
and in using raw milk instead of sterilized milk. Beef-juice squeezed from 
a half-cooked steak and orange-juice are also very useful. 



OBESITY. 

Definition. — The term obesity, or adiposity, is used to describe a state in 
which an individual suffers from an excessive deposit of fat in those parts 
of the body where a moderate amount of fat is found in health. In its 
advanced forms fat is also deposited in parts where it is never found in the 
normal state. 

Etiology. — It must be clearly understood that the mere presence of an 
unusual amount of fat does not in any way indicate ill-health or that the 
functions of the body are perverted. In many instances a considerable 
degree of obesity exists, because it is the natural state of the individual. In 
others, however, the deposition of fat in excess is a manifestation of disease 
or at least of perverted function. 

In the first class, of what may be called normally obese persons, the con- 
dition arises from inherited tendency. It is in this class that we find indi- 
viduals who have never been heavy eaters and who for years have deprived 
themselves of foods of which they are fond, but still gain weight. In another 
class it develops from overeating and lack of exercise, and in the third class 
it is due to disorders of metabolism, whereby foodstuffs are not properly 
dealt with by the economy after they are ingested. 

These three types are worth recalling, because when a patient seeks relief 
from obesity much depends upon the type to which he or she belongs, as to 
advice, prognosis, and treatment. 

Symptoms. — It is not necessary to describe all the symptoms of obesity, 
for the manifest increase in the size of the patient determines the diagnosis 
of an excess of fat. There are, however, certain other symptoms which are 
of importance, not only because they are part of the symptom-complex of 
obesity, but also because their presence determines the degree to which 
the excess of fat is really annoying or harmful. A symptom usually com- 
plained of by the patient is dyspnoea on exertion, which arises from the fact 
that the heart and lungs are put under stress because great muscular activity 
is needed to move the heavy body. This dyspnoea is also due to the fact 
that the vascular network is greater in the obese than in those who are lean, 
and therefore the heart has to drive the blood through a greater number of 
bloodvessels. Thirdly, the heavy deposits of fat on the chest walls, in the 
omentum, in the mesentery, about the diaphragm, and around the heart 
interfere, mechanically, with the free action of the respiratory and cardiac 
muscles. In many cases of severe obesity the layers of fat are projected 
between the cardiac muscular fibres, and thus seriously impede its move- 
ments, forming the so-called "fatty heart of the obese, " which is, of course, 
53 



834 DISEASES OF NUTRITION 

a very different state from the true fatty heart of myocardial degeneration. 
The pulse is often small and rapid. The arterial tension is also lower than 
normal, as a rule. 

While many of these patients are mentally and physically slow and some- 
what somnolent, others are active and restless and even unduly wakeful. 

Next to the dyspnoea the chief complaint is of constipation or indigestion 
and excessive sweating. Some cases of obesity, however, have a digestive 
system all too good. 

In some cases, too, there is an excess of urates in the urine, and these cause 
vesical irritability, chiefly because the larger surface of the body and the free 
perspiration cause a great loss of fluid, and this in time causes a scarcity of 
urinary flow with consequent concentration of the urinary solids. 

Treatment. — The first point in treatment, as von Noorden has said, is to 
determine whether we shall diminish the fat already present or content our- 
selves with the prevention, if possible, of an increase in the obesity. As a 
rule, the patient is not content with a plan of treatment which does not 
actually diminish the fat, partly because he has delayed consulting a physi- 
cian until the condition is far beyond what she desires. This is particularly 
the case with women who have arrived at middle life and who begin accu- 
mulating weight at the time of late childbearing, or in other cases immediately 
after marriage. These patients are often normally fat — that is to say, their 
condition is physiological — and they should be content in the majority of 
cases to try to prevent further obesity, rather than to remove fat already in 
existence. Such patients are often not unduly fat, and in their desire to main- 
tain a "girlish figure'' are willing to resort to almost any measure to become 
thin. Indeed, women in the fashionable walks of life, with little to think 
about, often make their lives miserable and destroy good health of mind 
and body by endeavoring, on the one hand, to get thin, or, on the other 
hand, to get stout. 

In such cases the physician should advise against severe measures, point 
out that the plumpness is natural, and, if need be, assert that it is better to 
be in good health, and a little more weighty than the average woman, than 
to be in bad health and slender. I have seen several splendid specimens 
of healthy womanhood made physical wrecks by ill-advised efforts to get 
thin. 

The great difficulty with all plans of treatment for the reduction of fat, in 
those women who desire to be slim for the sake of vanity, is that no plan can 
be so nicely adjusted as not to remove fat from where its presence is needful 
to good looks. With the decrease in the bulkiness of the hips and waist a 
hideous leanness of the chest and mammary glands ensues and leaves these 
parts covered with a skin thrown in wrinkles by disappearing fat, so that a 
well-preserved woman of middle age is soon converted into a hag. Further 
than this, pads of fat keep organs in place, and those who wilfully remove 
these pads may subsequently suffer from floating kidney, gastroptosis, 
uterine disorders, and constipation. 

There is a sad' lack of knowledge on our part as to the metabolism of 
obesity and nutrition in general, and the patient and physician must be 
careful how they attempt to disarrange processes so intricate and important. 



OBESITY 835 

On the other hand, it is often necessary to arrest a process which is mani- 
festly excessive and in need of control. 

In young persons whose nutritive processes are still in a formative stage 
and who are obese, we should not reduce weight already present, but simply 
try to prevent an abnormal increase. This holds true of those persons in 
later life who give a history of having always been fat. It is very unwise to 
ignore this rule if advanced years are already upon the patient, for under 
these conditions the effects of age and the efforts at reduction may produce 
disastrous nutritional changes. 

The most favorable period of life for reduction in weight is from twenty- 
five to forty years of age. 

Before ordering a diet and mode of life the patient should be subjected 
to a very careful physical examination; the urine should be repeatedly 
examined, and the state of the heart and vascular system carefully noted. 
If the urine contains albumin and sugar a reduction treatment is contra- 
indicated, and if the heart is weak from myocardial degeneration and if the 
vessels are fibroid it is dangerous to institute a plan of this sort. 

When it is determined that the patient is in normal health as to his vital 
organs the treatment for the prevention of increase is to be instituted, the 
patient being informed that a good result cannot be reached by a sudden 
and rapid process, and that patience and persistence are necessary for really 
valuable results. 

The first factor is exercise taken to the degree of moderate fatigue. Many 
patients take it to excess, and then not only eat and drink heavily, but lie 
down and rest while the nervous system lazily permits vital oxidizing 
processes to go on too slowly, and so more weight is gained than lost. 

In many cases no material reduction in fat can be attained unless the 
patient can be treated in a sanatorium, or at least in some place where an 
absolute diet can be maintained for a long period of time. It is not sufficient 
to order a reduced diet and but little to drink and much exercise. Such 
aids to reduction in weight w T ill not in the ordinary case produce much 
improvement, because the patient is not willing to persist in the annoyance 
of such a strict diet for a sufficient length of time to establish a new nutri- 
tional abscissa. Unless the state of reduced weight is maintained for a long 
period the patient often gains more flesh on returning to the ordinary diet 
than if no attempt at reduction had been made. 

The order for actual reduction of weight consists in cutting from the diet 
list all sugars and sweet articles, all fats and richly prepared foods, and in 
the prescribing of lean meat, and of vegetables which are bulky but contain 
little starch. Celery, lettuce, string-beans, spinach, cabbage, cauliflower, 
and limited amounts of tomatoes may be permitted ; whereas potatoes, bread, 
peas, and beans are to be forbidden. All alcoholic drinks are to be avoided, 
because the alcohol has to be oxidized in the body and so prevents an active 
oxidation of the foodstuffs and tissues. Alcohol is also contraindicated, 
because it stimulates the digestive organs and so increases the desire for 
food. 

If the avoidance of the fattening foods named above does not prevent 
an increase in weight, then a more rigid diet must be arranged. The patient 



836 DISEASES OF NUTRITION 

is not to be given all the food he desires, but must suffer from privation 
and hunger. Instead of ordering an amount of food which will give the 
2500 to 3000 calories necessary for comfortable existence, an amount cal- 
culated to allow about 2000 calories or less must suffice. 

For breakfast the patient is allowed 3 ounces of lean meat, 1 ounce of 
bread with no butter, and a cup of tea or coffee with no milk and no sugar, 
the sweetening being done by the use of saccharin. At an early luncheon a 
single soft-boiled egg may be given with an ounce of bread. At dinner a cup 
of clear soup, such as consomme* or Julienne (but no thickened soup or 
pure*e), may be allowed, followed by 2 ounces of fresh or salt fish, and this by 
2 or 3 ounces of lean meat. At this meal small quantities of the various 
green vegetables already named may be taken. The dessert should consist 
of some fresh fruit, such as an apple, an orange, a grape fruit, or a pear. In 
the middle of the afternoon a glass of milk or a cup of tea with a thick water 
cracker may be given, and at supper-time 3 ounces of lean meat, some 
lettuce with oil and vinegar, celery, 2 ounces of toasted bread or Zwei- 
bach or crackers may be given. At bedtime a biscuit and a glass of milk 
may be allowed. While excessive drinking of water is unwise, the patient 
should not be deprived of water to such extent that he suffers from thirst 
or has not sufficient liquid in his body to carry out to the full every physio- 
logical function. Although overfilling the tissues with water will make the 
patient appear fat, a certain amount of fluid is necessary to healthy life. 

In the way of drugs there is but one remedy which exercises a great influ- 
ence in reducing flesh, and that is the thyroid gland. This substance does 
not reduce the weight of all cases of obesity, and often fails unless it is 
given in doses which are so large as to cause distinct cardiac feebleness. 
The doses usually given vary from 2 to 6 grains of the extract of the gland 
once, twice, or thrice a day. It is important to give a large amount of nitro- 
genous food at the same time, for the thyroid causes a loss of nitrogenous 
tissue in the body as well as a loss of fat. Small doses of strychnine and 
of digitalis are also useful to protect the heart from depression. The patient 
should be warned against severe exercise while using this drug, and often 
will do best if confined to bed and given massage and electricity. 



ADIPOSIS DOLOROSA. 

Under the name of adiposis dolorosa my colleague, F. X. Dercum, first 
described in 1889 a condition in which masses of fat are deposited in differ- 
ent parts of the body, chiefly on the chest, arms, buttocks, and legs. These 
formations are usually symmetrical, and, as the name implies, are accom- 
panied by neuralgic pains which vary from slight dartings to severe suffering. 
The disease is of unknown origin, and affects women in or past middle life, 
as a rule. The deposits on the extremities are usually firm and even brawny, 
but they may be so soft as to be pultaceous in character. So far the best 
results in its treatment have been obtained by the use of thyroid gland to 
the point of tolerance. The condition is quite uncommon, but a consider- 
able number of cases have been reported. 



ACROMEGALY 837 



ACROMEGALY. 



Definition. — Acromegaly is a slowly developing chronic disease of nutri- 
tion characterized by an overgrowth of the extremities and head, and, to a 
less degree, of the trunk, with associated curvature of the dorsal and cervical 
spine. It is sometimes called " Marie's disease," because Marie first de- 
scribed it in 1886. 

Etiology. — Many theories have been advanced by various clinicians with 
the object of determining the causation of this extraordinary malady, but 
none of them are adequate. The one which seems most probable from our 
present knowledge is that the condition arises from disease of the pituitary 
body and that the enlargement of the thyroid gland, which is often present, 
is an effort of this gland to supplant its function. Acromegaly rarely appears 
before the thirtieth year. 

Symptoms. — The appearance of a patient suffering from this disease is 
so peculiar and striking that there is no difficulty in diagnosis, if the malady 
is well developed. The massive and gigantic appearance of the head, of 
the features of the face, and, on closer inspection, the enlargement of the 
hands, and the increase in the length of the long bones, combined with the 
kyphosis of the spine, make the clinical picture complete. The upper part 
of the forehead appears low because of the abnormally prominent super- 
ciliary ridges, and this effect is exaggerated by the projection of the lower jaw. 
As a consequence, the shape of the face is elliptical. The skin of the face 
is thick and sallow and greasy in appearance, and lies upon the forehead 
in heavy transverse creases. The cheeks appear sunken, chiefly because of 
the great overgrowth of the malar bones. The nose is not only greatly 
enlarged, but often increases in size more rapidly than the other features, 
so that it seems out of proportion with the rest of the head. The nostrils 
are heavy, thick, and immovable. Not rarely the superior maxillary bone 
fails to develop as rapidly as nearby tissues, and as a consequence the upper 
jaw may seem sunken, an effect increased by the enormous nose above and 
the overgrown lower jaw below it. This effect is also increased by the great 
enlargement and thickening of the lower lip. An examination of the mouth 
will reveal the fact that the tongue and uvula are broader and thicker than 
normal. The thorax on inspection will be seen to be greatly increased in its 
anteroposterior diameter, which is in excess, as compared to its lateral diameter. 
The ribs are enlarged and the clavicles thickened, but the abdomen often 
appears sunken because of the projection forward of the lower part of the 
thorax. The muscles may, in the early stages, seem increased in size and 
in power, but the dominant tendency is to muscular atrophy. No changes 
of importance take place in the internal viscera. Blindness, partial or com- 
plete, may develop, due to optic neuritis. Rarely nystagmus and squint 
have appeared. (See Figs. 108 and 109.) 

The subjective symptoms — that is, those complained of by the patient — 
consist in headache, dimness of vision, and pains in the joints. There is 
usually slowness of thought and perhaps actual drowsiness. 



838 



DISEASES OF NUTRITION 
Fig. 108 




Acromegaly, showing the large hands, nose, and superciliary ridges. 



OSTEITIS DEFORMANS 839 

Diagnosis. — Acromegaly must be differentiated from gigantism, leon- 
tiasis ossea, myxcedema, arthritis deformans, osteitis deformans, and pul- 
monary hypertrophic osteoarthropathy. Perhaps the most frequent error 
in diagnosis is that of confusing myxcedema with acromegaly, but in myx- 
cedema there is never any actual increase in the size of the bones. The face 
in myxcedema is round and full instead of elliptical, and the ends of the 
fingers are swollen and thickened instead of the whole hand being manifestly 
enlarged, as in the disease under consideration. Again, in myxcedema 
the skin is pale, puffy, and waxen in appearance, devoid of hair and also of 
wrinkles, whereas in acromegaly the skin upon the face is wrinkled and 
there is no marked falling of the hair. 

Gigantism is separated from acromegaly by the fact that there is a sym- 
metrical overgrowth all over the body, whereas, as has already been pointed 
out, the enlargements in acromegaly affects chiefly the extremities and the 
tissues of the face. Further than this, in gigantism the ends of the bones 
are not enlarged to such an extent as to be out of proportion to the shaft, 
and in acromegaly this disproportion is quite constant. 

Leontiasis ossea is characterized by the development of bony tumors or 
osteophytes on the face and cranium which produce great deformity, but 
there is no marked enlargement of any one feature nor of the extremities. 

Osteitis deformans is differentiated from acromegaly by the facts that 
the long bones are chiefly affected, are apt to be curved, and so produce 
great deformity. But there is no marked enlargement and the deformity 
is very apt to be asymmetrical. In osteitis deformans the facial bones are 
rarely affected, but the cranial bones are involved in the pathological process; 
whereas, in acromegaly it is the facial bones which are affected, the other 
cranial bones being but slightly diseased. Finally, and perhaps most impor- 
tant, the face of a case of osteitis deformans is broadened in its upper portion 
and narrowed in its lower portion, giving it a triangular appearance; whereas, 
in acromegaly the lower part of the face is broad, and therefore the general 
effect is elliptical. 

In pulmonary hypertrophic osteoarthropathy there is enlargement of 
the hands and feet, but no enlargement of the face, and there is always found 
marked chronic pulmonary lesions, such as bronchiectasis, empyema, or 
other serious thoracic disease. A close examination of the hands and feet 
will show that the enlargement is confined chiefly to the joints, and that the 
whole hand is not thickened and increased in size as in acromegaly. 

Treatment. — No plan of treatment is of any value. 



OSTEITIS DEFORMANS. 

Osteitis deformans is sometimes called "Paget's disease." It is charac- 
terized by enlargement and softening of the shafts of the long bones, by pain 
and deformity. The bones of the face are not affected, but the bones of the 
rest of the head are often involved. A careful examination of the long bones 
in a case of this kind reveals the presence of a rarefying osteitis associated 
with the development of new but imperfect lamellae in the bones. The face 



840 DISEASES OF NUTRITION 

has a curious triangular appearance because of the broadening of the 
upper portion and the narrowness of the chin. By the yielding of the 
bones under pressure, not only the tibiae but the femurs also undergo great 
deformity, so that an extreme degree of bow-legs develops. Occasionally, 
the bending of these bones is forward or backward. There is also some 
spinal curvature. Osteitis deformans rarely develops before the fiftieth 
year. No treatment which has yet been discovered is of any value. 



HYPERTROPHIC PULMONARY OSTEO-ARTHROPATHY. 

This is a condition first recognized by Bamberger, but the name was 
given by Marie. It does not affect the bones of the head or of the face, nor 
the long bones of the arms or leg. In every instance it develops in associa- 
tion with chronic pulmonary disease, such as chronic bronchitis, bronchi- 
ectasis, fibroid lung, and chronic empyema. 

The symptoms consist in the enlargement of the hands and feet, particu- 
larly about the small joints. The growth of the nails is often influenced so 
that they are thickened and incur vated. 



LEONTIASIS OSSEA. 

Leontiasis ossea is a disease in which there is a development of multiple 
osteophytes or symmetrical enlargement in the bones of the cranium, and 
sometimes in those of the face. It is a very rare affection. 



SCLERODERMA. 

Scleroderma is a chronic disease characterized by localized or general 
stiffening or rigidity of the skin, which is usually pigmented, and which 
seems to be bound over the tissues beneath it in much the same manner 
that a leather binding is sometimes placed over a wooden or metal object. 
In some instances the sclerodermatous process is sharply circumscribed. 
In other cases it shades off into the surrounding tissues, and may have a 
slightly reddened edge. 

The first symptom usually noticed by the patient is stiffness of the part 
affected, which gradually increases until movement may become almost 
impossible. The skin undergoes atrophic changes, and becomes silvery 
and shiny in appearance, with a certain amount of yellowish or light-brown 
discoloration. When the disease affects the skin of the extremities, it may 
cause much interference with the movement of the large joints, and be 
followed by atrophy of the muscles underlying the area involved. The 
lesions most commonly take place in the skin of the neck, in the neighbor- 
hood of the shoulders, and over the back and chest. It not infrequently 
attacks the skin of the face. The general health is not seriously impaired. 
There may be some local discomfort, with a sense of formication, or ting- 
ling. The skin is exceedingly dry, and rarely sweats. 



AINHUM 841 

Treatment. — In the way of treatment thyroid extract has been highly 
recommended by certain clinicians. Locally the parts should be treated 
by massage and the local application of oils, which should be of a sedative 
character. Occasionally, however, if the process is exceedingly chronic, it 
may be advisable to apply turpentine diluted with six times its amount of 
sweet oil. Even with the best of treatment the prognosis is anything but 
favorable as to cure, although the spread of the malady may be delayed. 



AINHUM. 

Ainhum is a peculiar trophoneurotic disease, commonly affecting the 
feet of negroes and other dark-skinned races. It is widely distributed in 
Africa, particularly along the west coast, and it occurs in India, and Brazil. 
It is a rare affection among negroes in the United States. The disease 
usually begins in the little toe of one foot or both feet, as a narrow fissure 
or groove, on the plantar surface at the junction of the toe and foot. The 
groove gradually surrounds the toe and slowly deepens until eventually it 
is amputated. Microscopic examination shows that the constricting band 
consists of dense fibrous tissue. As it tightens, the toe becomes very much 
enlarged, and disorganized before it finally separates. As a rule, the dis- 
ease is confined to the one toe, although other toes may be successively 
attacked and the disease may even appear in the leg. 

The cause of this condition has not been determined. It has been 
ascribed to traumatism, such as frequent cuts from blades of grass. By 
some writers it has even been regarded as an expression of a very much 
attenuated form of leprosy. It is evidently a trophic disturbance. 

Treatment. — The treatment is surgical, and consists in free division of the 
constricting bands in recent cases and amputation in advanced cases. 



INTOXICATIONS. 



ALCOHOLISM. 

Definition. — By alcoholism is meant a condition in which the patient suffers 
from the effects of alcohol when taken in sufficient quantities to act as a 
poison. 

Etiology. — An idea exists among the laity that chronic alcoholism is a 
manifestation of an inherited tendency in many instances, and this is some- 
times offered as an excuse by a patient for his unlimited libations. There is 
no such disease as alcoholism, nor does an alcoholic have any justification 
in this excuse. The tendency to consume alcohol is not an inheritance. 
The inheritance is a lack of self-control, a cowardly inability to meet the 
hard sides of life, and a willingness to escape, if only for a time, by drown- 
ing sensation in the stupor of a narcotic. In many cases, therefore, we may 
not only have to combat a habit, but a state of degeneracy which permits 
a habit to exist. 

Symptoms. — Alcoholism may be divided for readiness of consideration 
into the acute and chronic form. 

Acute Alcoholism. — The symptoms of the acute form are familiar to 
everyone who sees life in the town or city, and consist in disorderly 
conduct due to removal of the inhibitory functions of the brain, so that 
every silly thought or foolish idea is carried out in action. Later, as the 
drug affects the muscle sense, and consequently disorders co-ordination, 
the individual staggers and perhaps falls, and finally, if the quantity of the 
drug is adequate, passes into a deep sleep, or coma, from which he wakes 
more or less confused, with depression of the nervous system and a disordered 
digestive tract. In cases where the dose has been very large, death may be 
caused by depression of all the vital functions, of which the one most involved 
is probably that of bodily heat, the death being in part due to cold. In the 
majority of cases, however, in which death follows acute alcoholism, it is 
due not directly to the depressing effects of the alcohol, but to the fact that 
the lowering of temperature and the disorder of vital function in the various 
organs permits infection by the pneumococcus to take place so that pneu- 
monia causes death, or some complication such as acute nephritis is 
developed. 

The symptoms of profound acute alcoholism are pallor of the face, dulness 
of the eyes, widely dilated pupils, profound unconsciousness, stertorous 
breathing, and a temperature several degrees below normal. Occasionally 
convulsive attacks may develop. 

(843) 



844 INTOXICATIONS 

Although the symptoms of acute alcoholism are so familiar, there is no 
state so often confused with conditions of disease or with the results of 
injury. This is due to the fact that the symptoms of acute alcoholism are 
much like those of cerebral congestion, apoplexy, uraemia, or hemorrhage 
from a meningeal artery, or fracture of the skull. It is also due to the fact 
that alcohol often causes all these states directly or indirectly, and as there 
is a history of alcoholism or an odor of alcohol on the breath, it is natural 
to make a diagnosis of alcoholism without recognizing that another condi- 
tion is present. Again, it not rarely happens that an alcoholic takes a 
poisonous dose of opium, and so suffers and dies from the effect of this 
drug. The raised temperature in apoplexy is in contrast to the lowered 
temperature of alcoholism, as is also the full-bounding pulse as compared 
to the rapid-running pulse of alcoholic poisoning. Again, apoplexy is char- 
acterized by hemiplegia and facial palsy. Opium poisoning is characterized 
by pinpoint pupils, slow breathing, and a warm skin, as opposed to the 
normal or relaxed pupils, the cool, moist skin, and the normal or rapid 
breathing of alcoholism. 

Treatment. — Thetreatment of acute alcoholism consists in the administration 
of an emetic to empty the stomach of any alcohol still unabsorbed. Apomor- 
phine is probably the best drug for this purpose, as it can be given hypoder- 
mically, acts promptly, is sedative in its influence, and is safe in a moderate 
emetic dose of J grain. In other cases, or after the emetic has acted, an active 
cathartic, such as 30 grains of compound jalap powder or 15 grains of com- 
pound extract of colocynth, may be used to unload the bowels and the portal 
system, and decrease cerebral congestion. If circulatory feebleness is present, 
the aromatic spirit of ammonia in drachm doses, diluted with water, may be 
given. In other cases the physician must give full doses (^ grain) of strych- 
nine by the mouth, or by the hypodermic needle if depression is marked, 
and hot bottles must be applied to maintain body heat. Strong black coffee 
by the mouth or by the rectum may be given if active stimulation seems 
needful. The effects manifested on the next day are to be removed by the 
use of calomel, followed by a saline purge and the administration of elixir 
of celery and guarana, or, if the patient is very nervous, by the use of 
guarana and bromide of sodium, 5 grains of the extract of the former and 
30 grains of the latter at a dose. 

Subacute and Chronic Alcoholism. — Chronic alcoholism is divisible into 
three classes. In one the patient suffers from a prolonged alcoholic debauch 
lasting over days, or even weeks, during which time he is never com- 
pletely sober. In the other type he is never drunk, but always under the 
influence of the drug to an extent which eventually produces a train of 
symptoms even more grave than those which follow a debauch. Those 
who have made a special study of alcoholism also recognize that there is a 
certain class of persons, of the first division just named, who take no alcohol 
for a comparatively long period, varying from weeks to months, and then go 
on a terrific debauch, the so-called " periodical drunkard." It is the individual 
who takes alcohol up to the stage of intoxication for several days consecu- 
tively, and who has often used alcohol in large quantities for weeks before 
the acute exacerbation, who most commonly develops delirium tremens; 



ALCOHOLISM 845 

while the constant, moderate "soaker" is more prone to hepatic cirrhosis 
and affections of the peripheral nerves. Delirium tremens is very prone to 
develop in persons who are the subjects of subacute or chronic alcoholism 
if, perchance, they suffer from a severe injury, surgical operation, or great 
shock. Not rarely the onset of an acute illness may precipitate an attack. 

Morbid Anatomy. — The morbid changes produced by the continuous use 
of alcohol in excess are chiefly found in the organs by which the drug gains 
access to and egress from the body; that is, the stomach, the liver, and the 
kidneys. Next to the effect of the drug upon these organs it expends its 
deleterious influences upon the circulatory system. The passage of alcohol 
directly to the liver from the stomach through the portal vessels causes con- 
gestion, irritation, and finally atrophic cirrhosis of this organ. (See Hepatic 
Cirrhosis.) By reason of the direct effect of the drug upon the stomach, and 
the indirect effect produced by the impairment of its blood supply, which 
arises from the hepatic changes, chronic gastric catarrh develops. The 
changes found in the kidneys in very chronic alcoholism consist in a con- 
dition practically identical with that found in contracted kidney, and 
with this state an arteriocapillary fibrosis develops, just as it does in cases 
of cardiovascular change arising from other causes. The most common 
change in the kidneys, however, consists in a hypostatic congestion, or 
stasis, which causes them to be swollen, cyanotic, and to* be functionally 
inactive. Not rarely these patients develop acute tuberculosis, because of 
their lowered vital resistance. An alcoholic multiple neuritis may develop, 
and atrophy of the optic nerve may occur. 

Symptoms. — The symptoms of delirium tremens are great nervous rest- 
lessness and apprehension with anxiety, and finally delusions of persecution 
and terror. The delusions are largely those connected with vision, and all 
sorts of hideous objects are described as crawling about the patient. Because 
of these delusions the patient is often violent and difficult to control, but is 
rarely offensive unless he believes that the attendant is in league with the 
" objects of evil" about him. The pulse is usually rapid and feeble, the skin 
relaxed, and the tongue exceedingly foul. The bowels are constipated and 
the urine scanty. Hypostatic congestion of the lungs and congestion of the 
kidneys are very commonly developed, and these states often contribute to 
the death of the patient. 

It is not to be forgotten that acute croupous pneumonia at the apex not 
rarely is associated with an acute delirium not unlike that of delirium tremens. 

In that form of chronic alcoholism in which the patient is never drunk, 
but always has alcohol in his body, the chief symptoms are irritability of 
temper, gradual mental deterioration, localized sensory and motor palsies, 
and finally dementia. 

Treatment. — The treatment of this state consists in the use of an active 
cathartic, as already advised for acute alcoholism, and the use of full doses 
of morphine hypodermically, if the kidneys are not diseased, to produce 
nervous rest if the patient is becoming exhausted by his lack of sleep or 
struggling. Care must be taken that more than a few doses are not 
given, for such a patient may become a morphine habitue* very quickly. 
Strychnine and atropine are to be used hypodermically if any signs of 



846 INTOXICA TIONS 

pulmonary congestion arise, and they must be given boldly. Dry cups' 
should be applied to the back of the chest, and Hoffmann's anodyne is 
useful as a rapidly acting diffusible stimulant. Every measure must be 
taken to disperse and prevent the congestion, which, if it develops in full 
degree, means the death of the patient. 

The question as to the medicinal use of alcohol in these cases is debatable. 
In those who are not accustomed to its constant use, and who may have been 
intoxicated for but a few days, it is not necessary to give the drug; but if 
the patient has been in the habit of taking alcohol in considerable amounts 
prior to his acute alcoholic outbreak, whiskey must be used freely in many 
cases if signs of great nervousness develop. Aside from pulmonary and 
renal complications the most frequent one, and a most fatal one, is a state 
of nervous tension in which the symptoms are those of meningeal irritation 
with stiffness of the limbs and neck. This stage of tonicity in the muscles 
is preceded by muttering delirium, with periods of wakefulness in which 
hallucinations may make the patient difficult of control. The pupils are 
contracted and the pulse rapid and feeble. The temperature is often as 
high as 103° or even 104°, and not rarely hypostatic congestion of the lungs 
can be found if the bases are examined. Marked hyperesthesia of the 
skin usually exists. Patients with these manifestations usually die, but 
they may recover after a prolonged illness lasting several weeks. My 
experience is in accord with that of Dana, that if there is stiffness of the 
cervical muscles the patient usually dies. This condition is not due to a 
true meningitis, but to a toxaemia with serous effusion into the meninges. 
Dana and others have given the name "wet brain" to this condition. 

The diet, if food can be given to the patient, should consist of hot and 
stimulating liquid nourishment, such as highly seasoned beef-tea or pep- 
tonized milk, to which capsicum and salt have been added to stimulate the 
digestion to activity. The various highly seasoned broths are useful. 

The treatment of the alcoholic who continually takes the drug day in and 
day out presents grave difficulties. Those who have been wont to take this 
drug every day for many years are rarely willing to put up with the discom- 
fort which follows abstinence, and after a few days almost invariably return 
to the use of alcohol. The only treatment which is of any value in such 
cases is to send the patient to some isolated region where he is too far 
removed from the grog-shop to be able to obtain alcohol when his desire 
for it arises, and to take care that he does not provide himself beforehand 
with alcohol to be used during the trip. Usually, if the man is well-to-do, 
several weeks or months of hunting in isolated regions, and in the company 
of someone who does not drink alcohol and has considerable mental force, 
will be the best means of cure. 

For those who take alcohol more or less constantly to the point of 
intoxication, either this measure can be employed or the patient may be 
placed in a private room in a hospital, where he is under absolute control 
of the nurses and physicians attached to the institution, and the alcohol 
can then be immediately stricken off the list of permissible articles, or, if 
his condition is one of feebleness, it can be gradually diminished so that at 
the end of a week he is getting none of it. In the great majority of instances 



ALCOHOLISM 847 

it is utterly futile to attempt home treatment of these cases. Even if the 
family can prevent the man from getting alcohol, home life lacks the disci- 
pline which is necessary for the control of the patient, not only in the sense 
of preventing him from procuring alcohol, but in the sense of making a 
powerful mental impression. 

In those cases in which removal of alcohol causes nervous excitation and 
evidences of threatened delirium tremens, it is occasionally permissible to 
administer full doses of chloral and the bromides to produce nervous 
quiet at night. Small doses of these drugs practically have no influence 
whatever, and if the heart is at all feeble full doses of chloral are danger- 
ous. Morphine possesses the disadvantage that the alcoholic is very prone 
to develop the morphine habit in addition to his alcoholism. This drug is, 
however, exceedingly valuable if used on those occasions when the violence 
of the patient's nervous symptoms demand sedation. It should not be given 
day after day, but only occasionally, when insomnia is so pressing that the 
consequent exhaustion demands relief. 

Within the last few years very strong claims have been made for the 
use of hyoscine for the purpose of relieving the nervous irritation and craving 
for alcohol. The drug must be given in sufficiently large doses, hypoder- 
mically, to place the patient deeply under its influence. If necessary as much 
as -j-J-g- of a grain every two hours may be given hypodermically until the 
patient sleeps or is resting quietly. These doses, of course, produce the full 
physiological action of hyoscine and often cause great dryness of the mouth 
and talkative delirium. They may be continued for several days and then 
gradually remitted until the patient is no longer taking either alcohol or 
hyoscine. 

If the circulation fails in these cases strychnine and digitalis may 
be administered. For the purpose of combating signs of acute collapse 
Hoffmann's anodyne and strychnine are valuable, as is also the aromatic 
spirit of ammonia. Another drug which has been highly praised in this 
condition is apomorphine given in the dose of ^ of a grain hypodermically 
as a nervous sedative, the emetic effect of the drug not being desired. In 
some instances larger doses have to be given and may be used without pro- 
ducing emesis. 

It must be constantly borne in mind that the most important portion 
of the treatment consists in the isolation of the patient, and in a com- 
plete control of his methods of life for the period covering several weeks. 
Drugs are of little value except to support him through the period when his 
system lacks his customary doses of alcohol. If the patient is unwilling or 
unable to resort to this form of treatment, the employment of drugs is usually 
worse than useless. 

Careful attention to the digestive system is needful in all these cases. The 
liver should be unloaded by blue mass, followed by a saline purge, every 
few days, and bitter tonics, such as gentian with bicarbonate of sodium, are 
advantageous. 



848 INTOXICATIONS 



MORPHINISM. 

Chronic morphinism, or the morphine habit, is usually acquired as the 
result of the employment of this drug for the purpose of relieving insomnia. 
Sometimes the insomnia is due to neurasthenia, but more frequently the patient 
is one who primarily suffers from sleeplessness due to pain. If the condition 
producing the pain is continued over any considerable period of time, the 
patient finally becomes so dependent upon the use of morphine, as a nervous 
sedative, that he cannot sleep without it, and so even although the pain no 
longer continues he resorts to the drug for the nervous quiet which can be 
obtained only under its influence. Not infrequently these patients continue 
the use of the morphine long after the physician intends that it should be 
stopped, and so develop the habit of taking the drug without the knowledge 
of the physician who has first prescribed it. Because of the possibility of 
this occurrence he should only prescribe that quantity of morphine which 
is absolutely essential for the relief of pain upon a particular occasion, 
and if he writes a formal prescription ordering the drug from a pharmacist, 
this prescription should contain the words "Do not renew," so that the 
patient will not be able to continue taking the drug after the physician 
believes that he has stopped it. 

In a certain number of cases of morphine habit, the employment of the drug 
rests upon the fact that the patient is a degenerate without the necessary 
mental and nervous vigor to meet the vicissitudes of life. In other words, 
he is one who, in the presence of any condition which produces mental per- 
turbation or distress, at once resorts to some sedative to quiet his nervous 
system, instead of dominating it by his will power and conquering the depres- 
sion with a knowledge that any yielding either to that depression or to the 
desire for a drug is certain in the end to wreck his moral and physical 
condition. This is an important factor to be taken into consideration when- 
ever a morphine habitue is to be treated. This condition may be hereditary, 
or it may be acquired. Not rarely, when it is acquired, the mental and 
physical condition of the patient has been impaired by grief, excessive 
business worry, illness, or other cause. When the morphine has been used 
for any length of time this very fact tends to increase the lack of moral 
stamina on the part of the patient. 

Symptoms. — One of the most noteworthy symptoms of morphinism is 
great irritability of the nervous system so that slight causes may produce 
outbreaks of rage, or, on the other hand, a lacrymose state may develop. In 
some instances, where the drug has been used for a long time, there is not 
only a loss in mental power, but the patient develops melancholia or delu- 
sions closely resembling those seen in an ordinary case of insanity. Before 
the mental degradation is so complete that intellectual processes are greatly 
impaired, the patient develops a slyness quite different from his ordinary 
frank methods of life when in health. In association with this slyness there 
is always developed a skill at prevarication or lying which is quite remark- 
able. Persons who previously have been regarded as eminently truthful tell 
the most skilful falsehoods, and in such a way that the hearer is convinced 



MORPHINISM 849 

of their truth. As a rule, these falsehoods are never so clever as when they 
are intended to result in the obtaining of the drug which is desired, the 
patient resorting to every possible means, honest and dishonest, in order 
that he may obtain the nervous quiet which his system craves. 

Treatment. — It may be asserted with truth that it is useless to attempt to 
treat a patient who is suffering from the morphine habit, with the idea of 
curing him of his taste for the drug, unless he or she is willing to enter a 
private room at a hospital and be placed under the constant supervision 
of a night and day nurse. This isolation is necessary not only because it is 
a form of discipline which is advantageous for the mental condition of the 
patient, but it is the only way in which the physician can be assured that 
the patient is not surreptitiously continuing his daily dose of the narcotic. 
It must be remembered that the most pious individuals, when they become 
addicted to this drug, develop an extraordinary ability to tell lies which are 
so like the truth that they can deceive the most cautious. In one breath, 
the patient, with tears running down his face, will beseech the physician to 
cure him of the habit which is destroying his happiness, and, at the next 
moment, he will use every form of deceit and cleverness to obtain the drug 
which he craves. Even when the patient is under the observation of trained 
nurses night and day, any sudden improvement in his condition after with- 
drawal of the morphine, or failure to develop symptoms produced by its 
withdrawal, should make the physician believe that in some unknown way 
the drug has been obtained. In some instances the patient enters the hos- 
pital with the morphine carefully sewed in the hem of the night-dress ; in 
others, a friend or servant is bribed to bring the drug each day in some 
article of food. Nothing but ceaseless watchfulness can possibly prevent 
these patients from obtaining morphine. This being so, it can readily be 
understood that home treatment can rarely succeed. 

Having obtained special control of the patient, the method of treating 
him should consist in one of two plans which have found general accept- 
ance. The first of these is the gradual diminution of the morphine so that 
at the end of three or four days, or a week, none of the drug is permitted. 
If this method is carried out the patient usually develops after a few days, 
or sooner, great restlessness and irritability, not infrequently active purging, 
and profound mental and physical depression. Cramps in the extremi- 
ties also add to the suffering. Under these circumstances it is necessary to 
support the patient by the use of hot, stimulating foods, such as broths highly 
seasoned with pepper and salt, the use of digitalis and strychnine if the cir- 
culation fails, and the employment of hyoscyamus or hyoscine to diminish 
irritability of the nervous system. The employment of alcohol, coca wine, 
or similar stimulants for the purpose of aiding the patient at this time is 
unwise, because he is prone to develop the alcohol or coca habit. If the 
diarrhoea is so violent as to require control, aromatic sulphuric acid with 
a vegetable astringent, like the fluid extract of hsematoxylon, may be used. 
Hot compresses may be applied about the painful limbs. Great mental excite- 
ment may be relieved by chloral, but the danger of producing the chloral 
habit is not to be forgotten. In place of chloral, sulphonal or trional may 
be used. Occasionally nerve quiet can be produced by wrapping the patient 
54 



850 INTOXICATIONS 

in a hot, wet blanket, care being taken that the hot pack is not continued 
so long as to produce cardiac depression. 

A second method of treatment is one which has been largely employed 
in the last few years, and for which we are chiefly indebted to a Texas 
physician, Dr. Lott. This consists in putting the patient where we can 
have him under absolute control, and in the administration of full doses of 
hyoscine hypodermically, giving him as much as yj-g- of a grain every two 
hours, if need be, until a condition of nervous quiet is produced. In the 
writer's experience these large doses fail to produce sleep, and instead cause 
a condition in which the patient lies awake but stupefied, and often mum- 
bles continuously. Curiously enough the mouth does not become as dry 
as one would expect from the administration of such a powerful drug in 
these large doses. Should the circulation seem at all feeble, strychnine may 
also be given. The idea in employing hyoscine is to use that quantity 
which is necessary to keep the patient under control, and to prevent suffer- 
ing. These doses may be continued for a number of days, at the end of 
which time they are gradually diminished and the patient is permitted to 
return to his normal condition as the effects of the hyoscine pass away. 
By this means the acute mental and physical suffering caused by the sudden 
withdrawal of morphine is avoided, and in some instances the patient 
actually seems to be cured of his malady, although, of course, there is great 
danger in every case of his speedily returning to its use, particularly if any 
nervousness or mental stress is experienced. So common is it for the habitue* 
to go back to the employment of this drug habit that many men of experi- 
ence have gone so far as to assert that no case of the morphine habit is ever 
permanently cured. This view is, however, undoubtedly incorrect. The 
writer has seen a number of cases in which permanent cure certainly took 
place. 

ARSENICAL POISONING. 

Arsenical poisoning occurs in two forms, the acute and chronic. Usually 
after the first stage of acute poisoning, if the patient survives, there develops 
a second subacute stage due to the effects of the retained arsenic. Acute 
poisoning usually follows the ingestion of "Rough on Rats," Paris green, 
or Scheele's green. The symptoms are those of severe gastroenteritis, 
with vomiting and purging, followed by death in collapse. The antidote 
is the hydrated sesquioxide of iron with magnesia. When the patient sur- 
vives the acute stage he suffers from secondary lesions in the stomach and 
intestines, kidneys and liver. Widespread fatty degeneration also occurs 
and peripheral neuritis may be present. 1 

The causes of chronic arsenical poisoning are almost as numerous as 
are those of lead poisoning. It may find its way into the body through 
the lungs from the air of a room the walls of which are covered by a paper 
heavily laden with arsenical dyes; it may enter in beer made from glucose 
prepared by the use of iron pyrites contaminated with arsenic, as in the 

1 For this train of symptoms see the author's Text-book of Therapeutics, 10th edition. 



LEAD POISONING 851 

recent celebrated epidemic in England; or it may be given in moderate 
poisonous dose for a long time with homicidal intent, as in a case recently 
tried in the Philadelphia courts. 

Not very rarely a mild form of chronic arsenical poisoning is met with 
in cases to which a physician has found it necessary to give large doses of 
arsenic for long periods, as in chorea, in leukaemia, and Hodgkin's disease. 

Symptoms. — Chronic arsenical poisoning manifests itself chiefly in the 
form of a widespread peripheral neuritis, with the development of a secondary 
degeneration of the epithelium of the kidneys. The chief symptoms are 
tingling and pains in the limbs, followed, after a time, by paralysis which 
affects the distal portions of the body much more than it does the nerves and 
muscles of the thighs or arms. Atrophy of the muscles supplied by the 
paralyzed nerves soon takes place. Other trophic changes also develop, 
such as herpetic eruptions resembling those of herpes zoster or pemphigus, 
and glossiness of the skin sometimes supervenes. At times curious deposits 
of pigment take place in the skin. As in lead poisoning, the nerve supply to 
the extensor muscles suffers chiefly, but in addition the small flexor muscles 
are also affected much more commonly than they are in neuritis due to alco- 
hol or lead. The lower limbs are affected as much as the upper limbs, 
whereas in lead poisoning it is the upper extremities which suffer most. 
Again, arsenical neuritis affects the sensory and motor fibres, and for this 
reason pain as well as anaesthesia is often met with. The pulse is quickened 
and the mind confused in some cases. Because of the involvement of the 
sensory and motor fibres of the peripheral nerves the patient may present 
symptoms of tabes dorsalis (arsenical pseudotabes). The Argyll-Robertson 
pupil is a useful differential factor, for if it is present the cause of the 
disordered gait is probably due to true locomotor ataxia. 

Prognosis. — The prognosis in such cases depends upon the severity of 
paralysis and the state of the kidneys. If the latter organs are affected the 
outlook is more grave than if they are intact. Even when the symptoms of 
neuritis are severe, remarkable recovery may ensue if the patient is removed 
from the exposure to the drug. 

Treatment. — The treatment consists in the removal from exposure, the 
use of the iodide of potassium to aid in the elimination of the poison, the 
administration of strychnine in full doses if the nerves are not irritable, and 
in the application of massage and electricity to improve the nutrition of 
the affected parts. Iron may be used to combat the anaemia. 



LEAD POISONING OR PLUMBISM. 

Acute lead poisoning is not of frequent occurrence. Its consideration is 
distinctly toxicological in character, and for this reason it is not discussed 
in these pages. 

Chronic lead poisoning, on the other hand, is of exceedingly common 
occurrence, not only in those who are exposed to the poison by reason of 
their occupation, but in persons who have suffered no such exposure but 
have absorbed the lead from sources in which its presence would not be 



852 INTOXICATIONS 

suspected. Further than this, lead poisoning in its chronic form may pro- 
duce the most varied symptoms, which are oftentimes so unusual that no 
thought of lead as a cause is entertained. In speaking of the nervous mani- 
festations which are often present, a well-known teacher was wont to say: 
"When you cannot explain a curious train of nervous symptoms, always 
suspect syphilis, hysteria, or lead as the cause.' ' 

Etiology. — It is the insoluble rather than the soluble salts of lead which 
usually cause chronic lead poisoning. The most frequent sufferers are 
workers in manufactories where paint is made, and house painters who 
are continually engaged in the handling of lead paint. In rarer instances 
the patient is poisoned by the use of water which in passing through new 
lead pipes dissolves some of the lead; or lead is present in a hair-dye or 
cosmetics and is absorbed by the skin; or, again, it has occurred that a miller 
has filled holes in his grindstones with lead, which has then been ground 
with the flour and eaten in bread. In one instance, in Pennsylvania, a 
peddler sold a large number of crocks to farmers' wives. In these was 
placed apple butter, and as the acid in the fruit eroded the lead glazing 
which lined the jars, a widespread epidemic of chronic lead poisoning de- 
veloped. Perhaps the most notorious illustration of how lead may cause 
poisoning in unsuspecting persons is the celebrated "chrome-yellow cases" 
in Philadelphia, in which a wholesale druggist sold chrome yellow to a 
number of confectioners, who saved the cost of eggs by coloring their 
cakes with this substance. As a result a large number of men, women, and 
children died, and a much larger number suffered from chronic poisoning 
for months before the source of the trouble was discovered. An extraor- 
dinary cause, however, is the habit of chewing silk thread weighted with 
lead. At least two cases of chronic poisoning from this cause have been met 
with in seamstresses. 

The fact, therefore, that no history of exposure to lead is to be found in a 
given case does not negative the diagnosis of lead poisoning. 

Prevention. — Chronic lead poisoning is to be prevented in workers in lead 
by the exercise of the greatest possible cleanliness as to their hands, which 
should be thoroughly washed before food is touched, as otherwise lead may 
be taken in small amounts and finally cause poisoning. If the workman 
is employed in grinding lead, he must wear a mask to prevent the poison 
from being inhaled in dust. The use of vessels, the glazing of which 
contains lead, for holding food should be avoided. Small amounts of 
dilute sulphuric acid to form insoluble sulphates in the mouth and stomach 
may be resorted to, and purgation every few days by sulphate of mag- 
nesium is advantageous. 

Pathology and Morbid Anatomy. — There is no other poison from the mineral 
kingdom which taken into the body produces such widespread changes in 
different organs as does lead in the chronic form of poisoning. Even alcohol, 
that most ubiquitous poison, does not cause such a multitude of changes. 
The nervous system is the portion of the body which bears the brunt 
of the attack, and it is the peripheral nerves that suffer most. In them 
the lead produces a toxic neuritis. In advanced cases there is segmentation 
of the myelin and breaking up of the axis cylinder, with a proliferation of 



LEAD POISONING 853 

the nuclei in the sheath of Schwann. The early changes in the nerves 
affect chiefly the medullary sheath, which is affected in patches at irregular 
intervals — the so-called periaxial neuritis of Gombault. Although the 
lesions are more severe as the distal end of the nerves is approached, 
De*jerine has found them even in the anterior roots. Conspicuous changes 
in the spinal cord are almost never seen, but Oppenheim states that he has 
found alterations in the anterior cornua, and Gowers asserts that in some 
cases the cells in these cornua are degenerated. No constant lesions are 
found in the brain, even in those cases in which severe cerebral symptoms 
are present, except those dependent upon vascular lesions which are part 
of the general vascular disease produced by the poison. 

It is to be especially noted that the sensory fibres of the nerves are not 
affected, and that the musculospiral is the nerve chiefly involved in those 
cases which have peripheral neuritis. As a result of the neuritis, produced 
by the lead, atrophy of a severe character may develop in the muscles 
supplied by the affected nerves. Fatty degeneration of the muscles does 
not ensue. The second portion of the body to feel the effect of the lead is 
the kidneys, which are not rarely the seat of chronic interstitial nephritis, 
and with this renal lesion a process of arteriofibrosis develops, which asso- 
ciated conditions often cause the death of the patient. 

Sailer has recently shown that, in some cases at least, there is an absence 
of hydrochloric acid in the gastric juice. 

Symptoms. — From what has been said of the changes in various organs 
caused by lead, it is evident that the symptoms may be very varied. Paraly- 
sis of the extensor muscles of the forearm, causing wrist-drop, is the most con- 
stant symptom. This paralysis is nearly always bilateral, but occasionally 
but one arm is affected. The supinator longus muscle and the short extensor 
of the thumb, however, usually escape, which is curious in view of the fact 
that the supinator longus muscle receives its nerve supply from the musculo- 
spiral nerve. In atypical cases Oppenheim states that the supinator longus, 
the biceps, and even the deltoid are involved. 

In the legs palsy is far less frequent than in the forearms, and the muscles 
involved are the peroneal group, but the tibialis anticus is not affected. 

Although motor paralysis is present sensory disturbances are rare. 

Palsy of the ocular muscles producing squint may be due to lead, as may 
also optic neuritis. In very rare cases of severe plumbism cerebral symp- 
toms develop, consisting in epileptiform convulsions, or coma. This state 
is called " encephalopathia saturnina." 

Tremor of the forearms is sometimes present in lead poisoning. 

Chronic lead poisoning greatly aids in producing gouty lesions, probably 
by forming a urate of lead in the tissues about the joints. Others believe 
that the lead decreases the alkalinity of the blood and so permits the pre- 
cipitation of urates to occur. 

There still remain to be considered several symptoms of chronic lead 
poisoning which are so constant in their appearance and so characteristic 
that they are most valuable aids in diagnosis. The first of these is the blue 
line in the edges of the gums next the teeth, formed by the deposit of sul- 
phide of lead in the capillaries of the part. This sign is often absent in those 



854 INTOXICATIONS 

who are cleanly in the care of the mouth. The second is the characteristic 
pain in the belly, which is exceedingly severe in the region of the umbilicus, 
and is described as a pain due to twisting the bowels around a stick. This 
is called "painters' 00110," or " colica pictonum." The latter term is given 
to this state because it was frequently met with in Picton at one time. A 
third symptom of chronic lead poisoning is anosmia, which is in part due to 
the direct effect of the lead and in part to the renal changes induced by 
this agent. Microscopic examination of the blood will often reveal a granu- 
lar degeneration of the erythrocytes. 

Diagnosis. — In a case in which the blue line on the gum is present the 
diagnosis is easy. When wrist-drop is present it must be separated from 
that due to pressure, as by resting the head on the arm when sleeping or 
by the pressure of a crutch. As a rule, pressure palsy is unilateral and lead 
palsy bilateral, but this is not so invariably, and the history of the patient 
may be necessary to decide the diagnosis. When the palsy is distributed 
in various parts, particularly if it affects the legs, it must be separated from 
acute poliomyelitis Lead poisoning is rare in children and acute polio- 
myelitis is common. In adults chronic lead poisoning is more frequent than 
is acute poliomyelitis. Poliomyelitis in its acute form has a history of sudden 
onset with fever, and the onset of lead palsy is rarely so abrupt and is usually 
not febrile. The history of exposure to lead will aid in deciding the diag- 
nosis. In chronic poliomyelitis the only way to determine the question is 
by the history and the frequent examination of the patient's urine for lead. 
Often lead will not be found in the urine unless iodide of potassium is given 
to set it free from the tissues where it has been deposited. 

Saturnine epilepsy must be separated from true epilepsy by the history 
of the patient and by the association of other signs of plumbism. It must 
also be separated from ursemic convulsions, if possible, by the urinary 
examinations, but this may be impossible because the lead may at once 
cause encephalopathia saturnina and uraemia through its effects on the 
cerebral vessels and the kidneys. 

Prognosis. — The prognosis as to the duration of life in chronic lead poison- 
ing is good unless cerebral symptoms are present, or renal changes are well 
marked. The prognosis as to the paralysis depends largely upon the general 
nutrition of the patient and the stage to which the neuritis has advanced. 
If the muscles involved have lost all reaction to electrical stimulation, the 
prognosis must be bad as compared with that in a case in which the palsy 
has lasted for but a short time. Even when the reactions of degeneration are 
present the outlook is not hopeless, because if the patient is no longer exposed 
to the poison recovery sometimes ensues, particularly in young persons. 

Treatment. — The treatment of chronic lead poisoning consists in remov- 
ing the patient from continued exposure to the poison. If he is an artisan 
he must cease working in lead. If he has been poisoned by the metal through 
some accident, the source must be discovered and he must no longer be 
exposed to it. 

The second duty of the physician is to eliminate the lead already in 
the body as rapidly as possiple. For this purpose the iodide of potas- 
sium should be given in full doses, with the object of forming double 



FOOD POISONING 855 

soluble iodides with the lead. Not only have we every reason to believe, 
from a chemical standpoint, that this medicinal treatment is advantageous, 
but it is a well-known clinical fact that chemical examination of the urine 
in a case of lead poisoning will fail repeatedly to show lead, and will at once 
indicate its presence after iodide of potassium is administered, proving that 
by this means lead is carried to the kidneys and speedily passed out of the 
body. It must also be remembered that the liver eliminates lead freely in 
the bile. 

The third indication is to improve the patient's general health not 
only by the use of such tonics as iron and strychnine, but also by ordering 
an out-door existence, with as much sunshine as it is possible for the patient 
to find in the twenty-four hours. 

The paralysis of chronic lead poisoning is to be treated by the adminis- 
tration of full doses of strychnine and the simultaneous use of large doses 
of iodide of potassium. The paralysis of the extensor muscles of the arms 
and legs is to be treated not only by the use of strychnine, but by the employ- 
ment of the slowly and rapidly interrupted faradic current. In those cases 
in which cerebral symptoms develop, the patient should receive full doses 
of iodide of potassium, with the object of getting rid of the lead as rapidly 
as possible. If the symptoms are acute, and if a convulsion is already present, 
the patient should receive a hot pack in order that the sedative effect of this 
therapeutic measure may be exercised upon the nervous system, in order 
that the blood may be drawn away from the congested brain, and with the 
hope that by increasing the action of the skin the convulsions may be re- 
lieved of some of the work which they would otherwise be forced to perform. 
In other respects the convulsions should be treated, as are all other con- 
vulsions, by the use of nitrite of amyl inhalations, and by the employment of 
full doses of chloral and the bromides to quiet the brain and spinal cord. 

Painters' colic with its attendant constipation is not to be treated by the 
use of purgatives, but by the use of morphine given hypodermically. This 
drug, which so often causes constipation in the ordinary patient, often pro- 
duces active purgation in these cases, by quieting the intestinal irritation 
and spasm and simultaneously relieving the pain. 



FOOD POISONING. 

Bromatotoxismus. — Symptoms of poisoning produced by the ingestion of 
food which is impure by reason of faulty preparation, or the changes due to 
decomposition, are occasionally met with. It is rather remarkable, consider- 
ing the long period of time during which many foods are kept after they are 
prepared for the table, that more cases of poisoning do not ensue. Much of 
the information given in this article is obtained from the excellent summary 
of this subject which can be found in Vaughan and Novy's Cellular Toxins. 

Poisoning may be produced by the use of grains which have become infected 
by poisonous fungi. Animals may eat substances which may render their 
milk or flesh or both poisonous. The flesh of certain animals also becomes 
poisonous at certain stages of their life history. Foods may also become 



856 INTOXICATIONS 

infected by the discharges of human beings; the flesh of animals may suffer 
from some specific disease which may be transmitted to man, and milk may 
carry the disease of an animal to man or may be infected by the discharges 
of man, and so convey specific germs to other individuals. Food may also 
contain micro-organisms which in their process of development produce 
poisonous symptoms in man. 

The term sitotoxismus is applied to poisoning by vegetable foods which 
are infected by moulds or bacteria. 

The most familiar form of poisoning by grains, or vegetable food, is 
Ergotism due to the eating of rye flour made from rye which has been infected 
by the fungus Claviceps purpurea. This ergot is, of course, largely employed 
in medicine. Several poisons are found in ergot, such as ergotinic acid, 
sphacelinic acid, and cornutin. The first of these, however, seems to be 
poisonous only when it is injected hypodermically. Sphacelinic acid, on the 
other hand, is supposed to be responsible for the gangrene and cachexia 
which sometimes develop in persons who have eaten infected rye. On the 
other hand, cornutin seems to be the poison which affects the nervous system 
and produces spasms and convulsions. 

Mytilotoxismus. — Under the name of mytilotoxismus is described the 
symptoms of poisoning which are produced by eating poisonous mussels. 
These symptoms consist in some cases in violent gastrointestinal irritation 
with purging, but in the majority of instances the manifestations of the 
poisoning are nervous in character. A rash resembling urticaria and finally 
becoming vesicular may develop over the body, and the eyelids may be so 
swollen as to prevent vision by extravasation of the serum into their tissues. 
There is often difficulty in breathing, apparently due to intense hyperemia 
of the bronchial mucous membrane. Convulsions and coma may develop 
and death may be due to this cause. 

Treatment. — The treatment of mytilotoxismus consists in the use of an 
active saline cathartic to sweep the poisonous material from the alimentary 
canal, and in the use of ether as a diffusible stimulant. 

Ichthyotoxismus. — When fish produces poisonous symptoms the term 
ichthyotoxismus is used to describe the condition. As is well known, cer- 
tain fish are unfit to eat, and other fish become poisonous during the season 
at which they are spawning. In still other instances fish suffer from bacte- 
rial infections which render their flesh unsuitable as food. The ingestion 
of poisonous fish so seldom occurs, at least in this country, that the symp- 
toms produced need not be described. 

Poisoning from the flesh of fish which has undergone decomposition is 
often very violent in its manifestations. The most common symptoms are 
dilatation of the pupils, nausea, vomiting, and severe abdominal pain, fol- 
lowed by the development of a scarlatinal rash all over the body. In such 
cases a purge to sweep out the offending materials and also stimulants are 
needed. 

Kreotoxismus. — The word kreotoxismus is applied to poisoning result- 
ing from the ingestion of meat unfit for food, because of the presence of 
bacterial or animal poisons. Perhaps the most frequent instance of this 
is in so-called sausage poisoning. Sausages are often made from what 



PELLAGRA 857 

may be called the refuse following the butchering of animals ordinarily 
employed as food, and the treatment of this material is such that early 
decomposition changes may readily set in. In most instances the process 
of cooking destroys the poisons, but when cooking is not resorted to the 
symptoms which are induced are exceedingly severe, and death may ensue. 
There is, in many cases of sausage poisoning, difficulty in breathing and 
swallowing, violent vomiting, severe abdominal pain, hoarseness, dimness 
of vision, and delirium. In other cases the mind remains clear. From some 
of these forms of food ptomaines have been isolated. In other instances 
certain bacteria have been found which have been considered responsible, 
either directly or indirectly, for the symptoms. Meat-pie poisoning and 
poisoning by mince-meat are essentially similar to sausage poisoning. 
. Tyrotoxismus and Galactotoxismus. — Under the name galactotoxismus 
is described the poisoning which results from the ingestion of impure milk. 
When poisoning follows the use of bad cheese it is called tyrotoxismus. This 
term is also applied to the poisoning produced by impure ice-cream. The 
symptoms are sometimes exceedingly severe, and consist in evidences of 
gastroenteritis followed by collapse. To a substance which Vaughan 
states he is able to isolate from cheese and ice-cream he gave the name 
of "tvrotoxicon." 

PELLAGRA (MAIDISMUS) . 

Definition. — Pellagra is a chronic intoxication due to eating fermented 
maize. It is characterized by gastric and intestinal symptoms, by marked 
motor, sensory, and psychical disturbances, and by a constant skin eruption. 

History. — Pellagra has been known for about two hundred years. From 
that time until now it has been seen in various countries of Europe, particu- 
larly in Spain, Portugal, and Central Italy. In the Province of Venice 343 
cases occurred in the year 1901, and in the marshes of Umbria and Tuscany 
the cases are very numerous. In 1881 the number of cases in Italy was 
officially estimated at 104,607, or 0.36 per cent, of the entire population. 
The disease occurs in Hungary, in certain departments of Southern France, 
in Egypt and in Algiers. On this continent it is found in Mexico (Yucatan 
and Campeachy). 

Etiology. — Pellagra is primarily due to eating unsound maize or its products. 
Thus, whiskey prepared from such maize may give rise to pellagra just as 
corn-mush, corn-pap (polenta), or corn-bread may convey it. The cause 
of the fermentation of the maize is harvesting in unfavorable years, before 
the grain has thoroughly ripened, and storing in damp cellars or granaries. 
With respect to the specific changes in the grain, there is some conflict of 
opinion as to their exact nature. Lombroso isolated a watery extract, an 
alcoholic extract, and an oil with which he could produce the symptoms of 
pellagra in man and animals. Ceni and Besta have recently extracted, with 
ether, from the spores of Aspergillus fumigatus and Aspergillus flavescens 
a body which produced all the symptoms of pellagra. They have further 
shown that these organisms are constantly present in smutted maize. 

Both sexes are equally attacked. All ages are subject to the disease 



858 INTOXICATIONS 

although the majority of cases occur in later adult life. Bad food, priva- 
tion, and malaria predispose to the development of pellagra. Alcoholism 
is a very prominent factor in the etiology of the disease. Some writers, 
indeed, consider it to be the principal cause. 

Pathology. — The post-mortem changes observed in pellagra are extreme 
emaciation, with loss of the subcutaneous fat and extensive wasting of the 
muscles. The heart, liver, spleen, and kidneys are atrophied. Marked 
pigmentation is seen in the liver, spleen, heart, and spinal ganglia. In the 
central nervous system various changes are met with, principally chronic 
inflammation of the meninges with exudation, and occasionally hemorrhages. 
The spinal cord shows marked sclerosis of the posterior and posterolateral 
columns. The peripheral nerves are degenerated. 

Symptoms. — In pellagra there is first of all an ill-defined prodromal stage. 
The patient feels out-of-sorts and shows marked disinclination to work. He 
has dyspeptic symptoms and complains of constant pain in the head and 
spine. At this early stage insomnia is common and there may even be some 
degree of mental disturbance. These symptoms continue throughout the 
winter, until, with the advent of spring, the first marked symptoms of pellagra 
present themselves in an erythematous rash and marked gastrointestinal dis- 
turbances. The rash appears on the exposed surfaces of the body, particu- 
larly on the backs of the hands, the extensor surfaces of the forearms, and 
on the face and neck. It persists several weeks, when desquamation occurs, 
leaving a thickened patch of scurfy skin. The gastrointestinal symptoms 
consist in severe dyspepsia; there are flatulence, eructations, and anorexia. 
Diarrhoea is commonly present, sometimes approaching dysentery in severity. 
These symptoms persist throughout the spring. With the advent of summer 
the patient becomes very much better and continues in a fair state of health 
until, with the next succeeding spring, a recrudescence takes place. Thus, 
from year to year a cachectic state is developed, with marked nervous phe- 
nomena. 

The motor symptoms are spastic paralysis of the legs, toasting, and con- 
tracture. The superficial reflexes are normal, the deep reflexes increase. The 
sensory symptoms are severe pain in the head and spine, with intolerable 
burning and itching, referred to various skin areas. Girdle pains are com- 
mon. Disorders of vision and taste occur. Psychical symptoms are extremely 
common, and a large percentage of cases end in permanent insanity. In all 
Italy, out of every 100 insane patients, 10 are sufferers from pellagra. In 
Venice the proportion is 35 out of every 100. The common type of 
insanity is melancholia, with delusions of persecution and impulses to 
self-destruction, particularly by drowning. Mania occurs in a small pro- 
portion of cases and dementia is a common ending of all of them. 

In long-standing cases pronounced cachexia develops, with profound 
anaemia and marked emaciation. Alpago-Novello calls attention to the 
evidences of premature senility in these patients. They become prema- 
turely bald, prematurely gray, a marked arcus senilis may be present, and 
early atheroma is frequently observed. The disease is very chronic and may 
last from ten to fifteen years. Cases that have had more than three or four 
attacks, in succeeding springs, are regarded as hopeless. 



LATHY RISM 859 

Treatment. — Treatment consists, first of all, in the interdiction of unsound 
maize as an article of food, and the prohibition of alcohol as a beverage. 
With respect to medicinal treatment, Lombroso recommends large doses 
of arsenic. Wurzel confirms the value of arsenic and also advises the use 
of quinine and strychnine in large doses. For the nervous symptoms massage, 
electricity, and salt-water baths are of service. The patches of erythema 
should be kept moist and supple with oily ointments to which cocaine, 
carbolic acid, salicylic acid, or chloral may be added to control the itching. 

The prophylaxis of the disease includes education of the people in the 
infected area of the danger of fermented maize as an article of food. Maize 
should only be harvested when ripe and should only be stored in dry, well- 
ventilated granaries. When maize is a staple article of import it should be 
rigorously inspected at the first port of entry and all spoiled grain rejected. 



LATHYRISM (CHICKPEA DISEASE; LUPINOSIS). 

Definition. — Lathyrism is a chronic intoxication characterized by spastic 
paralysis of the lower limbs without disturbance of sensation. It is caused 
by the use of various species of lathyrus as food. That the vetches, or chick- 
peas, were capable of producing a disease of this type was known in the time 
of Hippocrates. 

History. — The disease was exceedingly common in Italy and France dur- 
ing the seventeenth and eighteenth centuries. It was first accurately studied 
by Irvin in 1859. The present geographical distribution is France, Italy, 
Algiers, and British India. 

Etiology. — Lathyrism is due to the use of different varieties of lathyrus 
as foods ; chiefly Lathyrus sativus, Lathyrus cicera, and Lathyrus clymenum 
(the common vetch, or chickpea). In time of famine and want the seeds of 
these legumes are ground and mixed with flour and other meal and used in 
bread-making. Observation has shown that they must be eaten for some 
length of time, several weeks or a month, before symptoms begin. The 
poison lies in the peas themselves, and mustiness or fermentation is not a 
factor as in pellagra. It is stated that "Teora" (Lathyrus sativus) in India 
only causes the disease when baked; when boiled it is said to be innocuous. 
As immediate exciting causes for the outbreak of the disease, exposure to 
cold, rain, and damp weather are recognized. Consequently men, being 
much more exposed to climatic changes in their daily avocations, are more 
frequently attacked than women. Cattle eating the peas also develop the 
disease. 

Symptoms. — There may be prodromal symptoms, such as fever, dyspepsia, 
and diarrhoea. Usually the disease begins suddenly, after exposure or a 
wetting. There is pain in the loins, legs, and knees, with weakness and 
tremors. From this point on there is a gradual and continuous development 
of a spastic paralysis of both legs with marked spasms, particuarly of the 
adductor muscles of the thighs. The reflexes are exaggerated. Sensation 
is not impaired. The bladder and rectum are not involved, as a rule, except- 
ing in severe cases, when the paralysis may include the sphincters. The 



860 INTOXICATIONS 

upper limbs are not involved. The course of the disease is exceedingly 
chronic and the paralysis is usually permanent. 

Death from lathyrism itself is very rare. In one patient who died of an 
intercurrent malarial infection Grandjean found a softened area in the cord 
extending 6 cm. above the lumbar enlargement. The clinical symptoms 
point to a degeneration of the lateral columns. 

Treatment. — Treatment consists in the withdrawal of lathyrus from the 
patient's food, and the education of the masses to the danger that lies in the 
use of these products. Scheube reports good results from sharp counter- 
irritation over the lumbar vertebra. 



ATRIPLICISM. 

Atriplicism (" intoxication par l'arroche") is an intoxication due to eating 
the coast orach, and is characterized by marked local disturbances of sensi- 
bility, by local oedema and trophic disorders. This disease was first 
reported by Matignon in 1898, from North China. He ascribes it to eating 
Atriplex augustissima and Atriplex serrata of the order Chenopodiacece, both 
common weeds in China. They are eaten baked or fried in dough, or raw 
as a salad. 

Within ten to twenty hours after eating the orach there is tingling and 
cold in the thumbs, fingers, and back of the hand, followed by itching and 
wdema, which spreads over the back of the hand and forearm and ends 
sharply at the elbow. Later, swelling and itching of the face occur. The 
parts are cold, the nose and finger-tips cyanotic. The oedema persists from 
two to ten days. After it subsides the skin is exfoliated. In severe cases 
large blebs may form which subsequently ulcerate. Matignon reports one 
case in which gangrene of the fingers occurred. The disease superficially 
resembles erythromelalgia. 

Treatment. — Treatment consists in free purgation at the beginning of the 
disease and the application of sedative lotions locally. 



LACQUER POISONING. 

This is a troublesome poisoning of the skin observed in China and Japan 
among workers in lacquer. Lacquer is derived from the balsamic exudate 
from the lacquer tree (Rhus vernicifera) . The poisoning is limited to the 
skin and is entirely analogous to that produced by the varieties of rhus, so com- 
mon in America, excepting that it is much more severe. The infection takes 
place not only through contact with the raw lacquer, but Scheube states that 
it may be conveyed from the vapors arising during the evaporation of 
lacquer, and that susceptible individuals may even acquire it by visiting 
lacquer warehouses where there are newly lacquered articles. The attack 
begins a few hours after exposure, with intense itching of the skin of the 
face and limbs. The skin becomes cedematous; numerous papules appear, 
which later become vesicular and are filled with a yellow seropus. The 



LACQUER POISONING 861 

vesicles may coalesce and form large blebs. The disease is limited to the 
arms, legs, face, and genitals. When the face is severely affected, the adjacent 
mucous membrane shares in the disturbance, and there may be a sharp 
febrile reaction. 

Treatment. — Treatment consists in soothing local applications. Lead- 
water with or without opium and lime-water are principally used. 

The gingko tree {Gingko biloba) causes a dermatitis exactly like lacquer 
poisoning excepting that it is not so severe. The question of gingko 
poisoning is of some little interest in the United States at present. The 
tree is a native of China, but has recently been introduced in America as 
an ornamental foliage plant. 



DISEASES DUE TO ANIMAL PARASITES. 



MALARIAL INFECTION. 



Definition. — By malarial infection we refer to a condition produced by the 
entrance into, and development in, the blood of specific micro-organisms 
known as the Plasmodium malarias, the haematozoon of malarial fever, or, 
more correctly speaking, the H (Entamoeba malaria?. 

The infection is manifested by four different types: First, the so-called 
intermittent type, in which the patient has recurring attacks which are 
characterized by a chill, a fever, and a sweat. These recurrences com- 
monly take place daily, on alternate days, or on every third day, and are 
called quotidian, tertian, or quartan. Second, a type in which there is 
present continued fever with remissions in its course, the so-called remit- 
tent malarial fever. Third, a type in which the infection is of a malig- 
nant or pernicious form with profound toxaemia. Fourth, that form in 
which more or less subacute, or chronic, and profound cachexia is present, 
associated with marked anaemia and enlargement of the spleen, and often 
of the liver. The first is due to the tertian or quartan parasite, the second 
and third to the aestivo-autumnal parasite, while the fourth form may be due 
to any one of the three parasites. 

History. — Malarial fever was recognized as a distinct disease as long 
ago as five hundred years before Christ, and Hippocrates divided it into the 
quotidian, tertian, and quartan types we recognize to-day. Empedocles 
(500 B.C.) recognized the relationship of the disease to stagnant water and 
stopped an epidemic by draining stagnant pools; but it was not until 1880 
that Laveran, a French army surgeon, first recognized the specific organism, 
and in 1886 Marchiafava and Celli described it more fully. In the same 
year Golgi showed that the malarial attack occurred simultaneously with 
the sporulation of the parasite, but not until 1898 did Manson and Ross, 
of England, and Grassi and Bignami, of Italy, prove that the infection is 
spread from man to man by a certain species of mosquito known as the 
Anopheles. In the United States excellent work has been done by a 
number of investigators, of whom the most noteworthy are Osier, Thayer, 
and Hewetson in Baltimore, James in New York, Craig of the U. S. Army, 
and Dock in Texas. 

Distribution. — Malarial infection is more widely diffused throughout 
the tropical and temperate zones than any other disease. It is, as a 
rule, prevalent and severe in direct proportion to the proximity to the 
equator and is rare in far northern latitudes. Certain parts of the world, 

(863) 



864 DISEASES DUE TO ANIMAL PARASITES 

which at one time suffered severely from the disease, are now free from it. 
Forty or fifty years ago, for example, the valleys of the Delaware and 
Schuylkill Rivers near Philadelphia suffered greatly, whereas at present 
cases of the disease are rarely met with in these localities. On the other 
hand, it is very prevalent on the shores of the Chesapeake Bay, which is 
not more than one hundred miles away. At present the disease appears 
in its mild forms in France, Germany, and England, and in the Middle 
Atlantic and Central United States, and in its severe forms in the Southern 
States, particularly in certain lower portions of the Mississippi Valley. The 
virulent forms are chiefly met with in Africa, in certain parts of India, and 
in the tropics, as in the West Indies and in the Philippines, and in the 
tropical parts of South America. On the Pacific coast of the United States 
the disease is rare. So far as season is concerned, it may be said that the 
greater proportion of cases occur in July, August, September, October, and 
November in semi-tropical or temperate regions. 

The frequency of malarial fever varies greatly and depends entirely upon 
the prevalence of the Anopheles, the sources for its infection, and the climate 
which permits of the growth of the mosquito. In the United States the 
greatest prevalence of this disease is in the States bordering the Gulf of 
Mexico and that tier lying immediately north of them. The death rate 
from malaria in this area is about 30 per 1000 deaths from known causes. 

Etiology. The Mosquito. — There is but one direct etiological factor in 
the dissemination of malarial fever in man, namely, that form of mosquito 
known as Anopheles. Many species of the genus Anopheles have been 
described, but only three have so far been found to be present as malaria- 
bearing hosts in the United States, namely, the Anopheles quadrimaculatus, 
which is the most common, the Anopheles punctipennis, and the Anopheles 
crucians. In Europe the infection is always borne by the Anopheles 
claviger, sometimes called Anopheles maculipennis. Fortunately, the ano- 
pheles is not universally distributed, the culex being the genus which is 
most commonly met with, at least in the temperate zones, and this mos- 
quito seems to be incapable of carrying the infection. The anopheles can 
be readily differentiated from the culex by the fact that when it rests 
upon a plane surface its body is held at right angles, or at an angle of 
forty-five degrees, whereas the body of the culex lies parallel to the plane. 
Again, the wings of the anopheles show very distinct mottling, as its names 
punctipennis or quadrimaculatus indicate. Most of the culex species lay 
their eggs in rafts or bottle-shaped masses, which remain intact until the 
larvse are discharged. The eggs of the anopheles are laid in groups that 
are readily broken up and scattered. Any stagnant or semi-stagnant accu- 
mulation of water is a suitable breeding-ground. 

The indirect factors in the causation of malarial infection are, therefore, 
stagnant or semi-stagnant water in which this mosquito can breed, and 
the presence of a source from which it can obtain the parasite so that it 
can transmit it to a healthy individual; for even if the Anopheles be 
present, it cannot inoculate a human being with malarial fever unless 
it has first bitten a person whose blood contains the hsemamceba. No 
more interesting experiments proving these facts can be adduced than 



MALARIAL INFECTION . 865 

those made by Patrick Manson on his son, who had never had malarial 
infection. Bignami and Bastianelli sent Manson in England relays of 
mosquitoes which in Italy had been fed upon the blood of patients 
suffering from pure benign tertian malaria. These mosquitoes were 
allowed to bite the younger Manson, and as a result he developed the 
same form of malarial fever as that suffered by the Italian patients, and 
the same parasite was found in his blood. 

The PLemamceba Malarije ix Max. — The parasite itself passes through 
two cycles of existence, namely, one which is carried out in the body 
of man, and another in the body of the mosquito. It appears in three 
distinct forms, namely, as the tertian parasite, the quartan parasite, and 
the sestivo-autumnal parasite. Each of these live in the red cells of the 
blood and to some extent exist in the plasma as well. 

Marchiafava, Celli, Bignami, and Grassi, of Italy, have endeavored to 
show that several species of the sestivo-autumnal parasite exist, but their 
views have not been generally accepted, and recently they have admitted 
that there are not sufficient grounds for advocating this proposition. 

In certain cases the patient suffers from a mixed infection in which the 
tertian and aestivo-autumnal parasite are both present at the same time. 

The young tertian parasite is a small colorless and hyaline body which 
occupies a small space in the corpuscle. \Yhen in a state of quiescence it is 
round, but if the specimen under the microscope is fresh and the temperature 
suitable it manifests active amoeboid movements. As the parasite grows, 
reddish-brown granules develop in its interior. These pigment granules 
move rapidly, and are often seen in the amoeboid projections of the para- 
site, so that it may appear that several parasites are in one corpuscle. As 
the growth continues the infected red cell becomes more and more pallid 
and swells up or expands, the amoeboid movements of the contained para- 
site diminish in activity, and the pigment granules arrange themselves 
about the periphery of the parasite. At this time the corpuscle is nothing 
more than a shell of its former self. Later the pigment granules accu- 
mulate near the centre of the body, and as they do so the process of seg- 
mentation begins; radial lines divide the parasite into twelve to twenty 
segments arranged around the central mass of pigment. Each segment 
has a nucleus, and as soon as the process of segmentation is completed 
these segments break out of the corpuscular shell and float freely in the 
blood plasma, where they speedily attack and enter fresh red cells. The 
evolution and segmentation require about forty-eight hours, and the chill 
and other acute manifestations of illness in the patient develop at the time 
of segmentation. In some instances the parasite becomes unusually large, 
the pigment bodies become stationary without aggregation in the centre, 
vacuoles develop in it, and the parasite seems to die. (See Plate V.) 

The tertian parasite is the one which produces that form of intermittent 
fever in which the paroxysm occurs every second day. If the attack occurs 
daily, it is due to a double infection, in which one set of parasites sporulates 
on one day and the other set on the next day. 

The following distinctions serve to separate the tertian from the sestivo- 
autumnal parasite: The nuclear body and chromatin mass of the young 
55 



866 DISEASES DUE TO ANIMAL PARASITES 

tertian parasite are achromatic to methylene blue, whereas the nucleus of 
the sestivo-autumnal parasite is densely stained by this agent (Ewing). 
The tertian ring is coarse and granular, whereas the sestivo-autumnal ring 
is a perfect circle and more delicate. The tertian ring is usually pigmented 
before the chromatin becomes subdivided, while in the sestivo-autumnal 
parasite the chromatin is subdivided before pigmentation appears. There 
are, however, exceptions to this rule. Lastly, the infected red blood cor- 
puscle is usually distended or swollen as soon as it is attacked by the tertian 
parasite, whereas it is shrunken in appearance when the sestivo-autumnal 
parasite enters it. 

The quartan parasite — that is, the organism that causes an attack every 
third day — resembles the tertian organism just described, but differs from 
it in the following respects : In the early stages it occurs as a hyaline body 
which is smaller than the tertian parasite. It speedily develops a sharper 
outline, it is more refractive, and the amoeboid movements are slower. The 
pigment granules are larger and darker, less active, and lie near the edge of 
the parasite. Again, it is noteworthy that the red cell does not swell as do 
those containing the tertian parasite, but grows smaller, darker, more 
refractive and metallic looking. The quartan parasite reaches its growth 
in from sixty-four to seventy-two hours, and then appears as occupying 
nearly the entire red blood cell, or it seems to float free in the blood serum. 
As the time for the paroxysm approaches the pigment granules at the 
periphery flow toward the centre in radial lines, so that it becomes arranged 
in stellate form and the protoplasm divides into from six to twelve pear- 
shaped segments, each of which has a refractive centre. These segments 
escape and infect new cells. Some of the parasites do not, however, go 
on to this development, but fail to sporulate and become sexual bodies 
or gametocytes. 

The third form of parasite, the oestivo-autumnal form, is smaller than 
the tertian and quartan organism, and presents a ringed appearance. It 
contains much less pigment and, moreover, it soon causes the corpuscle 
into which it enters to become shrivelled and brassy looking. After a time, 
possibly a week, the parasite increases in size, becomes refractive, crescentic, 
or round, or ovoid in form, and, in the centre, masses of dark pigment accu- 
mulate. It is these latter bodies which are indicative of infection by the 
sestivo-autumnal type, and it is to be remembered that, as a rule, they 
are not constantly present in the peripheral circulation but only in the 
blood of such internal organs as the liver, spleen, and in the bone-marrow. 
Because of their small size, slow development, and the difficulty of obtain- 
ing blood from deeply situated organs, they are less readily discovered than 
the other two types. It appears established that the crescentic and ovoid 
bodies do not undergo segmentation or sporulation, but correspond to the 
sexual bodies described above, the gametocytes. These crescentic and ovoid 
bodies do not continue their development in the human being, sporulation 
being the human cycle. The fertilization of the female by the male body 
occurs in the extracorporeal or intermediate cycle. (See Plate VI.) 

The three forms of malarial parasite as they appear in man have now 
been described. The mosquito cycle of its existence is as follows: 



DESCRIPTION OF PLATES V. AND VI. 1 

The drawings were made with great care and skill by Mr. Max Broedel, with the 
assistance of the camera lueida, from specimens of fresh blood. A Winkel microscope, 
1 II (oil-immersion) j ocular, I, was used. 



objective, 

Fi| 

camera 



L'tive, i 11 (^oil-immersion;, ocular, i, was used. 

Figs. 1, 13, 23, 21, and 42 of Plate Y. were drawn from fresh blood, without the 

jra lucida. 

PLATE V. 
The Parasite of Tertian Fever. 

1. — Normal red corpuscle. 

2, 3, 4. — Young hyaline forms. In 4 a corpuscle contains three distinct parasites. 

5, 21. — Beginning of pigmentation. The parasite was observed to form a true ring 
by the confluence of two pseudopodia. During observation the body burst from the cor- 
puscle, which became decolorized and disappeared from view. The parasite became, 
almost immediately, deformed and motionless, as shown in Fig. 21. 

G, 7, 8. — Partly developed pigmented forms. 

9. — Full-grown body. 

10-14. — Segmenting bodies. 

15. — Degenerative form simulating a segmenting body. 

16, 17. — Precocious segmentation. 

18, 19, 20. — Large swollen and fragmenting extracellular bodies. 

22.— Flagellate body. 

23, 24. — Degenerative forms showing vacuolation. 

The Parasite of Quartan Fever. 2 

25. — Normal red corpuscle. 
26. — Young hyaline form. 

27-34. — Gradual development of the intracorpuscular bodies. 

35. — Full-grown body. The substance of the red corpuscle is not visible in the 
fresh specimen. 

36-39. — Segmenting bodies. 

40. — Large swollen extracellular form. 

41. — Flagellate body. 

42. — Degenerative form showing vacuolation. 

PLATE VI. 

The Parasite of ^Estivo-autumNal Fever (Hcematozoon falciparum). 

1, 2. — Small refractive ring-like bodies. 

3-6. — Larger disk-like and amoeboid forms. 

7. — Ring-like body with a few pigment granules in a brassy, shrunken corpuscle. 

8, 9, 10, 12. — Similar pigmented bodies. 

11. — Amoeboid body with pigment. 

13. — Body with a central clump of pigment in a corpuscle showing a retraction of 
the hcemoglobin-containing substance about the parasite. 

14-20. — Bodies with central pigment clumps or blocks. Presegmenting forms. 

21-24. — Larger bodies with central pigment blocks. Presegmenting bodies. Seen 
in the peripheral circulation during a severe paroxysm. 

25-28. — Segmenting bodies from the spleen. Figs. 25-27 represent one body where 
the entire process of segmentation was observed. The segments, eighteen in number, were 
accurately counted before separation, as in Fig. 27. The sudden separation of the seg- 
ments, occurring as though some retaining membrane were ruptured, was observed". 

29-37. — Crescents and ovoid bodies. Figs. 34 and 35 represent one body which was 
seen to extrude slowrv, and later to withdraw, two rounded protrusions. 

38, 39.— Round bodies. 

40. — Pseudogemmation, fragmentation. 

41. — Vacuolation of a crescent. 

42-44. — Flagellation. The figures represent one organism. The blood was taken 
from the ear at 4.15 p.m.; at 4.17 the body was as represented in Fig. 42. At 4.27 the 
flagella appeared; at 4.33 two of the flagella had already broken away from the mother 
body. 

45-49. — Phagocytosis. Traced with the camera lucida. 

1 These plates are taken by permission from Thayer and Hewetson's classical report in the Johns 
Hopkins Hospital Reports, vol. v., 1895. Four figures — viz., Figs. 21, 22, 23, and 24 — have been added to 
Plate VI., and are also from the drawings of Mr. Max Broedel. 

2 The color of the pigment in these figures of the quartan parasite has too much of a reddish tint. 



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PLATE V. 
The Parasite of Tertian Fevei 



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The Parasite of Quartan Fever 



27 

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PLATE \ 
The Fbrasite of Aestivo-Aufum'nal tem. 











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MALARIAL INFECTION 867 

The ILemamceba Malarle in the Mosquito. — A mosquito of the genus 
Anopheles, when it sucks blood from an individual in whom the parasite has 
developed sexual forms, receives into its stomach bodies ready for the sexual 
process ; in other words, gametocytes. The male bodies, or microgameto- 
cytes, develop long, actively moving flagella, called microgametes, which 
break loose from the organism and penetrate and fertilize the larger female 
bodies or macrogametes, these bodies being simply macrogametocytes 
which have extruded from their nuclear substances. The impregnated 
female now penetrates the wall of the mosquito's stomach, within which 
further development occurs. Within forty-eight hours there may 
be seen encapsulated in the muscular wall of the mosquito's 
stomach small, round, refractive, and granular bodies which have 
in them pigment granules much like those present in the parasite 
existing in the red blood corpuscles. At the end of a week the parasite 
has grown considerably, and it is found to be marked by radial striations 
forming sporoblasts. When this stage is completed the mother body, 
sometimes called the oocyst, bursts, and so sets free in the ccelomic cavity 
of the mosquito a multitude of sporozoids. These sporozoids gain access 
to the veneno-salivary glands of the mosquito, and thence to the veneno- 
salivary ducts, from which they are ejected into the human being bitten 
by that mosquito. No sooner are the sporozoids deposited in the blood of 
man than they speedily become parasites which attack blood cells. Blood 
cells are therefore attacked in two ways: by parasites formed during the 
asexual or human cycle, and by parasites produced in the sexual or 
mosquito cycle. 

Prevention. — The prevention of malarial fever consists in (a) protection 
from the bites of the anopheles by the use of mosquito bars, particularly 
at night; (b) in the removal of all marshes by filling them in or draining 
them so that the breeding-place of the mosquito is destroyed; (c) in the 
destruction of the larvae of the mosquito by diffusing coal-oil over the surface 
of pools or ponds, and (d) by not permitting a patient who has the parasite 
in his blood to mingle with his fellows when the anopheles are present, for 
from him they derive their supply of infection. The latter measure can 
often only be carried out in private honses and barracks. Such patients 
should always sleep under a mosquito-proof canopy. Finally, it is a well- 
recognized fact that by the use of small doses of quinine taken daily (5 
grains) it is often possible to prevent infection. 

Pathology and Morbid Anatomy. — The changes produced in the body l>y 
the presence of the malarial parasite are much less pronounced if the tertian 
and quartan parasite is present than if the sestivo-autumnal is the offend- 
ing body. Indeed, in many cases the morbid changes are so slight that 
they are speedily overcome by the natural processes of repair, and hence 
rarely cause death. For this reason our knowledge of the acute changes 
produced in internal organs is very limited. These changes may, however, 
for the sake of study, be divided into two forms, the acute and chronic. In 
the acute type the parts of the body which suffer chiefly are the blood, the 
liver, the spleen, the kidneys, and the alimentary canal. 

The changes in the blood consist in a distinct decrease in the number of 



868 DISEASES DUE TO ANIMAL PARASITES 

red cells which are destroyed primarily by the growth of the parasites, and 
possibly secondarily by poisons produced by them. That some such agent 
is active seems to be proved by the granular degeneration of the red cells 
which is present in severe cases, and in the polychromatophilia which is 
met with in cells into which the parasite has not entered. There is also a 
diminution in the color-index, that is, of the individual richness of the cells 
in haemoglobin. The white blood cells are usually increased in the pro- 
portion of mononuclear leukocytes. Pigmented leukocytes are also found, 
and, if the infection has been severe, large white cells (macrophages) are 
to be seen heavily loaded with pigment. In some instances particles of 
pigment are seen floating in the blood serum, having been set free from red 
blood cells destroyed by the parasite. 

The liver, besides showing great congestion, may present areas of necrosis 
and the capillaries may be found filled with a multitude of the parasites in 
all degrees of growth. The capillaries of the liver may also contain many 
pigment particles. 

The kidneys are enlarged and congested. They may contain dotlets of 
deposited pigment, and their capillaries may be filled by leukocytes laden with 
pigment. The number of parasites found in the renal vessels, however, as 
compared to those found in the hepatic masses, is small. Rarely an acute 
diffuse nephritis may be manifest. 

The spleen is swollen, soft, and its pulp is very dark. Many of the red 
blood cells which it contains are inhabited by the parasites, and these are 
often in the stage of sporulation. So intense may be the swelling and con- 
gestion of the spleen that it may be ruptured by sudden stress. 

The mucous membrane of the stomach and bowels is engorged and its 
capillaries often contain the plasmodium. 

If the bone-marrow is examined it is found to be filled with segmenting 
parasites and with pigment. The crescentic parasites are also apt to be 
numerous in these areas. 

The chronic changes consist in profound anaemia, manifested by a 
diminution in red cells and in haemoglobin and by the presence of nucleated 
red cells. The liver is deeply pigmented, often slaty in color, the granules 
, being deposited in the endothelial lining of the capillaries and the so-called 
cells of Kupffer, that is, the perivascular cells. The hepatic epithelium is 
commonly granular and a certain degree of hepatic cirrhosis may also be 
present. 

The spleen also becomes markedly increased in size, slate colored 
from the contained pigment and later, due to increase in fibrous tissues 
it becomes very firm, the "ague cake." 

The kidneys are also markedly pigmented, and may suffer from 
chronic diffuse nephritis. In certain cases of the cerebral type the para- 
sites may be found in the vessels of the brain and a malarial neuritis has 
been described. As in the acute form, the bone-marrow is deeply pig- 
mented and the normal marrow may be replaced by red marrow in which 
normoblasts and megaloblasts are present in the majority of cases. All 
these changes are the result of aestivo-autumnal infection. 

The blood is to be examined for the malarial organism during life by the 



MALARIAL INFECTION 869 

microscope with an oil-immersion lens and by the use of the following 
methods i 1 

"There are two methods of examining the blood for plasmodia, in fresh 
preparations and in stained smears. Both require considerable training, as 
the artefacts produced by imperfect technique have often been mistaken for 
organisms. 

"The Examination of Fresh Blood. — To examine the fresh blood, a 
puncture is made in the pulp of the finger and a perfectly clean cover-glass just 
touched to the top of the drop of blood which exudes from the puncture. 
The cover is then dropped without pressure on a clean slide. The diameter 
of the drop on the cover-glass should never exceed 2 mm., because if more be 
taken the corpuscles cannot spread out in a perfectly thin layer, but will 
overlap each other, and the preparation will be useless. The search for the 
organism should be made with a -^ oil-immersion lens and a moderate 
illumination. The organisms are best recognized by the actively motile 
pigment in the clear, highly refractile cell body. 

"The Examination of Blood after Fixation. — If the examination 
cannot be made at once, stained preparations may be made. The smear should 
be made on a slide or large cover-glass. It is best fixed in a mixture of 
formalin and strong alcohol for one minute. The proportions are 2 c.c. of a 
10 per cent, solution of formalin to 100 c.c. of strong ethyl alcohol. The 
organisms are most easily found and studied in preparations colored with 
thionin. The formula for the stain is 20 c.c. of a saturated solution of 
thionin in 50 per cent, alcohol, added to 100 c.c. of 2 per cent, aqueous solu- 
tion of carbolic acid. The stain requires several days to ripen, and then 
keeps indefinitely. Its action is rapid, requiring only about fifteen seconds 
to color the malarial organisms deeply. 

"In order to demonstrate the nuclear chromatin of the malarial parasites, 
it is necessary to use special stains, the most useful being a modification of 
that originally devised by Romanowski for this purpose and improved by 
Giemsa. Two substances are necessary: First, an aqueous solution of 
* methylene azure II, Grubler,' 8 dgm. to the litre; and second, an aqueous 
solution of eosin, ' extra water-soluble, Hochst.' These two stock solutions are 
permanent if kept in dark-colored bottles. The smears to be stained are 
fixed in methyl alcohol for about ten minutes. The staining mixture is pre- 
pared by adding 1 c.c. of the methylene azure II to 10 c.c. of the eosin solu- 
tion. The staining mixture is poured into a Petri dish and the slide immersed 
in the fluid with the blood side down. The process is complete in from 
fifteen to thirty minutes. The slide is washed off for about ten seconds 
with a strong stream of distilled water, dried in the air without heat, and 
embedded in dammar dissolved in xylol. A simpler method has recenlty 
been published, which is better adapted for clinical work. The smear is 
fixed for two minutes or more in methyl alcohol, then stained for ten seconds 
with a 1 : 1000 aqueous eosin solution, the latter allowed to run off the slide, 
and the smear again covered with a few drops of a i per cent, solution of 

1 These directions are taken from the last edition of Pathology and Morbid Anatomy, by Delafield 
and Prudden. 



870 DISEASES DUE TO ANIMAL PARASITES 

methylene azure II. In about from fifteen to thirty seconds the staining is 
complete. The slide should be washed in distilled water, dried, and exam- 
ined directly with an oil-immersion lens, no cover-glass being necessary. " 

Symptoms. — The symptoms of malarial infection may be divided into 
two classes: those due to the tertian or quartan parasites, which are much 
alike, and those due to the sestivo-autumnal parasites, which are very different 
from those produced by the more benign forms. 

The Symptoms of Tertian and Quartan Infection. — The pre- 
dominant symptoms of infection by these parasites are the development at 
regular intervals of a chill followed by a fever, and this in turn by a sweat. 

The stage of onset begins with a feeling of malaise, in which headache and 
a general sensation of wretchedness are present. Patients who have had 
previous attacks are often able to recognize the fact that they will have a 
paroxysm in a few hours. 

After the lapse of from one to five hours the chill develops and is 
often in the form of a severe rigor, in which the teeth actually chattel 
and the patient is entirely unable to control his muscular quivering. 
At this time the skin is cold, the face is pinched and often anxious in 
expression; but while the patient complains of being cold and presents 
all the external signs of a lowering of body temperature, his actual 
internal temperature is raised so that fever is really well developed while 
the so-called cold stage is still manifest. Thus, it is not uncommon for the 
rectal temperature to be as high as 105° while the patient is shivering and 
trying to "get warm." Associated with this part of the paroxysm the 
patient is usually nauseated and may actually vomit, so that to the depression 
of the chill is added the relaxation and semi-collapse of excessive nausea. 
Headache of the congestive type is also severe. The urine is copious in 
quantity and light in color, and the pulse small, rapid, and of high tension. 

This stage of chill lasts from a few minutes to an hour or more, and is 
followed by the true febrile stage, in which the surface of the body becomes 
flushed and hot. In place of the cold, pinched expression the face now 
appears hot and flushed, the eyes may be brightened by the fever, and the 
pulse, which has hitherto been small and tense, becomes full and bounding. 
Headache, however, still persists, and active delirium may develop, but the 
actual temperature of the patient is rarely higher than during the stage of 
chill; indeed, it may be a little lower. The so-called febrile stage is not 
therefore any more febrile than the stage of apparent codlness, but the intense 
sensation of heat in the skin at this time when the physician touches the 
patient is noteworthy. This stage lasts from thirty minutes to several 
hours and comes to an abrupt ending by the development of the stage 
of sweat, in which the temperature drops to normal; the surface of the 
patient becomes bedewed with sweat, which may be so profuse that it is 
truly a "dripping sweat." The headache and general wretchedness now 
disappear and the patient drops to sleep exhausted bv the violence of his 
attack, but otherwise not ill. 

The accompanying charts (Figs. 110 and 111) show the typical temp- 
erature changes: 

As in all diseases, so in this one, it must be recalled that all cases do not 



MALARIAL INFECTION 



871 



go through these stages in exactly the same manner. Some individuals suffer 
from a very moderate chill and an equally moderate fever and sweat. Some 
suffer the paroxysm for twelve hours and some for a much shorter space of time. 
There are three important physical signs which may be demonstrable in 
many if not all these cases. The spleen is found on palpation and percus- 
sion to be distinctly enlarged, extending below the level of the ribs; some 
bronchial rales are usually to be heard in the chest, and the lips are apt to 
be affected by herpes at the close or after an attack. 



Fig. 110 



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Chart showing paroxysms of tertian fever, the segmentation of the organism occurring at 
about 12 o'clock every other day. 



The severity of all the signs depends, of course, upon the resistance of 
the patient and the virulence of the malarial infection. - 

There yet remains to be considered the periodicity of these attacks. 
They may occur daily, in which case they are called quotidian; or every 
other day, when they are called tertian ; or every third day, when they are 
called quartan. The tertian type is due to the tertian parasite, which sporu- 
lates every forty-eight hours, so that the next paroxysm develops at the 
beginning of the third day; hence the term tertian, or third. When the 
attack occurs daily it is due to the fact that a double infection of the tertian 



872 DISEASES DUE TO ANIMAL PARASITES 

parasite has taken place, so that a different set of organisms mature each 
day; in other words, it is a "double tertian infection." This form is more 
frequently seen in the United States than any other type. When the attack 
occurs at the end of every third day — that is, after the lapse of seventy-two 
hours, which is really therefore on the beginning of the fourth day of actual 
time — it is due to the quartan parasite. Sometimes, however, the infection 
with this parasite is a double one, the sporulation in each infection taking 
place separately, in which case the attacks occur on two successive days 
with a free day following. In still other cases a triple quartan infection may 
cause a daily or quotidian manifestation of the disease. A daily malarial 
attack may therefore be due to a double tertian or a triple quartan infection. 

On the days free from paroxysm the patient is entirely free from chills, 
fever, or sweats, and except for some impairment of strength may be almost as 
well as ever. It is for this reason that the disease is called " intermittent fever." 

Diagnosis of Intermittent Fever. — The diagnosis of this type of malarial 
fever is easy in the majority of cases, but the physician should not hurry to 
this conclusion until he has carefully excluded several other states that 
cause a similar temperature curve. These states are tuberculosis of the 
lungs with chills, fever, and sweats; septicaemia and ulcerative endocarditis 
with the same train of symptoms, and typhoid fever with chills of a sharp, 
distinct character. The number of poor human beings who are dosed ad 
nauseam with quinine for malaria when they have tuberculosis is appalling. 
The history of the case, the physical signs in the lungs, and the fact that the 
attacks of chills and fever do not cease if quinine is given, prove that malaria 
is not the cause of the illness. Careful examination of the patient ought to 
discover sepsis by the finding of a definite focus of pus, and in many cases 
ulcerative endocarditis can be discovered by the changes in the heart sounds. 
Typhoid fever can be discovered by the state of the tongue, that of the 
bowels, the rose rash, and the Widal test of the blood. Better than all for 
an absolute diagnosis is the discovery of the malarial parasite in the blood 
by the use of the microscope. Unfortunately, this is only possible to the 
expert. (For examination of the blood for the parasite see Pathology.) 

Prognosis of Intermittent Fever. — Intermittent malarial fever cannot be 
considered a self-limited disease. It is true that individuals affected by 
it recover without medication if they are otherwise healthy and have favor- 
able surroundings, but it is notorious that they are very liable to subsequent 
outbreaks of the disease when for various reasons their vital resistance is 
impaired or the system is affected by change of climate. Thus it is by no 
means unusual for patients seemingly well of the infection to be attacked by 
paroxysms on going to a higher altitude. If quinine is used with skill, and 
further infection is avoided, complete recovery usually is reached if no 
complication arises. 

Treatment of Intermittent Fever. — In the treatment of intermittent malarial 
fever the fact is always to be borne in mind that in quinine we have a true 
specific for the disease in that this drug, even in exceedingly weak solu- 
tion, is capable of causing the death of the malarial parasite. So complete 
is the cure produced by the proper administration of this drug that no other 
form of remedial measure can be considered until after it has been given 



MALARIAL INFECTION 873 

full opportunity to do its work. But, on the other hand, it must not be for- 
gotten that quinine cannot destroy the malarial parasite until it (the quinine) 
has entered the blood, that it cannot enter the blood until it is absorbed, 
and that it is impossible for it to be absorbed if the gastroduodenal and 
hepatic circulation is so disturbed that catarrh of the stomach and bowels 
is present, making it impossible for the quinine to be taken up by the circu- 
lation. It is therefore essential, in almost every case of intermittent fever, 
that the bowels shall be thoroughly unloaded, preferably by full doses of 
calomel of which not less than 5 nor usually more than 20 grains are required, 
this in turn being followed by a saline purge. If, in addition to these meas- 
ures, it is insisted upon by the physician that the patient shall rest in bed 
during the time that the quinine is being given, it is surprising how 7 little 
quinine is needed to destroy the parasites; w T hereas, if these precautions are 
not taken, enormous doses may be given with no curative effect. 

Quinine may be administered at two periods in connection w 7 ith the 
paroxysm of intermittent malarial fever. One method is to administer the 
drug several hours before an expected paroxysm, with the hope that it may 
prevent sporulation, or at least destroy the spores as soon as they escape. 
This plan is always to be resorted to when the physician is confident that 
an attack is threatened and that a sufficient time will elapse to make it 
possible for the quinine to be absorbed. The other method consists in 
administering the drug in the sweating stage of a paroxysm, for the purpose 
of destroying the young parasites w 7 hich have just escaped from the red 
blood corpuscles, in the hope that they may be destroyed before they can 
attack new cells. It is evident, therefore, that neither of these plans is 
contradictory, but are to be resorted to according to the period at which 
the physician sees the patient. It should always be the endeavor of the 
physician to have the quinine in the blood an hour or tw 7 o before an expected 
paroxysm, and this means that it should be given several hours before 
when taken by the stomach. 

When the attack is quotidian quinine must be given daily, when it is 
tertian it must be given every other day, and when it is quartan a full dose 
of quinine should be given on the day of the expected attack and smaller 
doses on the off days. If it is a double quartan infection the quinine should 
be given on the two consecutive days and only a small dose on the third day. 

The quantity of quinine which is required varies of course w 7 ith the severity 
of the infection and the rapidity of the absorption. Ten to 15 grains are 
usually sufficient in the milder types, but in the more severe types 30 to 60 
grains are often required, although a larger quantity is usually needless if 
attention is given to the processes of absorption. The quinine should be 
given in powder in soft capsules easily dissolved. 

So far as the attack itself is concerned, aside from the use of quinine, the 
physician may modify to some extent the effects of the paroxysm by the use 
of stimulants to support the circulation, and prevent congestion by using 
hot compresses or hot foot-baths. If the alimentary canal is overloaded 
with food or fecal matter, the stomach should be emptied by an emetic 
and the intestine by a purge or a large enema. Alcoholic stimulants, as a 
rule, are not advantageous. If the attack is exceedingly severe, a dose of 



874 DISEASES DUE TO ANIMAL PARASITES 

morphine may be given hypodermically, or deodorized tincture of opium 
may be used. During the fever the patient may be relieved by a tepid 
sponging, but usually antipyretic measures are entirely unnecessary, and 
coal-tar products ought never to be employed. The vomiting, if excessive, 
may be controlled by hourly doses of a grain of oxalate of cerium with 5 
grains of bismuth, and by counterirritation over the epigastrium. There is 
some evidence to prove that methylene blue has a destructive influence upon 
the malarial parasite. It may be given in the dose of 1 to 4 grains in capsules. 

The Symptoms of ^ffistivo -autumnal Infection or Remittent Fever. — From 
the standpoint of severity and danger to the individual attacked, this type 
of malarial infection is by far the most important, although it is not as 
widely distributed, and therefore not as commonly met with as the tertian 
and quartan forms, except in certain localities which are usually tropical 
or semi-tropical. The term " sestivo-autumnal fever," applied to it first by 
the Italian investigators, Marchiafava and Celli, indicates that it occurs 
most commonly in the summer and fall months. 

The symptoms of this type of infection differ markedly from the inter- 
mittent type of the disease in a number of particulars. Thus, it is not char- 
acterized by an intermittence of the fever and of the other signs of illness, but 
instead is typically remittent; that is to say, the fever and associated symp- 
toms diminish in severity at times, but they do not entirely disappear. On 
the contrary, they persist in some cases to such a degree that the amount 
of remission is very slight indeed. 

As the gastrointestinal disturbance due to this infection is very prone 
to be marked, and as the liver is usually much affected, this type of the 
disease is sometimes called "bilious remittent fever" or "bilious fever." 
Vomiting, which may be very persistent, and which may be markedly 
bilious, is a common symptom. 

The remissions just spoken of may occur regularly, but in the majority of 
cases they are very irregular, both as to the time of their occurrence and to the 
degree of their individual severity. In some instances the chills and sweats are 
distinct; in others they are so ill-defined as to be scarcely noticeable. Further 
than this, the febrile movement, which is so sudden in onset and which ends 
so sharply by crisis in the intermittent form, is usually gradual in onset and 
equally deliberate in its fall in the remittent type. The temperature falls 
by lysis, not by crisis, in each paroxysm. This lack of sharply defined 
waves of temperature may deprive the physician of one of the most important 
means of recognizing that the illness is really due to the sestivo-autumnal 
parasite, and may mislead him into the diagnosis of typhoid fever, to which 
conclusion he is aided by the heavily coated tongue, the somewhat apathetic 
face, the enlarged spleen, the tympanitic belly, and the state of the bowels, 
which are lax in some instances and constipated in others, just as they are 
in typhoid fever. As many cases of typhoid fever have chills and sweats, 
the confusion is all the more readily made, particularly as a subacute bron- 
chitis can often be discovered on ausculting the chest, just as it can be found 
in typhoid fever. 

The severity of the symptoms varies over a wide range. In some instances 
the patient is only moderately ill; in other cases he is manifestly suffering 



MALARIAL INFECTION 875 

from a severe malady. Delirium may be marked, and the mental stupor may be 
very noticeable. The pulse varies from 90 to 1 10, as it does in typhoid fever. 
There still remains to be discussed that form of aestivo-autumnal infection 
which is so violent in its course that the term ''pernicious malarial fever" 
has been applied to it. Pernicious malarial fever is very rare except in the 
tropics and in a few isolated places not far removed from these areas. It 
manifests itself in two forms : 

(a) The comatose form, in which a patient is seized with symptoms 
resembling intense cerebral congestion or apoplexy, or develops acute 
delirium followed by semi-consciousness or coma. The fever is usually very 
high and the skin intensely hot. The patient may die in twenty-four hours 
without regaining consciousness, but if he survive so long a remission in 
the symptoms sometimes appears and recovery takes place; or, instead, a 
second paroxysm comes on in which death is likely to occur. These 
cerebral symptoms are due in part to the profound systemic disturbance 
caused by the infection, but chiefly to the formation of thrombosis of the 
cerebral vessels by a host of the parasites. 

(b) The algid or cold form, in which the febrile movement is absent or 
very mild, and in its place signs of collapse and exhaustion appear, with 
great coldness of the surface of the body and a complaint of feeling cold on 
the part of the patient. With these symptoms of profound depression 
gastrointestinal disturbances, which are choleraic in type, may develop. 
There may be violent vomiting and active serous diarrhoea, the patient being 
at death's door by reason of the exhaustion. Here again the centralization of 
the symptoms about the intestines is due apparently to the accumulation of 
vast numbers of the parasites in the capillaries of the intestinal mucosa. 

Complications and Sequelae of .aSstivo-autumnal Infection. — The most serious 
complication of infection by the aestivo-autumnal parasite is the develop- 
ment of bloody urine, which is of two forms, namely, a true hematuria with 
free blood cells in the urine, and a true hemoglobinuria in which only the 
coloring matter of the blood is present. The former is obviously the result 
of a solution of continuity in the renal vessels, and the latter is equally 
obviously due to a destruction of a large number of red cells in the blood 
itself. This "black- water fever," as it is sometimes called, is practically 
unknown except where the aestivo-autumnal parasite is found. It occurs 
chiefly in certain of the Southern United States and in Africa and in Greece. 

The symptoms associated with the development of the bloody urine are 
those which are often manifested by ordinary cases of severe remittent 
malarial fever. If the blood is examined before the urine becomes bloody, 
a large number of aestivo-autumnal parasites are usually found. On the 
other hand, after the bloody urine has appeared, it is commonly stated that 
an examination of the blood does not reveal the malarial organism. 

The statement that quinine is capable of producing malarial haematuria is 
indorsed by so many practitioners of experience that it cannot be ignored, 
but we cannot help feeling that coincidence has been a large factor in the 
development of this view. 

As sequelae of malarial fever very marked anaemia, with chronic enlarge- 
ment of the spleen, sometimes called " ague cake," develops; the patient is 



876 DISEASES DUE TO ANIMAL PARASITES 

exceedingly pallid, the abdomen may be distinctly enlarged because of the 
swelling and congestion of the liver and spleen, and there may be some 
swelling about the ankles. There is dyspnoea on exertion. Hemorrhages 
in the retina may occur. Fever is usually not marked, unless there be 
attacks of malarial infection superimposed upon the chronic state. 

It is quite remarkable that in young children, who suffer from severe mala- 
rial anaemia and cachexia with associated enlargement of the spleen, recovery 
will take place under the administration of suitable tonic doses of arsenic, 
the avoidance of fresh malarial infection, and resort to a bracing climate. 
Even the spleen, which seems so hard and enlarged that any diminution in 
its size may appear impossible, undergoes an extraordinary degree of shrink- 
age, so that in adult life any evidences of it having been chronically enlarged 
may have disappeared. Similar improvement sometimes takes place in 
adults, but slight enlargement of the spleen is often a persistent evidence 
of earlier malarial infection, even after the disease has been apparently 
absent for years. 

Among the rarer complications of malaria may be mentioned neuritis, 
pleurisy, ascites, intestinal hemorrhage, splenic abscess, and inflammation 
of the lymphatic glands. Cases of orchitis have been reported by French 
military surgeons, and a rapidly developing and very painful form has been 
observed in Sumatra, by Martin, who describes it as a fulminating inflam- 
mation of the testicles. 

Choux has collected 147 cases of rupture of the spleen due to malaria. 
He recognizes two forms: one which occurs in persons who have not 
suffered very long from malaria, and whose spleens are not greatly enlarged, 
and one which affects the subjects of chronic malaria whose spleens are 
enlarged and deformed by splenitis. In the latter class rupture is usually 
caused by traumatism. Playfair, during a residence of two and a half 
years in the East Indies, observed twenty deaths from rupture of the 
spleen. 

Hemiplegia, either with or without aphasia, is the most common of local- 
ized cerebral complications. Paraplegia is less common, and monoplegia 
is of still rarer occurrence. Amaurosis, deafness, and perversions of taste and 
smell are occasionally observed. Symptoms of motor irritation, such as 
tremor and choreiform movements, have also been reported as rare complica- 
tions, and a case of posthemiplegic malarial chorea has been described by 
Boinat and Salebert. Paralysis of the lower extremities, due to lesions in the 
cord, occurs, and is often accompanied by loss of control over the rectum 
and bladder. All of these disturbances may be transitory. Occasionally 
some of the paralyses are rapidly fatal. Multiple sclerosis is a relatively fre- 
quent nervous sequela, and tetany and paralysis agitans are among the 
less frequent complications. Peripheral disturbances, such as hyperesthesia 
and ansesthesia ; occur in a few cases, and supraorbital, trigeminal, and 
intercostal neuralgia also complicate a small number of cases. 

Of functional nervous complications and sequelae, hysteria, neurasthenia, 
and insomnia may be mentioned. The various psychoses are of rare occur- 
rence. Pasmanik in an analysis of 5412 cases of malaria found 106 cases 
of mental derangement. None of these patients affected were known to 



MALARIAL INFECTION 877 

have an hereditary predisposition to insanity, and only 4.8 of the number 
were alcoholics. 

Diagnosis of JEstivo-autumnal Fever. — iEstivo-autumnal fever must be 
carefully differentiated from typhoid fever and from the so-called con- 
tinued thermic fever of hot climates. Its differentiation from typhoid 
fever is possible and should always be achieved; yet during the recent 
Spanish-American war the number of cases reported as malarial fever 
which were typhoid fever and the number called typhoid fever which were 
malarial was very large. 

The presence of sestivo-autumnal infection is determined by the fact that 
the patient is, or has been, living in a region in which this disease is prevalent 
or at least may occur. It practically never occurs north of the State of 
Delaware in the United States, or in any of the northern parts of Europe. 
Again, its presence is determined by the discovery of the sestivo-autumnal 
parasite in the blood. This is not an easy test for the tyro, and the blood 
is not easy to obtain from the deeply seated organs in which the parasite 
is found. After the first week of the illness the absence of rose spots and 
the Widal reaction will determine the case not to be one of typhoid fever. 
Finally, good-sized doses of quinine will modify the fever of this type of 
malaria, but will not affect typhoid fever at all. The physician should make 
it a rule that if a case of fever does not yield to quinine in four days it 
is not malaria; provided, however, that by the use of calomel and other 
measures he has been able to put the alimentary canal in such a state that 
the quinine can enter the blood. If this cannot be done, then the drug 
should be given hypodermically. 

Treatment. — The treatment of remittent fever is much more difficult 
than that of the intermittent form. The disease is more dangerous and 
often more rapid in its course. Further than this, the fever is so much more 
prolonged that it is of itself deleterious, and, as the patient does not have 
periods of intermittence in which he can make a partial recovery, strength 
is much more rapidly lost. The sestivo-autumnal parasite seems to be more 
resistant to the influence of quinine than either the tertian or quartan 
parasite, and, finally, it is much more difficult to cause the absorption of 
quinine in most cases of bilious remittent fever, both because vomiting is 
frequently a persistent symptom and also because absorption seems for the 
time being to be put aside. It is evident, therefore, that where vomiting is 
too persistent to permit of the administration of quinine by the stomach, it 
must be given hypodermically. The best way to administer it hypodermic- 
ally is in the form of the hydrochlorate of quinine, which is soluble in ten 
parts of water, and which may be injected in the following manner: Dissolve 
15 grains of hydrochlorate of quinine in 15 minims of alcohol and 2 J drachms 
of distilled water. Just before using, add a drop or two of dilute hydro- 
chloric acid. The difficulty with the administration of quinine by the 
rectum in these cases is that absorption is too slow. But, nevertheless, the 
drug may be given in this manner dissolved in starch-water whenever it is 
advisable to get quinine into the blood by every possible avenue. 

Even when it is impossible to administer quinine by the stomach, it is 
usually advisable to move the bowels freely, and this may be accomplished 



878 DISEASES DUE TO ANIMAL PARASITES 

by the use of a Seidlitz powder given in divided doses, or by the employment 
of citrate of magnesium. 

If the vomiting becomes so excessive as to be a dangerous symptom in 
itself, it may be controlled by hypodermic doses of morphine, or by 5 to 20 
minims of spirit of chloroform given with the same amount of compound 
spirit of lavender or of cherry-laurel water. Counterirritation may also be 
applied over the epigastrium in the shape of a mustard plaster. Some cases 
are also benefited by the application of hot compresses over the liver. The 
value of large doses of calomel, amounting to 20 or even 30 or 40 grains, for 
their effect in overcoming hepatic torpor cannot be denied. All practi- 
tioners of experience in intensely malarial districts are agreed as to this point. 

Should hematuria or hsemoglobinuria complicate a case, a careful con- 
sideration of the stage of the disease is essential. The value or harmfulness 
of quinine in malarial hsematuria is still a " bone of contention " with many 
practitioners, some claiming that the quinine is capable of actually producing 
bloody urine, and others asserting equally positively that it is always needed. 
The writer has expressed the view on several occasions that some of these 
cases of bloody urine, complicating malarial fever, may be due to an 
associated parasite upon which quinine has little influence. In a certain 
number of cases it is probably true that the bloody urine is a sequel rather 
than an accompaniment of the development of the parasite in the blood. 
Under these circumstances, as enormous doses of quinine can have little 
influence upon the malarial parasite and also may irritate the kidneys, it 
is conceivable that the use of this drug at such a time is distinctly contra- 
indicated; whereas, if an examination of the blood reveals the presence of 
the sestivo-autumnal parasite, then the quinine must be given, since the 
danger of producing hsematuria by its administration is more than counter- 
balanced by the desirability of destroying the cause of the illness. In other 
words, to give quinine in some cases of malarial hsematuria, when the 
specific parasite is not present, is like locking the door after the horse is 
stolen; while in others its administration is timely and appropriate. 

Many physicians of large experience strongly urge the use of hyposulphite 
of sodium in doses of from 15 to 60 grains every four hours for this com- 
plication. 

Latent Malarial Infection. — Latent malarial infection is probably 
much more common than physicians believe, although the laity have an 
exaggerated view of its occurrence. Craig has reported the results of exam- 
ining the blood of 47 men in one company of the United States Army, all 
of whom had been exposed to malarial infection in the Philippines, but all of 
whom were at least well enough to be on duty. Twenty-seven of them had 
the parasite in their blood, and 25 were infected by the aestivo-autumnal 
parasite. This persistence of infection not only possesses ordinary interest, 
but shows that by the distribution of returning troops to various parts of 
the country this parasite may be disseminated in areas hitherto uninfected. 
Further, as Craig points out, the development of a masked malarial infection 
may greatly mislead the surgeon, both before and after an operation. 



TRYPANOSOMIASIS 879 



PSOROSPERMOSIS. 

This term is applied to an exceedingly rare condition in which psorosperms 
become parasites, growing in cells and producing nodules. These nodules 
may be large enough to be felt through the abdominal wall. The patient 
presents symptoms which are like typhoid fever in character. There is 
diarrhoea, stupor, some fever, hepatic and splenic tenderness, and feeble 
circulation. Autopsy in such cases has shown the presence of masses closely 
resembling tubercles, which are scattered over the liver, the spleen, the 
peritoneum, and in the kidneys. 

Another form of infection by sporozoa has been described as occurring 
in the skin, but Stelwagon states that the condition called psorospermiasis 
by Darier is now known not to be due to this cause. On the other hand, 
Rixford and Gilchrist, in Baltimore, have recorded two cases in which 
tuberculosis of the skin was thought to be present for eight years. During 
this time the lymphatic glands were enlarged, other parts of the body became 
affected, and finally death ensued. Numerous nodules, looking like those 
of tuberculosis, were found scattered very widely through the body, and 
these were found to contain large numbers of sporozoa. 



TRYPANOSOMIASIS. 

Definition. — Two diseases, or rather two phases of one disease, are recog- 
nized in man as due to infection by trypanosomata. These are, first, an 
ill-defined fever resulting from invasion of the circulation by the Trypa- 
nosoma gambiense, and second, African lethargy, or sleeping sickness, due 
to the presence of the same parasite in the cerebrospinal fluid. 

The trypanosomata are flagellated protozoa, and were first discovered 
by Gruby in 1843 in frogs, and by Doflein in 1845 in rats and hamsters. 
Since that time they have been found in practically all vertebrates. These 
organisms were first supposed to be spirilli before their animal nature was 
understood. In the large majority of instances they are not pathogenic. 
As far as our present knowledge goes, the varieties represent distinct types, 
confined to the particular animal which they infect. At least six trypanoso- 
mata that are pathogenic occur in mammals. Thus, the Trypanosoma Evansi 
and the Trypanosoma Brucei are the causes of very fatal diseases, known as 
surra and nagana among horses, mules, camels, buffaloes, and wild animals. 
Trypanosoma equiperdum is the cause of an exceedingly fatal disease of 
horses in Algiers and the Mediterranean coast. Trypanosoma equinum is 
also the cause of a fatal disease of horses in South America. Trypanosoma 
Theileri, the largest of the known trypanosomata, is the cause of a serious 
cattle disease in South Africa. The most widely distributed is Trypanosoma 
Lewisi, the parasite infecting rats. This particular variety is very common 
in the rats of the United States, and has been found in practically every city 
where search has been made for it. Finally, we have the trypanosoma 
which infects man. 



880 DISEASES DUE TO ANIMAL PARASITES 

A trypanosoma consists of a leech-shaped, granular body from 13// to 
25// long and from 2// to 4/z wide. This body contains a nucleus and a 
rod-shaped centre known as the centrosome, or micronucleus. Along one 
edge of the parasite, beginning at the centrosome, is a delicate, fringe-like 
membrane known as the undulating membrane, upon the outer edge of 
which is a single flagellum extending from 7// to 15// beyond the anterior 
end of the parasite. In freshly drawn peripheral blood these parasites are 
seen to be in most active motion, progression being in the direction of the 
flagellum. In hanging-drop preparation they live several days, and as long 
as fifty days if the slide be kept cold and moist. McNeal and Novy have 
succeeded in cultivating Trypanosoma Lewisi and Trypanosoma Brucei 
on a culture medium of agar and defibrinated rabbits' blood. This is 
the first instance in which animal parasites have been obtained in pure 
culture. 

With respect to transmission of infection by trypanosomata numerous 
carriers have been found. Experimentally, animals may be infected by 
intraperitoneal and subcutaneous injection of the parasites, or by inges- 
tion of the parasites into the stomach. Infection may be carried by 
food and water, by the bite of fleas, lice, mosquitoes, ticks, and several 
varieties of flies. The infection of Trypanosoma equiperdum is conveyed 
during coitus. 

The prevailing evidence is that human trypanosomiasis is disseminated 
or conveyed and inoculated by suctorial flies. The view that one fly only 
can act as host for a particular trypanosome is generally held, but is by 
no means established. The known transmitters of trypanosomiasis, of 
which our knowledge appears accurate, are the Glossina palpalis for those 
of trypanosoma fever and sleeping sickness, and the Glossina morsitans for 
surra. Of other means of natural dissemination we know nothing. 

Human Trypanosomiasis (Trypanosoma Fever). — The first reported 
case of trypanosoma in man was made by Nepveu, and his paper contains a 
fair drawing of the parasite. Forde, in 1901, described the parasite in the 
case of a European from the Gambia River Colony suffering from an atypical 
fever. Since that time Manson, Dutton, Todd, and others have reported 
cases, nearly all of them from the Congo and Gambia River district. Man- 
son's case occurred in a woman aged forty years. The temperature ranged 
from 97° in the morning to 100° in the evening. The pulse was always 
rapid and feeble. Erythema was a constant feature in the case, and was 
first observed when the fever began. (Edema was also present, and was 
most pronounced on the back and face. There was marked enlargement 
of the spleen. Duthen reports a case of a European working along the 
Gambia River who suffered from an irregularly remittent fever. The 
trypanosomata were especially plentiful during the pyrexia. The symp- 
toms included extraordinary weakness, wdema of eyelids, enlarged and tender 
spleen, and rapid pulse. Malarial organisms were never found. This 
patient recovered under the use of arsenic. 

The clinical phenomena in the reported cases are chiefly these : In some 
cases the parasites occur in the blood without the patient manifesting any 
conspicuous symptoms. In other cases there is an irregular fever which may 



TR YPA NOSOMIA SIS 881 

be high, continuous, or remittent in type. It does not yield to quinine. 
After persisting from three days to two or three weeks, it is followed by an 
apyretic interval. During the course of the fever large erythematous patches 
occur all over the body, associated with irregularly distributed areas of 
cutaneous oedema. The oedema and erythema may or may not coincide. 
The oedema is most marked on the face, especially on the lower eyelids. The 
pulse is rapid and running, a peculiarity also observed in sleeping sickness. 
The lymph nodes enlarge and their expressed or extracted juice usually con- 
tains the parasite. 

In many cases the history of an inflamed and painful insect bite can be 
obtained. 

The parasites are found free in the peripheral blood and never in the 
corpuscles. They are not numerous, varying from one to twenty in a 
cover preparation. They may be absent for days at a time. In the case 
reported by Manson experimental inoculation on animals was negative, 
showing the distinct nature of the parasite. It now appears quite clear 
that infection results from the bite of a tsetse fly (Glossina palpalis) which 
is the carrier of the parasite. In Button's case there was the history of 
the patient being bitten by a rat. 

The blood condition is interesting. There is a moderate degree of anae- 
mia in all cases and a marked increase in the large mononuclear leuko- 
cytes, running as high as 22 per cent. The increase in these cells seems 
rather constantly associated with sporozoal infection, just as metazoal 
parasitism is accompanied by eosinophilia. 

Treatment. — Some of the reported cases have recovered on large doses of 
arsenic administered in the form of sodium cacodylate or arsenate of iron 
given hypodermically. Methylene blue and quinine in large doses have 
also been tried, but are not of any particular value. The patient should be 
kept in bed in a warm room, and should be fed on simple and nourishing 
food. Treatment of the fever is symptomatic. The most important pre- 
ventive measure is to keep the individual where be cannot be bitten by flies, 
and, if ill, where he cannot act as a centre of infection. 

African Lethargy (Sleeping Sickness) . — Sleeping sickness is a chronic 
disease characterized by increasing lethargy, and, after an exceedingly 
chronic course, death occurs from coma or from inanition — "a negro sleeping 
himself to death. " 

Sleeping sickness is at present confined to tropical Africa, principally 
along the west coast. The northern limit of its extension is the Senegal 
River; the southern limit is the Portuguese Colony. It is common in Sene- 
gambia, along the Gold Coast, and at Old Calabar. It has existed for a long 
time in the basin of the Congo River from Stanley Falls, in the heart of 
equatorial Africa, to the lower Congo. It has recently extended from Vic- 
toria Nyanza to the head-waters of the Nile. In the last two years the dis- 
ease has assumed epidemic proportions in Uganda and many thousands of 
the natives have perished. In the days of the slave traffic sleeping sickness 
was frequently carried to the West Indies, Southern United States, Brazil, 
and the Bahamas, but it never succeeded in establishing a foothold in any 
of these places. 
56 



882 DISEASES DUE TO ANIMAL PARASITES 

Etiology. — For a long time the Filaria perstans was supposed to be asso- 
ciated with sleeping sickness, principally on account of their coincidence 
in the infected areas. Later studies have shown that filaria has no connec- 
tion with sleeping sickness, and that many areas infected by sleeping sickness 
do not show infection by the Filaria perstans. 

The older views that sleeping sickness is due to poisoning, intoxication, 
and filaria have been superseded by the demonstration of a trypanosoma in 
the cerebrospinal fluid by Castellani, and the confirmation of this obser- 
vation by Bruce and other members of the English Sleeping Sickness 
Commission, who have successfully propagated the disease in monkeys. 
The trypanosoma of sleeping sickness is indistinguishable from that of 
trypanosoma fever, and, like the latter, is also found in the blood. Apparently 
the advent of sleeping sickness in a patient having trypanosoma fever is 
determined by colonization of the parasites in the cerebrospinal fluid. The 
exact relation of the hypnococcus, described by Castellani and other mem- 
bers of the Spanish Commission, as the cause of the disease is not as yet 
perfectly clear; apparently it is only a terminal infection. 

Sleeping sickness attacks persons of all ages. In the endemic area 
negroes are the most susceptible, mulattoes less so, and Moors contract 
the disease still less frequently. I know of but one authenticated case of 
sleeping sickness in a white man on record. The tsetse-fly (Glossina palpalis) 
is the intermediate host. It has been shown experimentally that this fly, after 
feeding on a case of sleeping sickness, is capable of conveying the dieases 
to healthy monkeys, and that flies from the endemic area were found to be 
infected even without such feeding. It is possible that the disease may 
exceptionally be conveyed in other ways. The negroes believe that con- 
tagion is carried by water and also by the saliva of the sick. 

Pathology. — Mott has shown that the lesion of sleeping sickness is an 
extensive meningoencephalomyelitis. In the cord and brain extensive 
round-cell infiltration is found about the capillary vessels. The cerebro- 
spinal fluid is deeper in color than normal owing to the presence of numbers 
of red blood cells. Besides these, numerous leukocytes and the specific 
trypanosoma are found. In the latter stages of the disease there is some 
ground for believing that there is a concomitant — in a terminal sense — 
streptococcus (hypnococcus) infection. 

Symptoms. — The incubation period is variable, but always long. The 
natives believe that the disease may develop as long as seven years after 
exposure. As a matter of fact numerous instances are on record where the 
disease has appeared in negroes several years after leaving the endemic area 
settling in other countries. It would appear, from the meagre knowledge and 
of the parasite now available, that it may be found in the peripheral blood 
without producing any symptoms. The causes that determine colonization 
of the parasites in the cerebrospinal system are unknown. 

The disease sometimes begins with marked psychical prodromata, includ- 
ing epileptiform seizures, melancholia, and even transitory mania. In the 
larger number of cases there is headache, vertigo, puffiness of the face, and 
slight fever. At this point the lethargy begins. The patient at first is somno- 
lent or stupid, but he can easily be roused for nourishment or to attend 



KALA-AZAR 883 

to the calls of nature. When so awakened his gait is staggering and the 
moment he is released he sinks into a deep sleep. In the early stages 
there are no evidences of paralysis, tremor, or convulsion. The patellar 
reflexes are decreased, sometimes abolished. Gradually the lethargy deepens 
until finally the patient can only be aroused with the greatest difficulty, if 
at all, and immediately falls again into a deep sleep. Partly from the disease 
itself, but largely because the lethargy prevents regular nourishment, nutri- 
tion fails, emaciation becomes progressively more marked, and bed-sores 
develop. Toward the close paralyses of various muscle groups develop, 
convulsions occur, and fatal coma supervenes. 

Diagnosis. — The symptoms are fairly characteristic, but a positive recog- 
nition of the disease is rendered easy by lumbar puncture, centrifugaliza- 
tion of the cerebrospinal fluid, and demonstration of the parasites by a 
microscopic examination of the sediment. 

Prognosis. — The course of the disease is chronic. Cases may last from 
three to four years. The prognosis is bad. There is no record of the 
recovery of an authentic case of African lethargy. 

Treatment. — With regard to treatment it has been found that purging 
in the early stages does good and in some cases temporarily arrests or delays 
the disease. Massive doses of arsenic are of some service and should be used 
on account of their supposed value in trypanosoma fever. 



KALA-AZAR. 

Definition. — Kala-azar or Tropical Splenomegaly, sometimes called Dum 
Dum Fever, is a chronic infectious disease, characterized by long-con- 
tinued fever, extreme emaciation, profound ansemia, marked enlargement of 
the liver and spleen, and a characteristic pigmentation of the skin. 

Much uncertainty has existed as to the nature of kala-azar, and our 
present knowledge rests largely upon the investigation of Leishman, who 
showed that it is a form of trypanosomiasis. (See Trypanosomiasis.) 
This investigator, with Marchand, James, Bentley, Rogers and others, has 
found the so-called Leishman bodies in persons suffering from typical 
kala-azar in various parts of the world, as in the Egyptian Soudan, Algiers, 
and in Assam. Airde has also made confirmatory investigations in China. 
These Leishman bodies are minute, spherical, oval forms closely resem- 
bling the chromatin masses seen in stained trypanosomes. They are 
found chiefly in the spleen and liver, and can be obtained during life by 
puncturing the spleen with a fine exploring needle, the fluid contained in 
them being expelled upon a glass slide and stained by the Romanowsky 
method. 

The Leishman bodies or parasites are capable of developing into flag- 
ellated organisms closely resembling trypanosomes, but differing somewhat 
in the position of the flagellum. 

Manson believes that the intermediate host of this parasite is some 
scavenger-fly which derives the parasite from the intestinal or other dis- 
charges of the patient and then infects the human being by a bite. There 



884 DISEASES DUE TO ANIMAL PARASITES 

may be a sexual multiplication in the fly, but in the human host the para- 
site multiplies by fission, and Manson thinks that this multiplication is 
asexual. 

Pathology and Morbid Anatomy. — The autopsy in a case of kala-azar shows 
enormous enlargement of the spleen, which is firm and friable. The liver 
is also greatly enlarged and toughened in texture. The bone-marrow and 
the organs just named are crowded with the parasites. Leishman bodies 
can also be found in the lymphatic glands, the suprarenal capsules, in the 
testicles, and in the inflammatory exudates in the pleura and peritoneum. 
The direct cause of death seems to be an associated dysentery or pneu- 
monia. 

Symptoms. — The symptoms in onset resemble those of malarial fever, 
being characterized by daily chills and fever, followed by free sweating, 
these symptoms recurring about the same time every afternoon. After a 
period of ten days or two weeks these symptoms diminish and a period of 
remission occurs followed after another period of ten days or two weeks by 
a return of the paroxysm. This may last for weeks or months. Occasion- 
allv the remissions already spoken of fail to occur, and profound inanition 
develops after some months. In still other cases the febrile movements are 
exceedingly irregular and varied. Enlargement of the liver and spleen 
begin early. The patient complains of languor, dyspnoea, and the general 
manifestations of profound anaemia. The constant symptoms are fever, 
enlargement of the liver and spleen, the progressive emaciation, and grave 
anaemia, 

Treatment. — No method of treatment has as yet been discovered which 
produces any good results. 



NEMATODES. 

Ascariasis. — Ascaris lumbricoides, or round worms, are found in the small 
intestine of man more commonly than any other parasite. 

They are not segmented as are the cestodes, but occur as smooth worms, 
not unlike an ordinary earth-worm, except that they are provided with 
small papilla? or hairs. The worm also possesses longitudinal striae and 
transverse rings, a mouth, and an anus. They are not hermaphroditic, but 
occur in the form of the male and female worm. 

They are met with far more frequently in children than in adults. The 
female worm is of a light-brown, or red, color, and is usually about 10 to 20 
cm. long and 0.5 cm. thick. The male is about one-half the size of the female. 

How these worms gain access to the body is not known, although it 
may be by ingestion. While they most commonly are found in the small 
intestine, they occasionally find their way from the intestine into the stom- 
ach, and cases are on record in which they have wandered into the oesoph- 
agus and mouth, and even into the nose and bronchial tubes. Cases have 
also been reported in which the migration of a worm into the gall passages 
has produced obstruction, and still other instances are recorded in which 
they have found their way through an ulcer, or through a perforation in the 



NEMATODES 885 

appendix vermiformis, into the peritoneal cavity. As a rule they are present 
in the intestines in numbers and do not occur singly. In rare cases coiled, 
mottled masses of lumbricoids have caused intestinal obstruction. 

A form of round worm, somewhat like that found in man, is found in the 
intestine of cats and dogs, but it is considerably smaller in size and does 
not infest man. 

Symptoms. — The symptoms of the presence of this worm do not differ 
materially from those produced by the tapeworm (which see). Occasionally, 
however, this worm seems to have the power of producing an irritant poison 
which not only causes intestinal irritation, but when absorbed may cause 
great nervous irritation and apparently be responsible for convulsions in 
young children. 

Treatment. — The treatment of a patient suffering from Ascaris lumbri- 
coides is abstinence from food for twelve or eighteen hours and the admin- 
istration of 1 drachm of the fluid extract of spigelia, or 2 drachms of the 
more old-fashioned, but efficacious, fluid extract of spigelia and senna. In 
other cases, 5 to 15 minims of the oil of chenopodium in capsule or emulsion, 
or on sugar, may be administered. In still other cases from 2 to 5 grains 
of santonin may be given in tablets or troches. All of these drugs should 
be followed by castor oil or a saline purge in order to sweep out the worms 
while they are poisoned by the drug. 

Oxyuris Vermicularis. — Under the name Oxyuris vermicularis or thread- 
worm, sometimes called pin-worm, a very small nematode worm exists in 
the rectum of young children and is sometimes found in adults. Occasionally 
it infests the entire colon. The length of the female is about 10 mm., and 
of the male about 4 mm. This worm may be present in great numbers 
without producing any symptoms whatever. Some irritation about the 
anus may be the only disturbance produced by their presence. 

Seat- worms are to be removed by the injection into the bowel of soap and 
water, which, after it is passed, is to be followed by a pint of warm water 
which has been medicated by boiling in it from \ to 1 ounce of quassia chips. 

Trichina Spiralis. — A patient infected by the parasite known as the 
Trichina spiralis is said to suffer from trichiniasis. This parasite was first 
described by Owen in 1835. It was found in the flesh of the hog by Leidy 
in 1847, and in a human being by Zenker in 1860, the patient, a young girl, 
being thought to be a sufferer from enteric fever until at autopsy the 
parasites were found free in the bowel and encapsulated in the mus- 
cles. 

Etiology. — In practically every case the infection of a human being comes 
from eating the flesh of an infected hog. It is scarcely necessary to state 
that infection does not occur if the pork has been well cooked. 

The frequency with which the disease occurs is not known, but it is not 
as rare as some have thought. Williams found it present 27 times in 505 
unselected autopsies in Buffalo, New York. 

If the muscle of a man infected by this parasite is examined, tiny little 
white or gray dots will be found upon its surface and through its texture; 
later the parasites encapsulate and look like deposits of calcareous material 
of about the size of miliary tubercles. If such a calcareous deposit be 



886 DISEASES DUE TO ANIMAL PARASITES 

opened it may be found to contain the embryo of the parasite, or if the 
worm be dead a granular detritus only is present. 

When uncooked meat containing this parasite is swallowed, the digestive 
juices dissolve the capsule of the parasite, and in this way the embryos 
are set free in the stomach. Here they rapidly develop and become sexually 
mature in about seven days. The female parasite gives off an immense 
number of embryos, so that it is estimated that one parasite may throw 
off from one to two thousand young. These parasites soon find their 
way through the wall of the intestine, enter the lymph spaces, and so reach 
the circulation, by which they pass to the muscles. Their favorite position 
for settlement is the striated muscles. They enter the muscular connective 
tissue and then the sarcolemma, where they coil themselves and cause a 
disintegration of the contractile substance. Here they become encapsu- 
lated in about six weeks, partly by the inflammatory exudate which is 
produced by their presence, and partly by the calcareous material which 
they seem to have the power of collecting. In these capsules the para- 
site remains alive for a very long period of time, possibly for twenty-five 
years. Occasionally, however, it dies, and the entire mass undergoes 
calcification. 

When one of the domestic animals swallows meat infected in this way, 
the same process takes place in the muscles as occurs in the muscles of 
man. In the muscles of the hog the parasite may escape notice, as it 
often lacks the calcified capsule. Moreover, an infected hog may be in 
excellent health. 

Pathology and Morbid Anatomy. — The lesions of trichiniasis consist in 
gastrointestinal irritation, overgrowth of the lymph nodes in the abdominal 
cavity, occasionally bronchopneumonia with great swelling of the bronchial 
glands, still more rarely fatty degeneration of the liver, and constantly a 
parasitic myositis due to the embryos invading the muscles. Almost every 
muscle of the body may be found infected ; but where the number of 
trichinae is not very great, the muscles of the neck, the intercostal muscles, 
and the diaphragm seem to be the parts in which the greatest aggregations 
occur. Furthermore, the greatest number of trichinae are usually found 
near the insertions of the muscles. 

Symptoms. — The symptoms consist in muscular soreness and pain, and 
disinclination to move. A diagnosis of muscular rheumatism is often made 
because of these symptoms. Headache, pufpness of the skin about the eyes 
and nose, and moderate fever are also present. Not rarely the symptoms 
may closely resemble those of typhoid fever, with great prostration and 
emaciation. For some unknown reason a marked leukocytosis develops, 
which is peculiar in the fact that the eosinophile corpuscles are chiefly 
increased. From investigations made by Opie it would appear probable 
that this eosinophilia is of some value from both a diagnostic and prognostic 
standpoint. The eosinophiles are not greatly increased, if the infection by 
trichinae is excessive, and their greatest development seems to occur at about 
the time that the embryonal trichinae are passing from the intestine by way 
of the lymphatics and blood to the muscular tissues — that is, during the 
third week after the ingestion of the trichinatous meat. 



NEMATODES 887 

Diagnosis. — In a suspected case the diagnosis may be reached by taking 
a small piece of muscle and examining it with a microscope. The stools 
of the patient should be flattened to a thin layer between two sheets of 
glass resting upon a black background, and then examined by means of a 
hand magnifying glass, when the parasite may be found as small, short, 
glistening, thread-like bodies. 

Prognosis. — The prognosis depends largely upon the severity of the infec- 
tion. In the worst outbreaks the mortality may be as high as 70 per cent. 
Many cases recover by the end of a fortnight. Others remain ill for weeks 
or months before recovery takes place. 

Treatment. — There is no treatment which can be directed to the removal 
of the parasite after it has entered the muscles. The only thing the physician 
can do is to give a nutritious diet, and relieve pain or other symptoms by 
symptomatic remedies. If the discovery is made that the patient has 
swallowed trichinatous pork within a few hours, then 5 grains of thymol 
followed by a dose of castor oil or sulphate of magnesium should be ordered 
to kill the parasite and sweep it out of the intestines before it can migrate 
into the tissues. 

Uncinariasis (Ankylostomiasis). Definition.— Uncinariasis is an infec- 
tion by different varieties of worm of the uncinaria species; it occurs not 
only in man, but in many of the lower animals. The parasite is often 
called the Ankylostomum duodenale, or hook-worm. The chief symptoms 
are severe anaemia, abdominal pains, asthenia without emaciation, and 
oedema. The parasite was described as uncinaria by Froelich in 1789; 
Dubini in 1843 gave it the name ankylostoma. 

The condition is also known as " brickmakers' anaemia," " Egyptian 
chlorosis," " miners' anaemia," " miners' cachexia," " miners' disease," 
" Porto Rican anaemia," " St. Gothard's tunnel disease," " tunnel dis- 
ease," "tunnel anaemia," "tropical chlorosis," and "hook-worm disease," 
besides a host of local names. It is one of the most ancient diseases 
known to man, for it was described by the Egyptians 3500 years ago. 

Frequency. — Uncinariasis occurs in all the tropical and practically all 
the subtropical world. According to Thornton it is the greatest enemy of 
the human race in the tropics; greater even than plague or cholera. In 
portions of India 75 per cent, of the population are said to be affected. 
In Egypt this worm is found at nearly every postmortem. It has been 
the most disabling of all diseases in the Egyptian army, as well as the 
greatest cause for the rejection of recruits. In Ceylon its ravages are 
said to be more serious than those of cholera. Harris has found it in 
Georgia and Florida, and believes it is the common cause of the severe 
anaemias of the Southern United States that have hitherto been re- 
garded as malarial. Stiles has also made very valuable studies of its 
characters and recurrence in the Southern United States. In Assam 
it is almost universal, 299 cases having been found in 300 postmortems. 
According to Alden, 22.5 per cent, of the total death rate of Porto Rico 
is ascribed to tropical anaemia due to uncinaria. In more temperate re- 
gions it has been found in nearly all our States as far north as New York. 
In the Cornwall and Westphalian mines the disability caused by this para- 



888 



DISEASES DUE TO ANIMAL PARASITES 



Fig. 112 





Male of Ankylostoma duodenale : a, head ; b, oesophagus ; c, 
gut; d, anal glands ; e, cervical glands ;/, skin ; g, muscular layer; 
h, excretory pore ; i, tri-lohed bursa ; k, ribs of bursa ; I, seminal 
duct ; m, vesicula seminalis ; n, ductus ejaculatorius ; o. its groove ; 
p, penis; q, penile sheath. Magnification, 20. (After Schulthess, 
from Ziegler.) 



site has become so great as to threaten the 
existence of these industries. 

Etiology. — The uncinaria is a nematode 
worm of the family Strongylidce. It is very 
widely distributed in the animal world, in 
distinct species. In man two species are 
recognized, viz., Uncinaria duodenale (Dubini) 
and Uncinaria Americana (Stiles), commonly 
spoken of as the old-world and the new- 
world uncinaria, or hook-worm. The two 
sexes are distinct; the male worm is from 8 
to 10 mm. long and the female slightly 
longer, 10 to 18 mm. They are grayish-white 
in color, cylindrical in shape, with a con- 
tracted head, and in the female a broad 
caudal bursa. When male and female worms 
are present, as they usually are in the propor- 
tion of one male to three females, the female 
produces an enormous number of ova. When 
deposited in favorable surroundings these ova 
develop into embryos in twenty-four hours. 
The embryo grows rapidly, passing through 
two ecdyses in about five days. The second 
ecdysis is the termination of the extra-cor- 
poreal phase, and the embryo is now infec- 
tive for man. When taken into its appropriate 
host the worm goes through three more ecdyses, 
making five in all; the fourth marking the 
formation of a provisional buccal armature; 
the fifth, the appearance of the definite arma- 
ture. It then reaches an adult or mature 
form in from five to six weeks. 

The sources of infection are the ingestion 
of infected water or food, the accidental inges- 
tion of infected earth from soiled hands, 
and infection through the skin during or after 
the second ecdysis of the 
worm. The mode of in- 
fection by earth is obvi- 
ous. In all regions af- 
fected by uncinaria, dirt 
and clay eating are very 
common habits. There 
is no doubt that geophagy 
in infected areas is a 
common manner of tak- 
ing the disease; but it is 
also true that this habit 
does not show itself, in 



NEMATODES 



889 



many cases, until the disease is fully developed. In these cases it seems 
clear that the earthy matter is eaten in obedience to an instinctive craving, 
and that it brings relief by mechanically loosening a number of the para- 
sites. That infection may take place through the skin, the experiments of 
Looss and many clinical observations, as well as accidental laboratory infec- 
tions, have made quite apparent. It has often been observed that children, 
walking barefooted through infected ground, became infected. The disease 
known as Pani-Ghao, and the "ground itch" of the South, are probably skin 
infections by this parasite, the lesions representing the point of entrance of 
the parasite into the human host. Looss experimented with the young 
worms in a mixture of earth and charcoal. This mixture was placed on the 
skin of dogs without scarification or friction. The parasites were found in 
the intestines as rapidly as when experimental infection by the mouth was 



Fig. 113 




Ova and embryo of Uncinaria Americana : a, unicellular ovum ; 6, c, d, e, ova showing various stages 
of segmentation ; /, g, ova containing larval uncinarise ; h, peculiarly shaped ovum ; i, larval worm 
just emerged from shell ; j, larva extended after emergence. (Stiles.) 



made. While making these experiments he accidentally allowed some of 
the mixture to remain on his own hand and himself became infected. 
Air-borne infection occurs very rarely, if ever. 

Prophylaxis. — Prophylaxis of uncinariasis demands the exclusion of all 
infected persons from earth-workings. Where large bands of laborers are 
collected in districts in which the disease is prevalent, in mines, in tunnels, 
and in excavations of all kinds, systematic examination of all cases of anaemia 
should be made. Defecation in the workings or tunnels should be rigorously 
prohibited. Water-tight latrines should be provided, and the contents 
rendered harmless by a cheap disinfectant. In the Arlberg tunnels the 
pail system has been recently used with good effect. Personal prophylaxis 
should include careful washing of the hands before eating, and the wearing 
of sound shoes when working in suspected soils. 



890 DISEASES DUE TO ANIMAL PARASITES 

Pathology and Morbid Anatomy. — Postmortem the subcutaneous fat, the 
panniculus adiposus, and the mesenteric fat are fairly well preserved. The 
parasites are found in the jejunum, still attached to the bowel wall if the 
section is early, or free in the intestinal contents if the section is delayed. 
They vary in number from 100 to 600 or more. The jejunum is covered 
with old and recent pinhead bloody extravasations. The bowel is thickened 
in spots, and there may be small cavities in the bowel wall rilled with blood 
and containing the heads of one or two parasites. The liver and kidneys 
commonly show some degree of fatty degeneration. The cause of the anaemia 
is probably twofold — the mechanical abstraction of a considerable amount of 
blood by the parasites, and a haemolytic effect from a toxin elaborated 
by the worm. That haemolysis occurs is indicated by increased iron in the 
liver, the occurrence of heematoidin in the liver and kidneys, as well as free 
iron in the stools. 

The blood shows the ordinary changes similar to those observed in 
pernicious anaemia. In early cases the color-index may be low, the loss of 
haemoglobin being more rapid at first than the red-cell loss. As the case 
advances, however, the haemoglobin index rises and may be plus. Megalo- 
blasts are not seen in as large numbers as in other pernicious anaemias. 
There is no marked leukocytosis; there is, however, a fairly constant rela- 
tive increase in the eosinophils, ranging from 3 to 30 per cent. 

The feces contain the ova. They also contain considerable blood, in 
which differential staining will demonstrate a great many eosinophiles, 
showing that there is not only a general increase in these cells in the circu- 
lation, but that there is an active determination of them to the intestinal 
lesions. Charcot-Leyden crystals are constantly present. 

Symptoms. — The symptoms vary with the number of parasites in the 
intestines and with the general condition of the patient. Recent obser- 
vations seem to make it clear that the new-world hook-worm is not nearly 
so fatal as the old-world hook-worm. If there be but a few worms, the 
general symptoms produced are very mild. If, on the other hand, the 
worms run up into the hundreds, or thousands, the blood destruction is 
extensive. In conditions of great deterioration, in the half-starved or ill- 
nourished, in acute or chronic dysentery the presence of only a few of 
these parasites may act as a very dangerous complication. 

In well-developed cases the symptoms are those of pernicious anosmia. 
The principal phenomena are dyspeptic symptoms with colicky pains in the 
early stages, followed by progressive anazmia with little or no emaciation, 
and with terminal oedema. The pain in uncinariasis is colicky in character, 
is one of the earliest symptoms, and is fairly constant throughout the disease. 
In cases in which only a few parasites are present, it may amount only to 
uneasiness; when there are many, it may be severe. Like all abdominal 
pains due to intestinal parasites it is relieved by food for the time being. 
The appetite is very variable ; it may be voracious or it may be diminished, 
and curious perversions of taste, such as earth-eating, may develop. 

Following the development of the colic, anamia appears and rapidly 
becomes profound. There is very little wasting, the subcutaneous fat being 
fairly well preserved. The skin is a lemon-white color; the conjunctivae and 



NEMATODES 891 

lips are exsanguinated; the sclera? pearly or muddy-white. All the subjec- 
tive phenomena of profound anaemia become marked. There is lassitude, 
breaihlessness on the slightest exertion, vertigo, and occasionally dimness 
of vision from retinal hemorrhages. Crises of fever occur that may last 
for days or weeks. Auscultation over the precordial area reveals soft 
hcomic bruits, propagated to a remarkable distance into the great vessels. 
The face and ankles become puffy, and there may be a slight general oedema. 
Harris has reported a case of uncinariasis with symptoms resembling 
pellagra. When the disease attacks children before the age of puberty, 
bodily and mental growth are stunted. The pubic hair, the axillary hair, and 
the hair on the face is scanty or absent, the limbs are thin and undeveloped, 
and the children are markedly pot-bellied. Stiles describes a fish-like, 
staring expression of the eyes in these cases. 

Diagnosis. — The diagnosis is easy, once the attention is directed to the 
intestinal parasites. The occupation of the patient, if it be one that predi- 
cates working in earth, is very suggestive. The anaemia is very commonly 
diagnosticated as malarial. There really is no diagnostic difficulty between 
malarial anaemia and the parasitic anaemia. This very common error has 
been made because, in the intensely malarial regions, the existence of this 
parasite has not been generally known. The disease has also been mistaken 
for beriberi, but there is a complete absence of paralytic symptoms in 
uncinariasis. 

A diagnostic sign, recently described, is the occurrence of triangular black 
or bluish patches on the dorsum of the tongue, looking as though a pen 
had been wiped on it. This appearance is quite striking. Recent obser- 
vations have shown that it is very constant; that it appears early, even 
before the advent of pronounced anaemia, and persists to the end of the 
disease. 

The diagnosis is definitely made by the demonstration of the ova or 
parasites in the feces. Search should be made in as fresh specimens as 
possible, to avoid confusion in case embryos have occurred and quitted the 
ova. A small amount of the material is placed on a large glass slide diluted 
with distilled water, and pressed down with a thick cover. The ova of 
uncinaria are very striking bodies. They are clear, transparent, light gray 
in color; they have a delicate, transparent capsule, containing in its centre 
from one to six gray yolk segments with granular nuclei. In shape, they 
are regularly oval, with an average length of 60 microns and an average 
width of 35 microns. Leichtenstern has found as many as 4,216,930 ova 
in a single stool. Care must be taken not to mistake the egg of the Ascaris 
lumbricoides for the egg of the uncinaria. The former have a thick, gela- 
tinous, often mammillated covering, and unsegmented protoplasm. So, too, 
the egg of the Oxyuris vermicularis, which is a thin, symmetrical shell, one 
side of which is almost straight and which contains an embryo, may be 
mistaken for the ova of the uncinaria. The egg of the whip-worm, Tricho- 
cephalus dispar, possesses a smooth, thick shell, apparently perforated at 
each end, with unsegmented protoplasm. 

Stiles has recently described a rapid and effective test, where micro- 
scopic evidence cannot be obtained. The stool is placed on ordinary white 



892 DISEASES DUE TO ANIMAL PARASITES 

blotting-paper, and allowed to stand for one hour. A rusty-red discoloration 
or stain develops along the edge of moisture, resembling somewhat that 
due to the presence of blood and the probable presence of uncinaria. Stiles 
directs that if uncinariasis is suspected, and it is not practicable either to 
make a microscopic examination or to delay matters until a specimen can 
be sent away for examination, still another method of diagnosis is possible. 
Give a small dose of thymol, followed by Rochelle salts, and collect all of 
the stools passed. Wash the stools thoroughly several times in a bucket, 
and examine the sediment for worms about half an inch long, about as 
thick as a hairpin or hatpin, and with one end curved back to form a hook. 

Treatment. — In the treatment of uncinariasis there are two drugs of value : 
male fern and thymol. Of the two the most effective is thymol or its deriva- 
tive, thymol urethane (thymol carbonic ether). Thymol should be given 
in capsule, or in emulsion with acacia, in 30 grain doses repeated in two 
hours for an adult. In these doses the drug occasionally causes vertigo, 
excitement, and smoky urine. For one or two days prior to the administra- 
tion of the remedy patients should be put on liquid diet and given a brisk 
saline purge the night before. On account of the high location of the para- 
sites in the intestinal tract, it will not be necessary to restrict the quantity 
of food. In administering thymol, it is essential that none of the solvents 
of the drug be given either with it or immediately after. Several cases of 
poisoning have occurred when alcohol or alcoholic drinks have been given 
with, or closely after, a dose of thymol. Similarly, ether, chloroform, 
glycerin, and most oils act as solvents, and may cause severe toxic symptoms 
owing to the absorption of the drug in bulk. In order to prevent poisoning, 
therefore, thymol should be followed by a saline purge, and castor oil should 
not be used. Weekly examinations of the stools should be made, and as long 
as ova or Charcot-Leyden crystals are found the use of this remedy must be 
repeated. Sometimes thymol is vomited, and in rare cases proves inactive. 
In these the male fern should be administered in the usual way. After the 
expulsion of the worm, the therapeutic indications are the same as for 
advanced anaemia from any other cause. 

Filariasis (Filaria Sanguinis Hominis). Definition and History. — The 
group of Filarice includes a number of species. The human parasite was 
first discovered by Demarquai in 1863 in a chylocele and demonstrated in 
the peripheral circulation by Lewis in 1872. The principal varieties 
affecting man are the following: Filaria nocturna, Filaria diurna, Filaria 
per starts, Filaria Demarquaii, Filaria Ozzardi, Filaria Magalhaesi, and 
Filaria loa. Of this group the Filaria nocturna and the Filaria loa are 
the only ones known to cause definite pathological conditions. 

The geographical distribution of the Filaria nocturna is very extensive. 
It is found in all tropical and in most subtropical countries. Its southerly 
limit of observation is Brisbane. In the United States it has been found in 
Alabama, Louisiana, South Carolina, Pennsylvania, Illinois, and New York. 
In the Samoan Islands from 10 per cent, to 50 per cent, of the inhabitants 
are said to be infected, and in the Friendly Islands 32 per cent. In Porto 
Rico the native troops showed 12 per cent., and small communities may 
have as high as 70 per cent, of the total population infected. 



NEMATODES 893 

Filaria Nocturna. — This parasite has two corporeal and one extra- 
corporeal phase. First, the parent worm, whose normal habitat is the 
lymphatic system; second, the embryo found in the circulating blood, and 
third, the intermediary stage in the body of the mosquito, which has been 
definitely shown to be the intermediary host for this parasite. When 
examined in a drop of peripheral blood the embryonic form is found as a 
minute transparent worm, one-eightieth of an inch in length and about the 
diameter of a red blood corpuscle. It has a transparent sheath, or sac, 
somewhat longer than the body of the embryo, and is usually present in 
very great numbers. 

The most striking characteristic of this filaria is the periodicity of its appear- 
ance. They are found only at night in the peripheral circulation, hence the 
name Filaria nocturna. In the daytime they entirely disappear and retire to 
the larger vessels, particularly the vessels of the lungs. The periodicity may 
be reversed by causing the patient to sleep in the daytime, when, after a 
few days, the embryos are found in the peripheral blood during the day 
and are absent at night. 

The microscopic demonstration of the worm is easy. The blood should 
be drawn near midnight, when the parasites are most numerous. A large 
drop of blood should be taken and a thick, coarse spread made. The slides 
are dried in air without covers, or, if it is desired to study the parasite in 
motion, the blood-drop is covered with a cover-slip and ringed with vaselin. 
In such a preparation the filaria retains its motility for days. The worms 
are quite large; an inch objective will be ample for the search and demon- 
stration. 

As already stated the mosquito is the intermediary host. When a mos- 
quito sucks the blood of a patient containing filarial the parasites escape 
from their sheath while the blood is still in the stomach of the insect. 
Thence they pass to the thoracic muscles. In this location, in from six to 
seven days, the metamorphosis from embryo to the young of the adult form 
takes place. The minute filarial migrate to the proboscis and are found 
lying in pairs in the labia, whence they are undoubtedly carried into the 
circulation of the first warm-blooded animal bitten by the insect. The 
possibility of the filaria? being passed into water when the mosquito lays her 
eggs, and being carried thence into the stomach in drinking water, is also 
to be remembered. Female mosquitoes, both of the culex and anopheles 
species, are capable of acting as the intermediary host. 

The adult form of the parasite, commonly known as the Filaria Bancrofti, 
is a long, delicate, nematode worm. It is from three to four inches in length 
and the thickness of a coarse hair or bristle. The sexes are distinct. The 
habitat of the parent worms is the lymphatic system, commonly the thoracic 
duct, although any portion of the peripheral lymphatics may be invaded. 
There may be only one worm of each sex or there may be many. 

The Filaria diurna presents minor differences in structure and appearance 
from the Filaria nocturna. The chief difference is in the periodicity, this 
parasite being found in the peripheral circulation only in the daytime. It 
is supposed that the Filaria diurna is the embryonic form of the Filaria loa- 
Nothing is known of its pathological significance. 



894 DISEASES DUE TO ANIMAL PARASITES 

The Filaria perstans is common in certain districts of West Africa, where 
it occurs in as much as 50 per cent, of the population. This parasite is 
found in the peripheral circulation at all times, day and night; hence its 
name. The pathological significance of this filaria is unknown. It was 
for a time supposed to be the cause of sleeping sickness, and was also 
found very commonly in association with crawcraw, an itching, pustular 
affection of the skin. 

Pathology and Morbid Anatomy. — Filariasis causes no symptoms in the 
large majority of cases. The embryos are innocuous. When symptoms 
develop they are due to the parent worm or an immature product of the 
parent worm. The lesions produced are divided into two broad classes, 
namely, those which are due to lymphatic varix from stasis, and those due 
to oedema from lymphatic obstruction. The parent worms, when present 
in numbers, may mechanically plug the thoracic duct or one of the larger 
lymphatic trunks. They may also initiate a lymphangitis, with thickening 
and occlusion of the lymphatics. Under either circumstance, stasis and 
retrograde movement of the lymph current are inaugurated and eventually 
a compensatory lymph circulation is established. The result is engorgement 
of some portion of the lymphatic system and the development of a peculiar 
group of phenomena: lymph scrotum, lymphatic groin glands, varices of 
the pelvic or lumbar lymphatic trunks or of the lymphatics of the bladder, 
ureter, or kidney. As these varicosities grow, they become more extensive, 
and rupture. If the rupture be in the genito-urinary tracts, chyluria 
develops; if into the tunica vaginalis, a chylocele; if into the abdominal 
cavity, chylous ascites. These are the lesions due to lymph stasis and 
lymphatic varices. 

In the second group the lymph stasis is associated with lymphangitis 
followed by obstruction, resulting in the formation of the peculiar solid 
cedema and the huge hypertrophies of the affected tissues known as elephan- 
tiasis. 

The majority of cases of elephantiasis are clearly due to filarial disease. 
The geographical distribution of elephantiasis and filariasis are identical; 
elephantiasis is most common in the areas most severely affected by filaria. 
Lymphatic varix and lymph scrotum are not only found in the same districts 
as elephantiasis, but very commonly terminate in elephantiasis. The disease 
is also seen in cases of operative removal of lymphatic varices. In a large 
number of these cases the embryo filarial cannot be demonstrated in the 
peripheral circulation. This is due to the fact that the parent female worm 
lies in the centre of the inflamed tissue and because the embryos cannot 
pass through the. occluded portion of the lymphatic circulation. Manson's 
theory as to the direct causation of elephantiasis is that the parent female 
worm migrates to one of the peripheral trunks. While in this position she 
receives an injury which is followed by premature parturition and the 
expulsion of ova instead of embryos. These ova are five times the diameter 
of the embryos, so that although the embryos pass freely through the finer 
lymphatic radicles the ova block up the smaller lymph channels, forming 
minute emboli. 

Following this stage of embolism, lymphangitis with inflammatory thick- 



NEMATODES 895 

ening occurs. When the inflammatory process subsides the deposit is in 
small part absorbed, but when the inflammation recurs an additional deposit 
is added to the remnant of the first. This concurs with the commonly 
observed clinical history of elephantiasis, which advances by crises of 
inflammation and a general symptom-complex known as elephantoid 
fever. 

As already stated, filariasis may occur without any symptoms being 
present until the lesions just described develop. 

Symptoms. Elephantiasis. — The most common location of elephantiasis 
is in the legs; next in the scrotum of the male and the labia of the female. 
It occurs in the breast, in the arms, and as interstitial or pedunculated 
masses in other parts of the body. These tumors occasionally grow to 
enormous dimensions. A scrotal tumor of 50 pounds is not at all uncommon, 
and one has been reported weighing 224 pounds. These large tumors 
develop as described with elephantoid fever. With each crisis of fever and 
lymphangitis there is not only an increase in the size and bulk already 
affected, but an extension into new territory. 

Elephantoid fever is the systemic expression of the lymphangitis origin- 
ating in filarial varices or in tissues already the seat of elephantiasis. The 
attacks recur at varying intervals of weeks or months. Exciting causes may 
be slight traumatism such as friction of the clothing over the occluded lymph 
channels. The attack begins with rigor and high fever, with all the usual 
manifestations of febrile disturbance, as anorexia, nausea, and, in severe 
cases, delirium. The skin over the inflamed lymphatic area is hot, tense, 
and red, with a marked degree of inflammatory thickening. After persisting 
a few days, the attack ends in a critical sweat. The inflammatory thickening 
remains. The attack may be so intense as to result in the formation of 
abscess. W 7 hen this takes place in superficial lesions, the condition is readily 
recognized and the treatment is obvious. When it occurs in the deeper 
varices, as in the pelvis or loin, there will be deep-seated pain, tenderness, 
and rapidly developing sepsis. 

Hamatochyluria is usually paroxysmal and is due to the leakage of chyle 
into some portion of the genito-urinary tract. The common location of the 
leak is in the lymphatics surrounding the pelvis of the kidneys or the lymph- 
atics of the bladder. The appearance of chyle in the urine is intermittent 
and is not accompanied by any increase of symptoms. The urine is opaque 
and varies in color from a milky-white to a deep red in proportion to the 
amount of blood that may be mixed with the chyle. Chylous urine coagu- 
lates on standing into a soft, jelly-like clot. In a few hours the clot contracts 
and forms a firm, white ball floating in a milky fluid. Microscopically, the 
urine contains fat, blood cells in varying amount, and occasionally embryo 
filaria. Chyluria may persist for many years without great deterioration of 
health. The only symptoms may be a dull pain in the loins or pelvis. Osier 
reports a case of intermittent chyluria which persisted for eighteen years 
without any special discomfort. When chyle escapes in large quantities, 
clots are occasionally formed in the bladder and may cause urinary retention. 
Medical treatment is of no avail in this condition, but the patient should be 
put at rest on dry diet, with as great restriction as possible in the fatty 



896 DISEASES DUE TO ANIMAL PARASITES 

elements of his food. Under this regimen the amount of chyle may be 
notably diminished. 

Varicose groin glands is a varicose condition of the superficial and deep 
inguinal lymphatics, and it is usually bilateral. It gives rise to doughy, 
soft, painless swellings in both groins. They cause little trouble until 
lymphangitis develops, when they may become very painful. They have 
been mistaken for the buboes of plague, and are commonly mistaken for 
hernia. 

Lymph Scrotum. — In this condition the filarial varix is situated in the 
lymphatics of the scrotum and is usually bilateral. It may be associated 
with the enlargement of the groin glands, and, like that state, it is prone to 
accessions of lymphangitis. When the deeper lymphatics are involved, the 
lymphangitis may extend to the testicle, forming what is known as filarial 
orchitis. 

Treatment. — The treatment of these conditions is surgical. When the 
tumors become so large as to be a burden to the patient, or when the inflam- 
matory symptoms cause great pain, their removal should be undertaken. 
The removal of an enormous scrotum or the amputation of a gigantic limb 
may be done to rid the patient of a drag that has, by its sheer weight, anchored 
him to his bed or chair for years. These growths may be removed with 
comparatively little risk. All surgical treatment in filarial disease must 
be regarded as palliative unless the parent female worm is included in the 
excised tissues, when the cure will be a definite one. 

As far as any plan of treatment aimed at the destruction of this parasite, 
adult or embryo, is concerned, there is no remedy of even the slightest 
value. During the attacks of filarial or elephantoid fever the affected part 
should be elevated, cooling lotions should be applied, and the patient freely 
purged. After the acute symptoms subside elastic bandages should be 
tried, and frequently give great relief. 

In countries where filarial diseases are common segregation is impracti- 
cable, but the danger of dissemination would be greatly lessened if patients 
harboring the parasites would so live as to avoid mosquitoes; such pre- 
cautions might be advisable for sporadic cases in countries wherein filariasis 
is only occasionally introduced. 

Guinea-worm Disease (Dracontiasis). Definition. — Guinea worm is 
sometimes called Dracunculus medinensis, or Medina worm. 

Distribution. — This parasite is distributed throughout the tropics. It was 
known in medicine long before the Christian era, and there is some reason 
for believing that the Biblical mention of the serpents affecting the Israelites 
near the Red Sea were these parasites. Though very widely distributed, 
the infection occurs in sharply defined areas. It exists on the west coast of 
Africa, particularly on the Gold Coast, in Abyssinia, Southern Egypt, and 
the Soudan. In Asia it occurs along the Caspian Sea, the Gulf of Persia, 
and in some sections of British India. It was common enough in the West 
Indies and Tropical America during the days of the slave trade, but seems 
to have established a permanent hold only in a few South American Islands 
and in isolated spots in Brazil. In the United States this parasite is encoun- 
tered from time to time in imported cases, although at least three cases have 



NEMATODES 897 

been recorded in persons who had never lived in or visited tropical regions. 
Thus, Van Harlingen reports it as occurring in a case of a man who had 
never lived outside of Philadelphia ; Jarvis, in the case of a man who lived 
at Fortress Monroe, Va., for thirty years; and Walker, in a case from Georgia. 

The Dracunculus medinensis is a nematode worm. We have definite 
knowledge of the female only. The adult female worm is cylindrical in form, 
from 60 to 80 cm. in average length and about 2 mm. in thickness. The 
head of the worm is blunt, with a triangular mouth and eight papillae. The 
tail is tapered and recurvated ventrally. The vascular tube and alimentary 
canal extend as straight canals the length of the worm, ending as blind 
pouches. 

Charles found in the mesentery of a cadaver two female guinea worms 
in conjugation with two smaller worms. These worms were about 4 cm. 
long and attached to the females, which were quite small, about 14 cm. 
from the head end. It is assumed that these were males. In the adult 
female the uterus occupies almost the entire body and is filled with myriads 
of tightly-coiled embryos averaging 0.6 mm. in length. 

Fedschenko and Manson have shown that the intermediate host of the 
guinea worm is a minute water flea (Cyclops quadricornis). The recently 
escaped embryos penetrate the Cyclops, in which they pass through one stage 
of larval development lasting about six weeks. 

It is assumed that infection occurs through swallowing the cyclops itself 
or the larva in drinking water. While this intermediate stage in cyclops 
is the usual history, Plehn has shown, experimentally, in monkeys, that 
direct infection by the embryos may also take place. 

Negroes and the laboring classes are more frequently attacked than others, 
and usually, in each small area, the infected well or spring may be identified. 
The greater number of cases occur at the close of the heavy rains, probably 
because these conditions are then more favorable to the development of cyclops. 

The worm is taken into the body through the stomach. The males and 
females probably pass through the intestine to the mesentery, where conjuga- 
tion takes place. The male dies and becomes calcified or absorbed and the 
female migrates into the connective tissue of the host. In these migrations 
she usually tends toward the lower extremity and appears in the foot or the 
leg, although she may appear in the subcutaneous tissues of the trunk, arm, 
or even the head. When the subcutaneous tissue is reached complete 
development takes place, and when the embryos are ready for expulsion a 
small boil or vesicle forms, which bursts and leaves a small sinus leading 
down to the head of the worm. The period of incubation from the ingestion 
of the embryo to the appearance of the adult embryo-bearing female in the 
subcutaneous tissue is about one year. The migrations of the worm are not 
attended by pain or any other symptoms. 

Symptoms. — At the time of development of the vesicle or boil there may 
be some slight febrile disturbance, and there is slight pain from the local 
irritation and inflammation. The rupture of the vesicle leaves a flattened, 
shallow ulcer, at the bottom of which is a small opening. At this opening 
the head of the worm may appear. If the ulcer be douched or sprayed 
with cold water a small quantity of a milky fluid exudes from the orifice, 
57 



898 DISEASES DUE TO ANIMAL PARASITES 

or the uterus of the worm may be protruded as a delicate tube which is 
seen to fill up and suddenly empty itself of a few drops of milky fluid which, 
examined microscopically, contains myriads of embryos. Usually when 
parturition is completed, or nearly so, the worm spontaneously leaves her 
host. In a case reported by Francis, in which five worms were observed in 
the feet, one complete worm containing its embryos and measuring twenty-six 
inches was passed in about half an hour. Usually a much longer period 
is required (fifteen or twenty days) before the worm emerges. Exception- 
ally, parturition being completed, the worm dies, becomes encysted, and can 
be felt as a firm, fibrous cord under the skin. 

Treatment. — The older method, and the popular one with the natives, is 
to grasp the presenting head of the worm, fix it to a smooth stick, and gradu- 
ally wind her out by twisting out a few inches every day. By this method 
the worm may easily be torn and a swarm of embryos liberated in the 
subcutaneous tissues. In the case reported by Francis, a temperature, with 
morning and evening variation between 98.8° and 104.5° lasting several 
days, occurred after rupture and retraction of a worm. These accidents 
have occasioned severe infections, resulting in death. Manson advises 
douching with cold water, application of a cold pack or cold baths to hasten 
expulsion of the embryos and the spontaneous emergence of the worm. 
Massage and electricity have been used with success. The best methods 
of treatment we owe to the suggestion of Emily. He advises injection of 
0.1 per cent solution of mercuric chloride into the head of the worm or into 
the swelling. This solution causes death of the worm, which may then be 
easily extracted. Similarly, Aoulkes advises injection of alcohol, and 
Tufnel, pure carbolic acid. 

Prophylaxis consists in careful filtration or sterilization of drinking 
water. 

Strongyloides Intestinalis. Definition. — Strongyloides ster cordis is a 
nematode worm infecting the intestinal canal. When present in large 
numbers it causes a chronic diarrhoea, with ansemia and emaciation. 

Distribution. — This parasite is widely distributed throughout the tropical 
and subtropical countries. It is extremely common in Cochin China, where 
it is supposed to be the cause of the severe diarrhoea of that country known 
as Cochin China diarrhoea. Powell has found it in India, in 15 out of 20 
cases of ansemia. It has been observed in Martinique, Sicily, Egypt, India, 
Porto Rico, and the Philippine Islands. In Italy, Germany, Brazil, and 
California it has been frequently observed in association with uncinaria. 
It was first reported in the United States by Thayer, and is now known to 
be fairly common in all our Southern States. 

Much confusion has arisen over the various nematode worms resembling 
this parasite. These are now believed by the majority of observers to 
represent morphological variations of the same worm. The following 
classification is given by M. L. Price: 

1. The rhabditiform embryo, formerly known as Anguillula stercoralis. 
found in the fresh stools, is a slender, active nematode worm, 0.3 mm. long 
and 0.04 mm. broad. 

2. Filariform embryo found in the stools after standing one or two days, 



NEMATODES 



899 



and supposed to develop from the rhabditiform embryos. This embryo 
is twice as long as the preceding form, and is also actively motile. 



Fig. 114 







A. Egg of Cochin-China diarrhoea worm (Strongyloides stercoralis) found in stools. B. Rhabditiform 
embryo of same, from the stools. C Filariform larva of same derived, by direct transformation, from a 
rhabditiform embryo. The figures were drawn from life, as seen under Leitz, objective 7, ocular 3. 
Bulletin of the United States Marine Hospital Service, No. 10, 1903. (After Thayer.) 

3. The sexually differentiated form, Rhabditis stercoralis, which may be 
developed from the preceding in five days. The male is a fine nematode 



900 DISEASES DUE TO ANIMAL PARASITES 

worm 0.7 mm. in length, the female 1 mm. in length, which, when cultivated 
extracorporeally, produces filariform embryos. Finally there is: 

4. The parthenogenetic mother-worm, Anguillula intestinalis , found in the 
intestinal canal at autopsy. A slender worm, 2 mm. in length, easily recog- 
nized by the string of five or six eggs in the centre of the body. Infection 
probably takes place by the ingestion of the filariform embryo in water or 
on uncooked vegetables. Leichtenstern has experimentally shown the 
incubation period to be seventeen days. 

Later researches have disproved much of the pathological importance 
previously attached to this parasite. It is a mistake, however, to say that 
the worm has no clinical significance. The principal symptom is a continuous 
diarrhoea, without pain or temperature disturbance. Secondarily, intestinal 
indigestion develops and nutrition is very much lowered. As a consequence, 
there is anamiia and wasting. Blood examination shows an ordinary anaemia 
and, in marked contrast with other verminous anaemias, shows neither 
leukocytosis nor eosinophilia. 

Treatment. — Thymol, given fasting, in the same manner as for uncina- 
riasis, is the best remedy for expulsion of strongyloides. If, for any reason, 
thymol should fail or if it should be rejected, or the patient show any intoler- 
ance to the drug, male fern should be used in large doses. 

Trichocephalus Dispar. — The Trichocephalus dispar, sometimes called 
a "whip-worm," is occasionally found in the intestinal canal of man. The 
male and female worms are about equal in size. The male is usually 
coiled in a spiral form, but the female is nearly straight. The posterior 
portion of the body is thicker than the anterior part, and by the slim 
anterior filament the parasite embeds itself in the mucous membrane of the 
intestine. This parasite is not common in the United States, but is frequently 
observed in France and Southern Italy. Its chief area of development is in 
the caecum, and more than one worm is usually present. Sometimes very 
large numbers are found. It is supposed to possess no pathological signifi- 
cance and to be incapable of producing serious symptoms, but some writers 
have claimed that it may cause diarrhoea and anaemia of a serious character. 
We know little about its history of development. 



CESTODES OR TAPEWORMS. 

Tapeworms are very frequently found in the intestinal canal of man. 
As their name indicates, they are flat, broad, white parasites, which consist 
of segments, each of which is rectangular in shape, but somewhat elongated. 
Each of these segments represents a single individual. From the head the 
segments just named develop. The technical name for the head and neck 
is the "scolex," and for the segment " proglottis. " By means of the head 
the worm is attached to the mucous membrane of the intestine, but there 
is no mouth in the sense that an opening exists which communicates with 
an intestinal canal. Each segment of the worm is hermaphroditic; that is 
to say, each segment contains male and female organs of reproduction. 

There are several varieties of tapeworms. The most frequently found 



CESTODES 901 

are the Tcenia mediocanellata, sometimes called the Tccnia saginata, or 
unarmed tapeworm, or beef-worm, the Taenia solium (pork-worm), and the 
Taenia echinococcus. Less common forms are the Dibothriocephalus latus, 
or Russian tapeworm, derived from eating infected fish; the Taenia nana, 
the Taenia confusa, and the " double-pored dog tapeworm," Dipylidium 
caninum. The Taenia nana is sometimes called the Hymenolepis nana, or 
dwarf tapeworm. 

The Taenia solium usually gains its entrance into the intestinal canal 
of man by the ingestion of imperfectly cooked pork, the Taenia medio- 
canellata by the eating of uncooked beef, and the Taenia echinococcus by 
the ingestion of food which has been fouled by the excrement of the dog. 

All tapeworms pass through three stages of existence. The segments 
of the worm give off eggs which are discharged from the intestinal canal 
of the host, enter the alimentary canal of some animal, and are hatched 
out as parasites which pass through the wall of the intestine, gain a place 
of rest in the muscles or other tissues, and there form cysts. When these 
muscular tissues are eaten, the parasite in the cyst once more enters the 
alimentary canal, becomes attached to its mucous membrane, and from it 
is developed the adult worm. 

The Tarda solium may be several yards in length. At one time it was 
thought to be solitary; hence its name. It not infrequently happens, how- 
ever, that more than one worm is present. The head, which is very small, 
scarcely larger than a pinhead, has a proboscis, or rostellum, about which 
is arranged a double row of horny hooklets. The hooklets in the anterior 
row are larger than those in the posterior row. Below these are four sucking 
disks at the sides of the head. By these means the worm attaches itself 
to the bowel. The segments of the worm are about 10 to 12 mm. in length 
and from 5 to 60 mm. wide, but they vary considerably in size; those nearest 
the neck of the worm being shorter and narrower than those which develop 
several feet away from the neck. When the egg of the Tamia solium is 
hatched out so that a scolex (or head) is set free, and this parasite becomes 
encysted in the muscles of a pig, the pork is said to be " measly." When it 
finds a resting place in the muscles of the brain, or other parts of the human 
being, it is known as the Cysticercus cellulosa. These cysts vary in size from 
that of a small pea to that of a bantam's egg, and are separated from the 
surrounding tissues by a formation of connective tissue which acts as a 
capsule. 

The Tamia mediocanellata possesses a head which differs materially 
from the head of the Tamia solium. There is no rostellum or hooklets, 
but there are four sucking disks, which are much nearer the point of the 
head than they are in the Taenia solium. This worm further differs from the 
Tamia solium in addition in that its segments are generally broader and 
shorter, and the entire worm is usually much longer. 

This worm may reach the length of about 25 or 30 feet, and it is not 
very rare for from 15 to 20 feet of a worm to be passed intact. When the 
scolex of this worm is found in the muscles of cattle it is called the Cysti- 
cercus mediocanellata. 

In Germany, where imperfectly cooked pork is largely eaten, the Taenia 



902 DISEASES DUE TO ANIMAL PARASITES 

solium is most frequently met with, but in this country, where the people eat 
largely of beef, the Tamia mediocanellata is much more common. 

The Tcenia echinococcus is very rarely met with in the United States. It 
is, however, exceedingly common in Australia. This worm possesses a 
double row of hooklets and four sucking disks. It is rare for more than 
three or four segments to be attached to any one head, but as the para- 
site is often present in numbers many disconnected segments may be 
discharged. Like the other forms of tapeworm, the segments increase 
in size as the distance from the head is increased. This worm does 
not inhabit the intestine of man, but produces its evil influence by 
reason of the entrance of its eggs into his alimentary canal, from which 
place they wander into other parts of the body, forming what are known 
as hydatid cysts. In other words, the infection of human beings by the 
Tcenia mediocanellata and the Taenia solium is quite different from the 
infection of human beings by the Taenia echinococcus, for in the first cases 
the patient swallows the parasite when it has reached the second stage of 
its existence and is prepared to develop its segments; whereas, in the case 
of the Taenia echinococcus the patient takes food which has in some way 
become contaminated by the fecal discharges of the dog, which fecal dis- 
charges contain the eggs of the parasite, and from these eggs are developed 
cysts. A patient infected by the Tamia echinococcus therefore suffers from 
the cystic stage of development of the worm. 

The hydatid cysts formed in this manner most frequently infest the 
liver, but almost any portion of the body may be affected. Such cysts, in 
the liver in particular, are always surrounded by a layer of connective tissue 
which is thrown out in an endeavor to circumscribe the invading parasite. 
The wall of hydatid cysts, therefore, is formed of two layers; the outside 
layer is lamellated and is sometimes called the cuticula. The inner wall 
of the cyst often contains muscular fibres and bloodvessels, and is called 
the parenchymatous layer. Not rarely the primary cysts give rise to sec- 
ondary cysts called daughter-cysts, and these daughter-cysts may develop 
in themselves cysts which are called granddaughter-cysts. 

On the inner surface of these cysts the scolices, or heads, of the worm 
are formed. At the posterior end of the scolex is a stem, or pedicle, by 
which it is attached to the wall of the brood capsule. In some instances the 
scolex may be found free inside of this capsule. In most cases, after the 
cyst has existed for a long period of time, the scolices die, the fluid is 
absorbed, and a granular mass remains. This granular mass may contain 
the hooklets, or the hooklets may be found free in the contents of the cap- 
sules, or in the primary cyst itself. Occasionally, a hydatid cyst is found 
which is sterile, that is, in which neither sub-cysts nor scolices are devel- 
oped. 

In addition to the scolices, the cysts contain a clear, limpid fluid 
which sometimes becomes turbid after the cyst has existed for a con- 
siderable period of time, the turbidity being due to disintegration of the 
lining layer of the cysts and the formation of crystals of cholesterin, and to 
the presence of lime-salts. Occasionally the cyst shrinks, its contents 
become inspissated or thickened, and the entire mass, including the con- 



CESTODES 903 

nective tissue which has been formed around the cyst, may become calcified. 
Sometimes, too, the daughter-cysts instead of growing inside grow outside. 
Indeed, this variation is more commonly seen in man than it is in animals 
that are affected by this parasite. This is called the echinococcus 
exogena. 

Under the name of echinococcus multilocularis a variety of echinococcus 
cyst is found in the liver, which is characterized by a somewhat irregular 
distribution of groups of small cysts walled off by connective tissue, as 
are the larger cysts already described. These cysts are often sterile; 
that is to say, they do not contain scolices or hooklets. It is probable that 
this formation is due to a somewhat different parasite from the ordinary 
Tamia echinococcus. 

The Bothriocephalus lotus, or Dibothriocephalus lotus, is the largest of all 
human tapeworms, and has very broad, square segments. The head is 
egg-shaped, but possesses no disks or hooklets. On the contrary, its head 
is marked by long grooves by which it attaches itself to the intestine. Its 
neck is longer and more slender than that of other tapeworms. Two 
species have been described, the Bothriocepholus cordatus and the Bothrio- 
cephalus cristatus. Infection by this parasite occurs most frequently by the 
eating of imperfectly cooked fish, probably because the eggs develop to 
some extent in water and are swallowed by various fish, in whose flesh the 
cysts are formed just as the other scolices already described form in the 
flesh of the hog or ox. 

Teenia nana, or dwarf tapeworm, Hymenolepis, is only from one-fifth 
to two inches in length. It has four suckers and a single row of hooklets on 
its head. Stiles states that it may be present singly or by thousands, and 
is probably more frequent than is generally thought. Its intermediate host 
is usually the rat, from the stools of which food is infected. In the rat the 
cyst stage may occur in the intestinal wall and is called a cercocystis. 
Like other tapeworms, the embryos burrow into the wall of the intestine, 
but do not remain there, falling back into the lumen of the bowel to reach 
adult development with eggs in about fifteen days. The only tseniafuge 
which has proved effective for the removal of this worm is aspidium. 

The Tamia cucumerina is slightly larger than the Tamia nana, and its 
head possesses four rows of hooklets. It is not infrequently found in the 
ileum of dogs and cats, but rarely affects man. Its scolices inhabit the 
dog-louse and by means of this parasite, or by the carrying of the embryos 
to the mouth by the hands after handling a dog or cat, infection of a human 
being may take place. 

Symptoms. — The symptoms produced by the presence of tapeworms in 
the alimentary canal are not pathognomonic. Not infrequently the worms 
exist for a long period of time without their host having any knowledge 
of their presence, and the infection is only discovered by the chance observa- 
tion of one or more segments in a stool. The patient may suffer from 
symptoms of gastrointestinal catarrh produced by the irritation caused by 
the worm, and sometimes an inordinate appetite is present, but this is by 
no means as constant a symptom of tapeworm as most persons imagine. 
Not infrequently, the host of a tapeworm suffers from anorexia rather than 



904 DISEASES DUE TO ANIMAL PARASITES 

from excessive hunger. In children there may be a good deal of nervous 
irritation and peevishness. 

In some instances, however, the presence of a tapeworm produces a very 
much more serious train of symptoms, which consist in an intense anoemia 
that may be so severe as to give rise to the suspicion that pernicious anaemia 
is present. The Bothriocephalus latus is said to be more prone to produce 
grave anaemia than any other of the tapeworms. 

Treatment. — The treatment of a patient infected by tapeworm consists 
in the abstinence of all food for eighteen hours prior to the administration 
of one of the following drugs, which are known to possess the power of so 
paralyzing or killing the worm that it lets go its hold, and then is readily 
passed from the bowel under the influence of a purge. One-half to one 
drachm of the oleoresin of aspidium may be given in capsule or emulsion 
to an adult, and followed in four or five hours by a saline purgative, such 
as citrate or sulphate of magnesium or Rochelle salts. In other instances 
pelletierine given in the dose of 3 to 5 grains may be used under the same 
conditions. It is commonly given in syrupy solution, and this syrupy solution 
is put up in a small container which holds one dose. If it is desired pelle- 
tierine may be followed by castor oil in place of the other purgatives named, 
but castor oil must not be used after aspidium is given, as it aids in the 
absorption of the drug into the body and so tends to poison the individual. 
A less agreeable method of destroying the worm is to administer a confection 
made of pepo, or pumpkin seeds which have been deprived of their hard 
coverings by the process of bruising. Several drachms of these seeds are, 
without doubt, very efficacious. The patient should always be instructed 
to pass the stool through a sieve and not to seek so much for the segments 
of the worm as for the small head. The mere passage of a large number 
of feet of segments does not indicate in any way that the patient is perma- 
nently relieved unless the head, from which other segments will grow if it 
remains in the bowel, is also passed. 



TREMATODES. 

Definition. — A large number of worms belonging to the Trematodes live 
as parasites in the body of man or of the lower animals. When the body 
is so infested the condition is said to be one of Distomatosis, this term 
arising from the fact that the word Distoma is oftentimes applied to these 
parasites. 

Up to the present time no less than thirteen species of Trematodes or 
Flukes have been described as occurring in human beings. Eleven of these 
belong to the family of the Fasciolidoe, one to the family Paramphiscus, and 
one to the family Schistosomidce. 

When the human being is attacked the parasite is usually found in the 
genito-urinary tract, when it causes what is known as Bilharzia Disease or 
Endemic Hematuria. Less commonly it infests the lung and the condition 
is then called Distomatosis of the Lung, Endemic or Parasitic Haemoptysis 
or Lung Fluke; and it is also met with in the liver, forming the so-called 



TREMATODES 



905 



Liver Fluke or Distomatosis of the Liver. The fluke found in the genito- 
urinary tract is the Schistosoma haematobium, that met with in the lung is 
the Paragonimus Westermanni, sometimes called the Distoma Ringeri or 
Distoma 'pulmonale, and that discovered in the liver the Fasciola hepatica 
or instead Dicrococlium lanceatum, Opisthorchis sinensis, the Opisthorchis 
felineus, and the Opisthorchis noverca. 

Bilharzia Disease. — Bilharzia disease, or endemic hematuria, is due to 
the development in the body of the Schistosoma haematobium, and is charac- 
terized by hematuria and the formation of papillomatous tumors in the 
genito-urinary tract. 

Etiology. — The male worm is about 4 to 15 mm. in length and 0.6 mm. in 
breadth. The female averages 15 to 20 mm. in length and 0.28 mm. in 
breadth. The male has flattened sides, rolled up on both edges so as to 
form a deep groove, the gynecophoric canal, in which the female lies during 
conjugation (Fig. 115). 

Fig. 115 




Male bilharzia worm carrying the female, showing the papillae on his skin. The small figure is a 
cross- section showing relative position of the sexes. (Looss.) 



History and Distribution. — Endemic hematuria has been observed in 
Egypt for centuries. At the present day it is said to be present in fully one- 
half of the population. According to Looss it is equally frequent in Uganda. 
It is practically limited to the African continent, although cases have been 
reported from Cyprus and Sicily, and Manson reports a case from the West 
Indies. It occurs frequently in British India, but always as an imported 
infection. A few cases have been reported in the United States. The 
parasitic nature of the disease was discovered in 1851 by Bilharz. 

The ova of these worms are found in very great numbers in the urine. 
They are oval, and have a marked terminal spine and contain a ciliated 
embryo. It is supposed that the spine is the organ by means of which 
the embryo bores through the peripheral tissues. Ova with lateral implan- 



906 DISEASES DUE TO ANIMAL PARASITES 

tation of the spine are frequently observed. Looss supposes these are 
examples of faulty development, and that the faulty position of the spine, 
limiting the mobility of the ovum, is the reason many more of this form 
are found in sections than free. In urine or in water the embryos very 
soon escape from the ovum and move about very actively by means of their 
cilia. In undiluted urine they die when it cools. In water they remain 
active for a long time. 

The embryos are probably taken into the stomach in drinking-water, 
penetrate the gastric or intestinal wall, and they develop into mature worms. 
Looss surmises and brings some evidence to show that, like the uncinaria, 
this parasite may also penetrate the skin. 

Pathology. — The affected bladder is covered with a bloody, tenacious, 
mucous layer; the submucosa is greatly thickened; the muscular and serous 
coats, as a rule, are unchanged. In older cases papillomata are found, vary- 
ing in size from a small pea to large tumors filling the entire bladder. Micro- 
scopically the changes consist in marked degeneration of the epithelial 
layers, going on to complete destruction of the mucosa. The pseudomem- 
branous covering then consists of ova, leukocytes, and urinary salts. In 
the submucosa enormous masses of ova are found, many of them calcified. 
The papillomatous tumors spring from this layer, and are very similar in 
their histological structure to nasal polypi. Similar changes occur in the 
rectum, urethra, ureter, seminal vesicles, prostate, and uterus. Second- 
arily these lesions produce stricture, urinary fistula?, pyelitis, prostatitis, 
and urethritis. 

The papillomatous tumors show some tendency to undergo malignant 
change, but by far the commoner complication of the disease is stone forma- 
tion. In old cases a beginning deposit of lime-salts is found in the mucus 
covering the bladder wall, as small calculi embedded in the folds and loculi. 
In other cases large, free calculi are found with clumped masses of calcified 
ova as their nucleus. 

Tumors and masses of ova are sometimes found in the pelvis of the kid- 
ney, rarely in its parenchyma. 

Symptoms. — The symptoms vary with the intensity of the infection, the 
number of adult worms, and the location and extent of the lesions already 
described. The only constant symptom is hematuria. The amount of 
blood present in the urine may be so small as only to be evident on micro- 
scopic examination, or so large as to form clots of appreciable size in the 
bladder. As a rule, the blood is passed at the end of urination. The micro- 
scopic examination, in doubtful cases, should therefore be directed to the 
last few drops of urine expelled. In the large majority of cases hematuria 
will be the only symptom. In the severe infections, however, cystitis usually 
develops and becomes very troublesome. Following the development of 
inflammation the ordinary symptoms of tumor or stone develop. In severe 
cases, with diminished resistance, suppuration of these lesions occurs, with 
formation of extensive fistulous tracts. When the lesions are confined to or 
are most marked in the bowel, the early symptoms may resemble acute 
dysentery and, in older cases, chronic dysentery, with pain, tenesmus, and 
bloody and mucous stools. When tumors occur in the bowel they are readily 



TREMATODES 907 

recognized, although when situated low in the rectum they have been mis- 
taken for hemorrhoids. 

The urine contains red blood cells, leukocytes, principally eosinophiles and 
polynuclear cells, besides large numbers of ova. With these the ordinary 
evidences of an extensive chronic cystitis are also found. The number of 
ova present varies very widely and bears no relation to the amount of blood 
in the urine. When they are very few in number they may only be found 
in the last few drops of urine passed. 

The blood changes, in severe cases, are marked. There is a pronounced 
fall in the number of red cells and a still greater reduction of haemoglobin. 
With this there is a moderate degree of leukocytosis, the increase consisting 
almost entirely of eosinophile cells, which are present in proportion varying 
from 9 per cent, to as high as 52 per cent. 

Diagnosis. — The blood condition pointing to a toxic or parasitic anaemia, 
with the demonstration of the ova in the urine, make the diagnosis of Bil- 
harzia disease. 

Prognosis depends on several factors, namely, the extent of the infec- 
tion, the number of adult worms present, and, more important still, the 
conditions favoring reinfection. W 7 hen all opportunity for reinfection is 
avoided, as by removal from the endemic area, after a time the adult 
worms die, and eventually all the ova are evacuated. This process may 
be a very long one. In some observed cases it has extended up to eight 
years. The prognosis also depends on the character and extent of the 
surgical complications and sequelae. 

Treatment. — There is no treatment that will influence either the worm 
or the ova in the slightest degree. All the anthelmintics have been tried 
and found useless. Similarly, local application of antiseptics and proto- 
plasmic poisons to the bladder have failed. In most cases the haematuria 
does not require treatment. When it becomes severe, rest in bed should be 
enjoined. Cystitis should be treated on general lines by local medication, 
as well as the internal administration of urotropin, salol, benzoic acid, 
and remedies of this group. The complications of the disease, such as 
stricture, extensive tumors of the bladder and rectum, accessible ulcera- 
tions of the vagina or cervix, and prostatic involvement, call for appropriate 
surgical measures. In a general way, all the conditions which predispose 
to or aggravate cystitis should be avoided. These are exposure, chill, violent 
muscular effort, alcoholic debauches, spices, and highly seasoned food. 
With a view to obtaining an eventual cure, patients should if possible be 
removed from the endemic area. When this is not possible, proper means 
should be taken to ensure a good water supply. In this manner the constant 
reinfection of the patient is avoided. Similarly, in view of the possibility 
of infection through the skin, sound shoes should be insisted on and work 
in alluvial oozes should be avoided. 

Distomatosis of the Lung (Lung Flukes; Endemic or Parasitic Haemop- 
tysis). — The lung fluke (Paragonimus Westermanni) is widely distributed 
in Japan, Formosa, Corea, and North China. It has been carried by Oriental 
emigrants to many other countries. Isolated cases have been reported from 
the United States and Mexico. 



908 DISEASES DUE TO ANIMAL PARASITES 

The parasite is a small, fleshy, trematode worm or fluke. It is 8 to 
20 mm. long and 6 mm. in its transverse diameter. It is usually 
found in the lungs, but has been observed in other organs, notably 
the liver and brain. The worms discharge a vast number of ova. These 
ova are dark brown, oval, 0.08 mm. long by 0.05 mm. wide, possess a small 
operculum, and contain a ciliated embryo. They are found in great numbers 
in the sputum. Infection probably takes place through contaminated water, 
although nothing is known of the extracorporeal phases of the parasites. 
By far the larger percentage of cases is observed in young males. Alcoholism 
is supposed to predispose to the disease. 

Pathology. — Patches are scattered all over the lungs, but particularly in 
the periphery, resembling hemorrhagic infarcts. On section these patches 
are found to be infiltrated and honeycombed with small tunnels and 
cavities, each of which contains one or more distoma and masses of eggs. 
Occasionally large cavities are formed by coalescence of the smaller 
lesions. 

In cases in which the parasite invades the brain, analogous conditions are 
found, but they are almost entirely limited to the cortical areas. 

Symptoms. — The commonest symptom is chronic morning cough, with a 
rusty, prune-juice, or bloody sputum. The amount of blood in the sputum 
may be so small as to be only demonstrable by the microscope, or there may 
be periodical and severe hemorrhages from the lungs. The rusty color of 
the sputum is due not only to the blood and the bloody pigments contained 
in it, but also to the large numbers of dark-brown ova. The sputum also 
contains eosinophile cells, Charcot-Leyden crystals, and elastic fibres. The 
course of the disease is essentially chronic. Cases last from ten to twenty 
years without much discomfort and without much deterioration in the 
general health, excepting where marked secondary anaemia results from 
repeated and severe hemorrhages. 

Prognosis. — The prognosis is good, excepting in the rare instances in 
which hemorrhage is sufficiently severe to cause a fatal ending. When the 
parasite attacks the brain, epileptic symptoms have been observed and the 
prognosis is grave. 

Treatment. — A large numer of drugs have been administered to patients 
suffering from this condition, both by the mouth and by inhalation, 
in the hope that benefit might accrue. It is evident that the nature of 
the lesions renders any therapeutic measure of little value. 

Distomatosis of the Liver (Liver Flukes). — Liver flukes occur endem- 
ically in certain sections of Japan. For instance, Baelz estimates that 20 
per cent, of the inhabitants of Okayama Province are infected with the liver 
fluke. Inouye found in various sections from 19 per cent, to 71.9 per cent, 
of the population infected. Infection has been carried all over the world by 
Oriental emigrants. In the United States an entirely analogous affection is 
seen in cats and cattle and several cases have been met with in man. 

The parasite commonly invades the biliary tract or the pancreatic duct, 
and is also found in the duodenum, the stomach, and spleen. The obstruc- 
tion of the biliary ducts by the parasites causes dilatation and chronic 
catarrh. There is also overgrowth of the hepatic connective tissue, with 



DHOBIE ITCH 909 

atrophy of the parenchyma. Small but constant hemorrhage from the 
biliary passage may cause a grave anaemia. 

Postmortem the parasites are found in great numbers in the walls of 
the gall-bladder and biliary ducts, or free in the ducts. They lie in small, 
cyst-like cavities connecting with the gall-bladder or ducts. 

Symptoms. — The symptoms depend on the number of worms. The first 
symptom is rapid enlargement of the liver, with voracious appetite. The 
liver may reach to the umbilicus, it is tender on palpation, and there are 
recurring attacks of jaundice. Sooner or later diarrhoea begins, and with 
it marked failure of nutrition. The patient becomes weak, emaciated, and 
anaemic. The diarrhoea in marked cases is severe, and the movements 
contain much blood besides the ova of the parasites. Later, dropsy of the 
legs and belly develop, and the patient dies exhausted. The course of the 
disease is very chronic, and likewise depends on the number of parasites. 
Recovery never takes place. 

Treatment. — There is no treatment save the use of stimulants and good 
food. 

With the idea of prophylaxis Inouye advises against drinking or swim- 
ming in canal water or eating raw fish or mussels. He states that in one 
region notably infected with the disease the mortality from distomiasis has 
been reduced to zero by following these simple precautions. 



PARASITIC INFUSORIA. 

The parasitic infusoria w T hich are found in man are protozoa of the sub- 
class flagellata. They are rarely met with. The Plagiomonas urinaria 
has been found in the urine of a man who suffered from chronic suppura- 
tion. The Trichomonas vaginalis is found in acid vaginal mucus, and the 
Trichomonas hominis has been found in the bowels and stools. They all 
possess but little clinical interest. 

DHOBIE ITCH. 

Definition. — Dhobie itch is a term applied to a large group of mycotic and 
bacterial, itching skin diseases affecting persons living in hot climates. These 
eruptions may occur anywhere on the body, but usually in the crotch, 
axilla, on the soles of the feet, and between the toes. The term dhobie 
is derived from the "dhobie" or washerman, owing to the widespread 
belief that the contagion is conveyed by the clothing passing through his 
hands. 

Etiology. — Epiphytic skin diseases are exceedingly common in the 
tropics, and all forms of ringworm grow with the greatest freedom under the 
exceedingly favorable conditions of heat and moisture afforded by the climate. 
Three types of the disease are recognized. The first is thought to be 
due to the Microsporon minutissimum; the second type probably represents 
a very extensive group of different varieties of tricophyton, or ringworms. 
The third type, classed as dhobie itch, is that described by Manson as 



910 DISEASES DUE TO ANIMAL PARASITES 

Pemphigus contagiosus, in which he has isolated a diplococcus, the exact 
significance of which has not yet been fully determined. 

These skin diseases have all been imported into the United States by 
soldiers returning from the Philippines, and there is every possibility of 
spreading them in the States that lie in the subtropical belt. Tropical skin 
infections of this type are usually spread by direct contact with infected 
persons or their clothing. In many instances sexual intercourse serves as a 
means of spreading the disease. Bathing in the waters of sluggish streams 
and tanks sometimes causes dhobie itch. The natives of Luzon believe 
that sea bathing is one of the common causes, and among men who habit- 
ually bathed in the sea I (Kieffer) saw a larger proportion of itch cases 
than in those who did not. The washing of underclothing in cold water, 
and without boiling, must also be considered a cause. Clothing washed in 
cold water invariably becomes overgrown with moulds when laid aside for 
a day or two. These mouldy clothes frequently cause ringworm infection. 
Ringworms are also very common among the domestic animals in the tropics, 
and are undoubtedly cenveyed from them to man. 

In the two mycotic forms the disease usually attacks the crotch and 
axilla. The appearance of the lesion is that of an ordinary ringworm with 
festooned, scaly margins. The interior of the patch is red, glossy, and bare. 
Secondary infections frequently occur from scratching or chafing, or from 
simple contact with the denuded epithelium. These diseases affect almost 
all ages, and are found in the native as well as in the foreigner. In the Philip- 
pines very few Americans escape without contracting one or another of them. 
The smarting and itching are very severe. The suffering from the chafing 
of the clothing may be so great as to entirely prevent the patient from 
moving about. Unless vigorously treated the disease persists until the cool 
season, when the patch heals up, leaving a scaly, pigmented area which 
breaks out again with the approach of the hot weather. 

Pemphigus contagiosus occurs in the form of vesicles, or blebs, which 
break and leave a raw, red, and shiny, denuded surface, with a sharp, clear- 
cut zone one-sixteenth to one-eighth inch in width of undermined epithe- 
lium surrounding them. When the blebs are small its resemblance to 
varicella may be very close. The disease occurs in foreigners of all ages. 
Among the natives adults are as a rule immune, and it is principally seen 
in children. The eruption may be scattered over the entire body or may 
be limited to the crotch and axilla. 

When any doubt exists of the nature of these eruptions, the mycotic 
elements can be readily demonstrated microscopically. Pemphigus con- 
tagiosus is to be differentiated from varicella in that the constitutional 
symptoms of the latter are wholly lacking. 

Treatment. — The parts should be thoroughly cleaned with green soap, 
following which a parasiticide remedy should be used. Manson advises 
Vleminck's solution of the sulphuret of calcium, applied every night for 
three or four times. Tincture of iodine painted over the area daily is a valu- 
able remedy. Similarly, an ointment of chrysophanic acid or the oleate of 
mercury is very efficient. A saturated solution of salicylic acid in collodium, 
applied twice daily, is a convenient and excellent remedy. The main diffi- 



MYIASIS 911 

culty is that in the majority of cases, as soon as the diseased area is sterilized 
by these remedies, it becomes reinfected by the clothing or hands of the 
patient. Pemphigus contagiosus should be treated by bichloride of mercury 
washes and a dusting powder. Prophylaxis includes careful boiling of the 
underclothing, and keeping the crotch and axilla as dry as possible with a 
good dusting powder. 



CHIGGER (SAND FLEA). 

The chigger, or sand flea {Pulex penetrans), is distributed widely over 
tropical and many parts of subtropical America and the West Indies. It 
is supposed to have been carried in 1872 from South America to Africa. 
At present it is widely distributed on both African coasts and in certain sec- 
tions of India. It is a very common pest in the Philippine Islands, where 
it is known as " tungau." The chigger is a minute, reddish-brown flea, and 
attacks both man and animal. When impregnated the female attaches 
herself to the skin surfaces and burrows under the skin, head first. Ovula- 
tion takes place in the cutaneous tissue and the female increases to the size 
of a small pea. If unmolested the ova, when mature, are expelled through 
the point of entrance, through which also the female is ultimately extruded. 
The chiggers may vary in number from one to several hundred. They 
usually lodge in the feet and legs, but the hands, arms, genitals, and face 
may also be invaded. The bite of the insect causes little pain, and the female 
is usually detected when she commences to enlarge beneath the skin. There 
is then intolerable itching, with formation of small papules, with red, in- 
flamed heads, and a black spot on the summit. The papules become pustu- 
lar, discharge, form small ulcers, and eventually heal, leaving small, pitted 
scars. When the lesions are numerous, particularly when neglected in the 
unclean and the physically deteriorated, extensive infections and sloughing 
wounds may occur. Rarely tetanus and phagedenic areas develop. 

Treatment. — Treatment consists in complete enucleation with a needle or 
the point of a fine scalpel. Chloroform, turpentine, infusion of tobacco, 
mercurial ointment, and the essential oils allay the itching and kill the para- 
sites. The essential oils, particularly the oil of eucalyptus, act not only as a 
cure, but also as a preventive against the bites of the insects. 



MYIASIS. 

Infection by Larvae of the Diptera. — Screw-worm (Lucilia Macellaria), 
the larva of the common blue-bottle flesh fly, a very common fly in 
the United States, West Indies, and South America, causes infection in 
man through the female laying her eggs on wounds in the skin and in the 
noses or ears of people sleeping in the open. During the campaign at San- 
tiago de Cuba, in 1898, numerous cases of infection by this larva were seen 
in wounds and abrasions about the feet of the men and horses. In the 
tropics they have also been seen attacking the vagina of recently delivered 



912 ' DISEASES DUE TO ANIMAL PARASITES 

women. The eggs deposited in these locations hatch out in a few hours 
into the larva, known as the screw-worm on account of the circles of minute 
spines running around the body of the worm very much as does the thread 
of a screw. The larvse are about three-quarters of an inch in length. They 
are extremely active, and burrow widely, causing extensive destruction of 
all the tissues. On account of the circles of spines they are extremely diffi- 
cult to extract from their burrows in firm tissue. Screw-worm infections of 
the nose are very painful and exceedingly fatal. The larvse bore into the frontal 
and ethmoidal sinuses, and eventually may even enter the brain. There is 
intolerable pain at the bridge of the nose, with a bloody, fetid discharge from 
the nostrils. A very large percentage of the cases die from extension of the 
infection into the sinuses or meninges. When the larva? develop in the ear 
they penetrate the tympanic cavity, causing severe otitis media and even fatal 
meningitis. Numbers of such cases have been reported by army surgeons 
from the Rio Grande border. 

Treatment. — Treatment consists in the injection of strong parasiticides, 
such as carbolic acid and chloroform. Better still, chloroform is taken up 
on a small probe tipped with absorbent cotton, and, with a good light, the 
nose or ear is explored and each worm as it lies embedded in the tissues 
is touched with the chloroform-saturated cotton. This kills them immedi- 
ately and they may then be readily extracted with small forceps. In super- 
ficial wounds the destruction of the larvse is much more simple. 

Intestinal Myiasis. — The larvse of diptera are very frequently found in 
the alimentary canal of man. They usually gain entrance by being swal- 
lowed on fly-blown food. No less than nineteen different species have been 
identified in human evacuations. As a rule no symptoms are produced, 
and the first the patient knows of the existence of the larvse is to find per- 
haps a copious mass of them in the stools. In tropical climates the passage 
of larvse is very much more frequent than in temperate countries, for 
obvious reasons connected with the difficulty of preserving food supplies. 
The appearance of the larvse is usually viewed with the greatest alarm by 
the patients, but, as a rule, they are entirely harmless. Occasionally they 
produce some symptoms of gastrointestinal disturbance, such as vomiting, 
diarrhoea, and abdominal pains. Free purgation is indicated whenever 
larvse are seen in the stools, to ensure evacuation of those remaining. For 
this purpose calomel is the best drug, as it exercises not only an evacuant 
but a toxic effect on the larvse. 

Dermatobia Cyaniventris. — This common American fly deposits its eggs 
on the skin of man and cattle. The larvse penetrate the cutaneous structure, 
producing large pustular lesions (locally known as ver macaque). Besides 
this fly there are great numbers of diptera whose larvse attack the skin of 
man. In all of them the lesions are similar to that above described. In 
America these are principally the Musca vomitoria. the ordinary blue-bottle 
fly, and the bot-fly of the ox and sheep. 



DISEASES OF THE NERVOUS SYSTEM. 



DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN 
THE BRAIN AND ITS MEMBRANES. 



HEMORRHAGE INTO THE BRAIN, CEREBRAL THROMBOSIS, 
AND EMBOLISM. 

Definition. — Apoplexy consists in the sudden onset of paralysis and loss 
of consciousness from an abrupt intracranial lesion. In its most typical 
form it is due to hemorrhage in the cerebrum, but it may also be due to 
hemorrhage into the cerebellum, into the brain-stem, or into the meninges, 
and it may result from embolism or from thrombosis. When it arises 
without being accompanied by a demonstrable brain lesion it is spoken 
of as an " apoplectiform attack." An inflammatory process in the central 
nervous system, so acute that minute hemorrhages occur in the affected 
area, is also spoken of as apoplectiform, as, for example, ''apoplectiform 
bulbar paralysis." 

The term "apoplexy," as commonly employed, is nearly equivalent to 
the popular term "stroke." and is used so indefinitely that it is better to 
use the more accurate terms cerebral hemorrhage, cerebral thrombosis, or 
embolism when describing the condition present. The symptoms pro- 
duced by thrombosis and embolism are almost identical with those due 
to hemorrhage, and will be found discussed in the consideration of the 
differential diagnosis of the disease. 

Etiology. — As already stated, the usual cause of apoplexy is the rupture 
of a bloodvessel in the brain or its meninges. This is due in the great 
majority of cases to changes in the bloodvessel produced by disease or bv 
injury. These changes are described in the article on Arteriosclerosis. 
The immediate causes which produce rupture of an intracranial vessel are 
numerous, for all factors which cause a sudden increase in blood pressure 
may result in so great a strain on a weakened vessel wall that it gives 
way. Thus, apoplexy not rarely follows a paroxysm of rage, a severe 
nervous shock, a sudden muscular effort, as in running for a car, in 
straining at stool, and during sexual intercourse. The use of alcoholic 
and other stimulants may also cause rupture. 

Frequency. — Men are more frequently attacked by apoplexy than are 
women, because they suffer so much more commonly from arteriocapillary 
fibrosis. The ratio is about as 80 to 20 per cent., according to Starr, but 
58 ( 913 ) 



914 DISEASES OF THE NERVOUS SYSTEM 

Gintrac puts it at 56.6 to 43.4 per cent. Of 816 cases of cerebral hemorrhage 
collected by me from various sources, 454 occurred in men and 362 in women. 
The period of life at which cerebral hemorrhage most commonly occurs is 
from fifty to eighty years of age. This is the age period during which the 
patient is actually most liable to this accident; but if the ages of the entire 
number of persons dying of apoplexy in a given series of statistics be added 
together and an average obtained, the largest number of cases is found 
between forty and sixty years, because so few persons live to eighty years 
that not many persons of that age are to be found in such a series. The fol- 
lowing table is a combination of the cases of Gintrac and Breese, and shows 
the age incidence of cerebral hemorrhage by decades from thirty to eighty 
years. 

Between 30 and 40 years of age 74 

" 40 " 50 ' " " 98 

" 50 " 60 " " ..... . 138 

" 60 " 70 " " 172 

70 " 80 " " 124 

The question of age in its relation to apoplexy is, however, more dependent 
upon the state of the bloodvessels than upon the actual years of existence, 
for not infrequently a syphilitic of thirty years of age may suffer more from 
degeneration of the arteries than another man at seventy. 

Available statistics do not show any increase in the frequency of cerebral 
hemorrhage. Thus, from 1879 to 1884, 12,408 patients were admitted to 
the medical wards of St. Bartholomew's Hospital, London, and of this num- 
ber 79 were affected with cerebral hemorrhage. During the five years from 
1897 to 1902, 12,089 medical patients were admitted to the hospital, and 
among them there were 62 cases of cerebral hemorrhage. 

Pathology. — The changes which take place in the bloodvessels of the 
brain which result in apoplexy are those of arteriosclerosis as we meet it in 
other parts of the body; the intima becomes roughened and eroded, the 
muscular sheath undergoes fatty degeneration, and the fibrous sheath 
becomes less elastic than in health. Aneurysmal dilatations frequently 
develop, and these are the parts of the vessel from which hemorrhage often 
ensues. In the article on Arteriosclerosis it was shown that the causes of 
this state are syphilis, lead, gout, renal disease, and, not least important, 
advanced years; but of all these causes renal disease is probably the one 
which most frequently produces vascular rupture, because it is usually 
associated with cardiac hypertrophy and a high arterial tension, which 
increases the stress on the weakened vessel wall. 

Rupture of a vessel occurs very much more frequently in certain areas 
than in others, as already pointed out. This is because certain vessels 
suffe from arterial sclerosis earlier than others, and also because of the 
anatomical relationship. Thus, the blood current reaches the left middle 
cerebral artery more directly from the heart than it does on the right side, 
where it first passes through the innominate artery, which diminishes its 
force. Durand Fardel states that 75 per cent, of the miliary aneurysms 
which affect cerebral vessels involve the branches of the middle cerebral 



HEMORRHAGE IXTO THE BRAIN 915 

artery which enter the anterior perforated space, namely, the lenticulo- 
striate and the lenticulo-thalamic vessels. For this reason the lenticulo- 
striate branch was called by Charcot the "artery of cerebral hemorrhage. " 
About 50 to 60 per cent, of all cerebral hemorrhage is from this vessel, and 
therefore occurs in the internal capsule or near it. (See Hemiplegia.) The 
sharp spurt of blood which follows rupture of the vessel wall may break 
through the corpus striatum in either direction, often internally through 
the caudate nucleus, or it may break through the optic thalamus; and when 
the rupture is large and the blood pressure high, the blood thus finds its 
way into the lateral ventricles (see Fig. 118), into the third ventricle, 
and even into the fourth ventricle, where it causes death by pressure on the 
vital centres, if death has not already ensued from shock and the damage 
to the cerebral tissues. 

When these "capsulo-ganglionic" vessels do not give way the cause of the 
symptoms is usually rupture of some of the outer branches of the Sylvian 
artery, producing lesions in the cortex. In still other cases, which are less 
frequent, the hemorrhage takes place into the pons and still more rarely 
into the cerebellum. 

Cerebellar hemorrhages are especially prone to inundate the fourth ventricle. 

A very much rarer form of apoplexy is that in which by reason of disease 
of the blood, or of the vessels, small oozings or extravasations take place 
through the vessel walls, which on subsequent examination do not reveal 
any rupture. This extravasated fluid finds its way alongside the vessels, 
and so does damage to a wide area without causing any very gross lesion 
in the brain tissues. Such a state may develop in the course of purpura or 
leukocythemia. Extravasations of blood into the meninges and cortex also 
occur as the result of injury 7 . 

In those cases in which the hemorrhage is arrested before it does great 
damage much depends upon the part of the brain which is affected. 

If the hemorrhage occurs on, or in, the cortex, and is small in amount, 
the convulsions and paralysis which ensue may only involve part of the 
arm, or leg, or face, or one of the special senses, or a particular function 
controlled by the centre that has been destroyed, or such a monoplegia may 
be due to a small hemorrhage in the subcortex cutting off the fibres of the 
corona radiata descending from the cortical centre. But an equally small 
hemorrhage still lower down, where the fibres from the entire cerebral 
hemisphere come together in the internal capsule, will produce a complete 
hemiplegia (Fig. 116, lesion of ordinary hemiplegia). On the other hand, 
if the lesion occurs still lower down — that is, in the brain-stem, where 
bundles of fibres are separating from the main paths and crossing to 
the opposite sides to connect with cranial nerves — it will produce crossed 
paralysis — for example, the face is paralyzed on one side and the body on 
the other. Ordinary "crossed paralysis" indicates a lesion in the lower 
third of the pons because at this point the motor fibres for the face have 
crossed but the fibres for the limbs have not done so (Fig. 117, lesion of 
crossed paralysis). If the posterior third of the internal capsule is affected 
as well as the anterior and middle thirds, we find hemiansesthesia as well 
as motor paralysis on the opposite side (Fig. 118); and if the very posterior 



916 



DISEASES OF THE NERVOUS SYSTEM 



portion of this limb is affected the optic radiations are implicated and 
hemianopsia is added to the symptoms. (See Fig. 118, "optic") If the 
patient survives the attack the extravasated blood coagulates and is sur- 
rounded by a protective wall of lymph, which undergoes organization 



V. QWEB 



Fig. 116 

LIMB 




Diagram showing the fibres from the cortex forming the corona radiata, which after they are approxi- 
mated pass into the internal capsule. It also shows the decussation of the pyramid of the left side, which 
passes to the right side of the spinal cord, and the direct or uncrossed tract (Turck's column). Finally, it 
also shows the secondary degeneration which occurs after cerebral hemorrhage or softening, and which 
follows the course of the motor tracts into the spinal cord. H. Site of lesion. The continuous lines are 
fibres going to the legs, the dotted are those going to the arms and motor cranial nerves. The Roman 
numerals refer to the origins of the cranial nerves. (Modified from Van Gehuchten.) 



HEMORRHAGE INTO THE BRAIN 



917 



while the clot softens, and contracts as its contents are being absorbed. 
The permanent lesion of apoplexy is thus commonly a cyst, but some- 
times, absorption having been complete, only a scar remains. Not only do 
these changes take place at the site of the hemorrhage, when it affects the 
the cortex or motor fibres in the corona radiata or in the internal capsule, 
but degenerative alterations follow along the motor pathways through the 
peduncles of the cerebrum, the pons, the pyramids of the medulla, and so 
on into the direct and crossed pyramidal tracts of the cord. (See Fig. 116.) 



Fig. 117 



Lesion of cerebralmo- 
noplegia (brachial) 



Lesion of ordinary 
hemiplegia 



Lesion of cross paralysis 
(face of same side with 
limbs of other side) 



A lesion causing paraplegia 



A lesion causing hemi- 
paraplegia 




Cortical centre for op- 
posite leg 



Cortieal centre for op- 
posite arm 



Cortical centre for op- 
posite side of face 



Internal capsule (pos- 
terior limb ) 



Motor nerve to face 

Decussation of pyra- 
mids 

Crossed pyramidal tract 



■Motor nerves to upper 
limb 



Crossed pyramidal tract 



Sensory nerves entering 
cord, and decussating 
soon after entry 



Motor nerves to lower 
limb 



Diagram showing the general arrangement of the motor tract and the cflect of lesions at 
various points. (Ormerod.) 

Symptoms. — The symptoms of apoplexy depend upon the site of the lesion 
and upon the suddenness and severity of the hemorrhagic extravasation, 
as already stated. A few cases have some premonitory symptoms such as 
numbness or tingling in the part of the body about to be affected, but most 
cases are attacked without warning. When the hemorrhage takes place 
from the middle cerebral artery the symptoms are usually as follows: 



918 



DISEASES OF THE NERVOUS SYSTEM 



An Individual who is apparently in his normal health is suddenly seized 
with vertigo, which causes him to stagger and fall. The face is at first pallid 
and later somewhat congested. The respiration is altered almost imme- 
diately. At first it may be slightly gasping and irregular, but soon becomes 
full and deep. The air is drawn into the lungs with considerable force 



Fig. 118 




Cross-section of the brain, showing the lateral ventricles, the cerebellum, and, most important, the 
section of the motor fibres in the internal capsule. (Modified from Fuller.) 

and then equally forcibly expelled. As it enters it causes the relaxed soft 
palate to vibrate and as it escapes through the angle of the mouth, which 
is paralyzed, it produces a noise to which the term "stertorous breathing" 
has been applied. The pulse is slow and full and its tension high except 
for a few moments after the onset of the symptoms, when it may be rapid 



HEMORRHAGE INTO THE BRAIN 919 

and irregular from the shock. In some cases, too, in which the hemorrhage 
into the brain is very great and death imminent, the pulse may not 
become full and strong. 

An examination of the patient's limbs may show that both sides are almost 
equally relaxed and powerless, but this is usually a temporary state due to 
shock, and in a very short time it will be found that the limbs on one side 
are moved, or at least are not quite powerless, while those on the opposite 
side are paralyzed. In other words, the typical paralysis of cerebral hemor- 
rhage called hemiplegia is present. 

The muscles of the trunk are never as completely paralyzed as those of 
the limbs. The muscles of the lower part of the face share in the paralysis, 
and for this reason the features w T ill be drawn away from the paralyzed side 
because the normal balance between the muscles on the two halves of the 
face has been destroyed. Unlike the facial paralysis due to a lesion in the 
facial nucleus in the pons or in the facial nerve itself, the upper muscles 
escape, and so we find that the muscles of the forehead and eyes are 
not paralyzed; the forehead can be wrinkled and the eyes can be closed. 

In the stage of onset we sometimes find the head and eyes turned 
sharply to one side (conjugate deviation), usually away from the para- 
lyzed side. When this occurs it is said that the eyes "look at the lesion." 
The pupils are sometimes contracted, but more commonly are dilated, 
the pupil on the side upon which the hemorrhage has taken place being 
more dilated than its fellow. 

Pricking or pinching the skin of the paralyzed side is not followed by 
any reflex contraction soon after the onset, though the deep reflexes may 
be present, but later, when the primary shock has passed away, it will be 
found that the skin reflexes as well as the knee-jerk and other deep reflexes 
are exaggerated, particularly upon the paralyzed side. Irritation of the sole 
of the foot almost invariably causes extension of the big toe (Babinski's 
reflex), a reversal of the normal plantar reflex, which is flexion of the 
toes. Ankle-clonus is also frequently present. 

In cases in which the bladder and the bowel are full at the time of the 
"stroke," the shock of the hemorrhage may result in involuntary evacua- 
tions, but in some cases the bladder and rectum are not only retentive, in 
the ordinary sense, but fail to empty themselves when they become full. The 
bladder of an apoplectic patient should, therefore, be frequently examined, 
and if the urine accumulates in excess it must be withdrawn by the catheter. 
If the urine is examined a trace of albumin is usually found in it, even if 
actual renal disease is not present. The temperature of the body immediately 
after a hemorrhage is usually subnormal. With reaction from the primary 
shock, which is often of brief duration, the temperature rises from one 
to three degrees, the chief change being on the paralyzed side. 

The unconsciousness of the early stage of apoplexy may last from a few 
hours to several days, according to the severity of the lesion. When it 
persists for any length of time the prognosis is correspondingly bad. 
In some cases the depth of the coma decreases and the patient emerges 
to some extent, only to sink back again into deep coma and high fever a few 
days later when a secondary hemorrhage takes place, perhaps bursting into 



920 DISEASES OF THE NERVOUS SYSTEM 

the ventricle, or secondary irritation of the brain, produced by the pres- 
ence of the extravasated blood, develops. In other cases in which the 
extravasation of blood has been limited, and the parts damaged are not of 
vital importance, the patient gradually improves in his mental state and 
progresses toward recovery. In most cases, however, the mind never com- 
pletely recovers its previous acuity. 

The persistency of the hemiplegia also varies greatly in different cases. It 
may remain absolutely unchanged, one-half of the body being helpless, or 
it may diminish in severity and even greatly improve to the extent that the 
patient can walk about and write. In most of the cases, however, in which 
this much to be desired result is attained, the lesion has probably been due 
to embolism or thrombosis rather than to an actual hemorrhage. 

Many patients after an attack of apoplexy not only suffer from a degree 
of mental failure, but in addition become exceedingly irritable or emotional, 
crying, laughing, or getting into a furious temper at slight causes. Distinct 
loss of emotional control has been said to be particularly prone to occur 
when the lesion involves the frontal lobes. 

There still remain to be considered several additional symptoms of apo- 
plexy which are often present. The most important of these is aphasia. 
It is most common in cases in which the right side is paralyzed, because the 
speech centre is chiefly in the third left frontal convolution. If the patient 
is left-handed, however, the aphasia is present when the left side is paralyzed. 
The symptom aphasia varies very greatly in the time at which it is first 
evident and in its severity. Not infrequently it is one of the first signs of 
a beginning apoplexy, the speech becoming suddenly confused and indis- 
tinct. In most cases, however, the aphasia is first noticed after the patient 
recovers from the immediate effects of the stroke. The persistency of the 
aphasia varies greatly. In some cases it remains so severe that the patient 
has great difficulty in making himself understood. In others it improves 
so greatly that it may entirely disappear, or only be present when the patient 
becomes very tired or excited. 

Another special symptom is hemianopsia, which is of the homonymous 
type, that is, the corresponding halves of the visual fields are darkened 
because the temporal half of one retina and the inner or nasal half of the 
other retina has lost its visual function. 

Hemianesthesia persisting after recovery from the primary shock is a rare 
symptom and is never complete, thereby differing from the hemiansesthesia 
of hysteria- The sense of heat or cold or touch may be impaired, but total 
loss of the senses does not take place. 

When the power of recognizing objects placed in the hand is lost (astereog- 
nosis) it indicates a lesion in the superior parietal portion of the cortex 
on the opposite side. (See Fig. 121.) 

In some cases of hemiplegia of a severe type bed-sores develop on the heel 
or buttock of the affected side. The tendency to this accident can be greatly 
decreased if the patient is not permitted to lie in one position for long periods 
of time, and if great care is taken as to the cleanliness of the skin in the 
places where pressure is marked. 

As a sequence to an apoplexy we find not only persistent paralysis, but 



HEMORRHAGE INTO THE BRAIN 921 

as time goes on contractures occur in the affected limbs. The forearm 
and hand, however, suffer far more than the leg. The flexor muscles 
being stronger than the extensors, the hand is usually found in marked 
flexion upon the wrist, and the fingers are turned into the palm of the hand. 
The leg is usually held in the position of extension so that it cannot be bent 
at the knee, and for this reason it is often swung with a lateral movement 
from the hip when the patient attempts to walk. These contractures are 
usually much diminished when the patient is asleep, and are due to 
degenerative changes in the crossed pyramidal tracts. (See Fig. 116.) 
Occasionally, that curious mobile spasm of the fingers or other members, 
called " athetosis," is a sequence of apoplexy and posthemiplegic chorea 
may develop. This is commonest in the hemiplegias of childhood, but 
occurs in adults. Full doses of strychnine may produce spastic contractions 
in old cases of hemiplegia. Next to signs of spasm the most common 
symptom as a sequel is muscular atrophy, which is due in part to disuse 
of the muscles in the paralyzed limbs and does not develop till some 
time after the acute stage of the attack. Charcot has reported instances in 
w 7 hich true trophic joint changes took place, but they are exceedingly 
rare. 

The symptoms of an attack of apoplexy in which the lesion has been due 
to rupture of a branch of the middle cerebral artery having been described, 
there still remain to be considered those additional symptoms which develop 
when other parts of the cranial contents are affected by the giving way of 
other vessels. 

When a vessel in the dura mater is ruptured, usually as the result of an 
injury, it is the middle meningeal artery or vein which suffers as a rule. 
The clot which is formed is either outside the dura mater (extradural) 
or beneath it (subdural). The noteworthy peculiarity of these cases is 
that the primary unconsciousness due to a blow speedily disappears, the 
patient may recover his normal mental state, and then, after an interval 
varying from some minutes to several hours or days, becomes heavy and 
dull, and finally comatose. Spasmodic movements of the muscles on one 
side of the body, followed by paralysis, may develop. If the extravasation 
of blood is large, the pupil on the paralyzed side is contracted and that on the 
side of the hemorrhage is dilated. This is called the ''Hutchinson pupil." 
The eyes are turned away from the lesion, whereas in the acute stage of an 
ordinary apoplexy they are turned toward it. It is in this form of apoplexy 
that surgical interference is absolutely essential to save life. Such hemor- 
rhages sometimes occur in the insane without a history of injury, particularly 
in paretics and in chronic alcoholics. 

In hemorrhage from a vessel upon the cortex, as one of the branches of 
the Sylvian artery, it is important to recall the fact that muscular spasm, or 
a convulsion, usually ushers in the attack due to the disturbance of the 
cells in the motor area. 

When the blood finds its way into the lateral ventricles, a general convul- 
sion affecting the entire body may develop. Such cases usually pass into 
deep coma and soon die. 

When the lesion is in the pons the temperature is usually soon hyperpyretic, 



922 DISEASES OF THE NERVOUS SYSTEM 

the pupils are tightly contracted, swallowing is difficult, and the respiration 
is very slow. Death comes rapidly in these cases as a rule. 

Under the name of u ingravescent apoplexy" a condition is met with in which 
the symptoms develop very gradually, beginning, it may be, by an attack 
of vertigo or aphasia, followed by the slow development of the other 
symptoms already described, so that several days may elapse before the 
entire symptom-complex of apoplexy is present. 

Diagnosis. — An attack of apoplexy, or hemorrhage into the brain, must 
be separated from a number of conditions which may closely resemble it. 
Two conditions which resemble it so closely as to be inseparable in some 
cases are thrombosis and embolism of the cerebral vessels. The symptoms 
produced by these accidents will be found described below. 

An ordinary attack of syncope can readily be differentiated by the pallor, 
the feeble pulse, the weak heart of a fainting attack, and the quick recovery 
of the patient after receiving some rapidly acting diffusible stimulant. 

In epilepsy the peculiar initial cry, the bloody froth at the mouth, the general 
convulsion, and the deep unconsciousness are more constant and severe than 
in apoplexy, even if the hemorrhage takes place in the cortex. Epilepsy is more 
common in the young, apoplexy in those of advanced years, and there may 
be scars to indicate previous severe falls in epileptics. A history of epilepsy 
will practically settle the diagnosis, although the epileptic is liable to apoplexy. 
The respiration in the coma of apoplexy continues deep and noisy, the 
lips and cheeks of one side flap in the air current, showing paralysis, 
and weakness of one arm and leg may be ascertained. In the coma of 
epilepsy the breathing soon becomes quiet. Rarely in epilepsy weakness 
of one side of the body or of one limb may appear as the patient emerges 
from the coma; this postepileptic hemiplegia is ascribed to exhaustion, for 
it passes off in a few hours or days, but it may put the diagnosis in doubt 
for a time. 

From the stupid stage of acute alcoholism apoplexy can be differentiated 
by the history of the patient, by the odor of alcohol on his breath, by the fact 
that both legs are moved if they are irritated by pricking, proving the absence 
of hemiplegia, and by the cool skin as compared to the hot, dry skin of 
apoplexy. It is, however, possible for an apoplectic to have induced an 
attack by the use of alcohol, and therefore the odor of alcohol on his 
breath is not of great importance from a diagnostic standpoint. 

Opium poisoning is differentiated by the presence of contracted pupils, 
by the fact that by shouting the patient can be aroused, by the absence 
of paralysis, and by the presence of the corneal reflexes, 

The coma of uraemia and of diabetes may also be mistaken for apoplexy, 
but in uraemia there may be oedema of the lower extremities, and there is a 
urinous odor about the body and breath of the patient. If the renal disease 
is of the parenchymatous type, the peculiar waxen appearance of the patient 
and the urine heavily loaded with albumin will make the diagnosis clear. 
If the uraemia is of the type caused by chronic contracted kidney, these latter 
signs will not be present nor will oedema be found, and as apoplexy often 
complicates this disease the diagnosis may be most difficult. Unless the 
coma is very deep one side may be moved far more than the other, reveal- 



HEMORRHAGE INTO THE BRAIN 923 

ing the hemiplegia of apoplexy. However, in uraemia the cerebral affection 
may be more pronounced in one hemisphere, thus causing a hemiplegia 
("ursemic apoplexy"). In diabetic coma the sweet odor of the breath and 
the presence of sugar and acetone in the urine will make the diagnosis 
possible. 

In sunstroke likewise hemiplegia may be found, which is not an apoplexy 
in the ordinary sense. 

Finally, it must not be forgotten that apoplectiform attacks not rarely 
develop in the course of general paralysis of the insane. In this disease the 
speedy return to consciousness and recovery of power in the affected limbs, 
with the physical signs of this disease and the mental symptoms, will 
render a diagnosis possible. 

The separation of the paralysis due to hemorrhage from that due to 
thrombosis depends more upon the history of the patient than upon the 
symptoms actually present. As already stated, hemorrhage usually fol- 
lows some effort and takes place during waking hours, whereas the paralysis 
of thrombosis develops during periods of quiet and rest, as during sleep, so 
that the patient wakes to find the palsy present. In cases of hemorrhage 
premonitory symptoms are not common, but in thrombosis they are nearly 
constant. Thrombosis is most frequent in the aged or prematurely senile, 
and in syphilitics. Again, thrombosis does not cause such violent symp- 
toms nor is the onset of the symptoms so sudden, but consciousness is pre- 
served or is not so completely lost, or if moderate coma is present it is 
brief in duration and is followed by mental clearness. Finally, in cases of 
thrombosis, the recovery of power in parts of the paralyzed side may be 
quite rapid, and at the end of a few days only a few muscles, as one arm or 
leg, are affected. Such cases are, however, often mentally feeble, emotional, 
and forgetful after the attack. There is often to be found a history of 
syphilis, of arteriosclerosis, or an infectious disease, which has predisposed 
the patient to a formation of a clot by causing disease in the lining of the 
bloodvessel or producing changes in the blood. 

Embolism can be determined by the sudden onset of symptoms during 
the waking hours, as a rule, and by the discovery of some source of clot or 
foreign body, as in an endocarditis with vegetations or a septic focus else- 
where. Unconsciousness, when it develops, may be as profound, but is 
usually more transient than in hemorrhage (Mills), and is often entirely 
absent. The appearance of the patient is not so alarming as in hemor- 
rhage, and localized or general twitching may be present in the affected 
limbs. Not rarely as a collateral circulation is established, the symptoms 
improve with great rapidity and after a few days may amount to only a 
partial monoplegia. It must be recalled, however, that in some cases of 
thrombosis and embolism the symptoms may be so like those due to hemor- 
rhage that a differentiation is almost impossible. 

The chances of the case being one of hemorrhage rather than embolism 
or thrombosis is as 6 to 1, according to Dana. 

Prognosis. — Many cases of hemorrhage into the brain survive the first 
rupture, but if so they nearly always fall victims to subsequent attacks. Out 
of 441 cases occurring in St. Thomas' and St. Bartholomew's Hospitals, 



924 DISEASES OF THE NERVOUS SYSTEM 

London, 375 proved fatal, a mortality percentage of 85. This per- 
centage is, however, far too high for private practice, where milder cases 
are often seen. In the severe cases in which the coma is profound, the 
temperature low and then quite high, the paralysis severe, and control 
of the bladder or bowels impaired, death will probably occur in the first 
attack, and if Cheyne-Stokes breathing is present death nearly always takes 
place within a few hours. If the hemorrhage affects the pons or cerebellum 
death may come on speedily, but when the hemorrhage is small the patient 
often survives. When the hemorrhage is cortical the prognosis is better 
than in the other forms unless the pressure symptoms are severe. The 
patient not rarely dies from pulmonary oedema or pneumonia as an inter- 
current disease. 

Treatment. — Apoplexy, like other forms of internal hemorrhage, cannot 
be materially benefited by medicinal treatment. If nature does not form 
a clot to plug the bleeding vessel, the hemorrhage must continue until it 
has done so much damage that death is inevitable unless the vessel is on the 
surface or in the meninges, when surgical relief should be given. Again, the 
pressure with which the blood escapes into the soft textures of the brain is 
so great that if the leak is of any size the mechanical injury to the cerebral 
tissues must be very great, and for this reason the organ is permanently 
disabled. 

Until the recent researches of Cushing, of Baltimore, in regard to the 
significance of high arterial pressure in cases of hemorrhagic extrava- 
sations inside the skull, it was universally taught that the presence of 
a full, bounding pulse in a case of apoplexy indicated venesection, par- 
ticularly if at the same time there was distinct venous engorgement, the 
thought being that by this means the blood pressure would be lowered, and 
that there would be a corresponding decrease in the leakage from the rup- 
tured vessel. Cushing's investigations have apparently shown beyond all 
doubt that the high arterial pressure which is so constantly found in persons 
who suffer from hemorrhage inside the skull is an effort of nature to main- 
tain the blood supply to the vital centres at the base of the brain, and that 
if this blood supply cannot be maintained because of a fall in arterial pressure 
death speedily ensues. In other words, the maintenance of a high arterial 
pressure in these cases is an advantageous sign, and any marked diminution 
in arterial tension is an indication that the vasomotor centre is becoming 
paralyzed and that the blood supply to the centres at the base of the brain 
is becoming impaired. If Cushing's studies are correctly interpreted by him, 
venesection or the administration of vascular sedatives, with the purpose 
of lowering tension, is therefore a distinctly harmful method of treatment, 
and truth demands that we should admit that the physician can do little 
if anything in the way of controlling the escape of blood. 

For the purpose of apparently making an effort to do good for the sake of 
the friends who may demand activity rather than masterly inactivity, a hot 
mustard foot-bath may be given, and some diffusible stimulant like 
Hoffmann's anodyne may be used if the patient is able to swallow, or 
atropine may be given if arterial tension falls and the surface becomes cold 
and clammy. 



INFANTILE CEREBRAL PARALYSIS 925 

If vomiting occurs, the patient should be promptly turned on one side 
so that free drainage from the mouth may take place, and in order that 
particles of food may not be drawn into the respiratory passages. 

If the tongue falls back in such a manner as to make the breathing 
difficult it should be drawn forward by means of the fingers covered with 
a towel. If, by chance, the patient is convulsed, his tongue should be pro- 
tected from damage by placing between the teeth a penholder or tooth-brush 
handle covered with a piece of muslin. 

The patient's body should always be put in that position in which breathing 
is most easily carried on. 

The treatment after the hemorrhage has ceased consists in absolute 
rest, in the application of an ice-bag to the head, and attention to the 
bowels and bladder to prevent them from becoming overdistended. 
Gentle purgation is probably advantageous for its influence upon the 
brain. If any evidence of nervous excitation exists, it may be controlled 
by small doses of the bromides or morphine. If any tendency to sec- 
ondary reaction develops in the course of a few days, cold to the head 
and small doses of aconite to quiet the circulation may be administered. 
Later on, with the hope of diminishing the paralysis, iodide of potassium 
may be given in moderate doses in order that it may aid in the absorption 
of the extra vasated blood and remove products of inflammation. There is 
little use in giving the iodide of potassium for the purpose of causing absorp- 
tion earlier than two or three weeks after the hemorrhage. Strychnine is 
usually not valuable in these cases, as it is very apt to produce spasm or 
contracture in the parts which are paralyzed by irritating the motor tracts 
in the spinal cord. 

From three to four weeks after the hemorrhage it is often advantageous to 
apply a slowly interrupted faradic current to the paralyzed muscles, with 
the object of maintaining their nutrition by exercise and keeping them in 
the best possible condition, in the hope that eventually they may receive a 
sufficient amount of nervous impulse from the cerebral centres to be able 
to respond sufficiently to permit the patient to move his limbs. Massage is 
another excellent means to combat the loss of power. Passive and active 
movements followed by a course of systematic exercises will render valuable 
service in combating secondary contractures of the paralyzed extremities. 
Great care should be taken that all stimulants which increase circulatory 
activity, and all foods which readily cause indigestion, be avoided, as these 
two factors tend to produce that most unfortunate complication, another 
hemorrhage. 

INFANTILE CEREBRAL PARALYSIS. 

Definition. — As a result of injury or disease of the brain during fetal life 
or soon after birth, it not rarely happens that certain portions of the cere- 
brum fail to develop, and as a consequence a number of very characteristic 
conditions are produced, which depend in their nature upon the site and 
size of the atrophied region. 

These conditions can be grouped in three divisions: In the first there is 



926 DISEASES OF THE NERVOUS SYSTEM 

a spastic paralysis which may be limited to one side of the body (spastic 
hemiplegia), or it may be bilateral (spastic diplegia). In spastic diplegia 
the legs may be affected alone or the arms and legs may both be involved. 
The second class is chiefly characterized by mental failure varying in severity 
from slight intellectual deficiency to absolute idiocy. In some instances the 
defect is manifested by epileptic attacks. The third class presents disorders 
of the special senses, such as blindness, deafness, mutism from deafness, 
and it may be epileptic seizures as well. 

Etiology. — Acute infectious disease occurring in the mother during preg- 
nancy may result in lesions in the fetal brain. Syphilis may also act in 
this manner. It is probable, too, that definite developmental defects 
may be hereditary, as when the parent or parents are epileptics, neurotic, 
alcoholic, or otherwise degenerate. Premature labor is a frequent cause of 
diplegia. A very large proportion of cases develop as a result of injury 
during birth because of a meningeal or cerebral hemorrhage. In a few 
cases the damage is due to a fall in early infancy, and in still others there 
develops some time during the first three years of life a cerebral thrombosis, 
a hemorrhage, an encephalitis, or a meningitis which is followed by the 
brain symptoms about to be described. Such a condition may arise as a 
complication or sequela of any one of the acute infectious diseases of child- 
hood. A convulsion may be said to be the cause in certain cases, but it is 
probable that the lesion in the brain is responsible for this symptom rather 
than that it is the provoking factor. Finally, there are certain cases in which 
it is impossible to discover any cause whatever. 

Pathology and Morbid Anatomy. — When spastic paralysis is present it is 
due to a lesion which involves the motor portion of the cerebral cortex and 
neighboring convolutions. The lesion itself in long-standing cases is scle- 
rotic or atrophic in character and is associated with similar changes in the 
motor fibres, which pass from the cortex, and in the basal ganglia as well. 
In some cases the sclerotic change is limited to these ganglia. When there 
is diplegia both sides of the brain are involved. In that type of case in 
which mental impairment is present the atrophy and sclerosis affect the 
anterior convolutions of the brain, and when disorders of special sense are 
present it is because the perceptive centres of the senses affected are involved 
in the damaged area. It is readily seen, therefore, that as the lesions are 
distributed so are the manifestations of the disease varied. 

The exact nature of the cerebral lesions has been found to be of several 
types: (1) A localized atrophy, or failure of development, may produce 
an excavation of the surface of the brain, usually due to meningeal 
hemorrhage at birth, with formation of a clot which indents the delicate 
cortex permanently. This indentation is called porencephaly (poros, the 
Greek word for "hole"). (2) A sclerotic process with overgrowth of con- 
nective tissue and atrophy of the nervous protoplasm may be present. (3) 
Imperfect development of the cerebral cells may be found. (4) Atrophy 
may follow cerebral softening produced by the closure of a vessel by an 
embolus or thrombus. (5) An inflammatory process in the pia mater 
may cause an adhesion to the cerebrum and so cause atrophy (meningo- 
encephalitis). (6) A cerebral hemorrhage may not only destroy the cerebral 



INFANTILE CEREBRAL PARALYSIS 927 

tissue, but cause a cyst to develop. (7) A cyst may cause atrophy from 
pressure. (8) Hydrocephalus, in which state the cerebral ventricles may be 
so distended that the brain tissues atrophy from pressure. (9) Rarely an 
external hydrocephalus may produce the same results. 

Symptoms. — The symptoms in a child affected by this accident, like 
those of ordinary apoplexy, vary greatly in speed of onset, in severity, and 
in type. AYhen the lesion occurs at birth there are often no symptoms for 
several days or even weeks, except it may be an unusual limpness of the 
limbs and some difficulty in swallowing. In other cases unilateral spasms 
or general convulsions speedily develop, but these are not of long duration, 
and it is noticed that the child's head is not held erect, but falls from side to 
side, backward or forward. The convulsions may affect the entire body, 
or be confined to the side in which paralysis is about to develop. Associated 
with these convulsions there is a marked rise in temperature, the fever some- 
times reaching as high as 105°. After the convulsion there may be post- 
convulsive coma, which may last several days. Gradual improvement now 
takes place, and as the child returns to consciousness it is found that there 
is loss of power upon one side of the body. Shortly afterward it is also noticed 
that the arm upon the affected side is not only paralyzed, but that it is in a 
somewhat spastic state. The leg suffers in a similar manner. Later on, 
clubfoot and a sharply flexed hand develop from secondary contractures. 
The paralyzed limbs fail to develop as they should, become atrophied, and 
are often considerably shorter than the limbs upon the healthy side. The 
reflexes are exaggerated. Sensation is not impaired. 

If the child survives, the paralyzed parts gradually become markedly 
distorted and tenotomies may be necessary to prevent the contracture from 
causing so great a deformity as to make any motion impossible. Even these 
means may not make walking possible. If the intellectual portions of the 
brain are not involved, and if the patient reaches the years of puberty, it not 
infrequently happens that by prolonged training a very remarkable degree of 
ability is developed in the non-paralyzed side so that the individual can follow 
some pursuit which will render him self-supporting. In other instances, how- 
ever, the spastic condition of the affected limbs is very marked, the hand is 
sharply flexed at the wrist, and athetoid movements of the fingers may be 
present whenever any attempt is made to move them. These athetoid move- 
ments occur very soon after the paralysis is noticed in certain cases. In 
others they do not develop for a long time. The state of the legs is even more 
noticeable, if such a thing be possible. Here we find that the parts are at 
once placed in strong extension if they are touched, the muscles of the calf 
are tightly contracted and the feet are inverted and turned inward. The 
thighs are abducted. When the attack comes on after the child has learned 
to speak, there may be marked aphasia for a time, but this symptom often 
gradually disappears. 

Spastic diplegia may affect either the arms or the legs, usually both arms 
and legs, and is characterized not only by loss of power in these parts, but 
by rigidity, which is particularly marked in the lower extremities. The 
symptoms usually develop slowly, not acutely as they do in spastic hemi- 
plegia. 



928 



DISEASES OF THE NERVOUS SYSTEM 



Fig. 119 



Various deformities of the lower limbs occur, and the muscles of the 
trunk, particularly at the back, are so rigid that the child is as if fixed 
in a plaster cast. In other instances where the condition has developed 

some time after birth, the patient can 
sometimes walk by the aid of a cane 
or crutches, but in those instances in 
which the lesion is severe the contrac- 
tures and athetoid movements, the exag- 
geration of the reflexes, and the imper- 
fectly developed muscles all combine to 
make the child absolutely helpless. 
There is no loss in the control of the 
sphincters nor any trophic disturbances 
in the way of bed-sores, nor are there 
any sensory disturbances. 

Both of these types not infrequently 
suffer from epileptic convulsions, which 
may be of the Jacksonian type. In 
those cases which are due to lesions in 
the intellectual area of the brain, idiocy 
may be present. In those instances in 
which the defect of mental power is not 
complete the patient is called an imbe- 
cile. Such patients are often subject to 
violent outbursts of anger, to attacks of 
malicious mischief, and are often exceed- 
ingly filthy in their habits. 

In the cases in which the posterior 
portions of the brain are affected, the dis- 
orders of special sense do not usually 
make themselves manifest until the child 
is at least a year or eighteen months old. 
Often prior to the discovery of any 
symptoms of disorder of special sense, 
epileptic convulsions have called atten- 
tion to the fact that the cerebral de- 
velopment is imperfect. In some in- 
stances the disorders of vision may amount to nothing more than a hemia- 
nopsia. In others there may be total blindness, or deafness, or loss of 
smell and taste. In these cases also ordinary epilepsy and Jacksonian 
epilepsy are often present. In some instances minor epilepsy takes the 
place of major epileptic attacks. 

When a hemiplegia develops in a child of a year or more it is usually due 
to hemorrhage or embolism or to the polioencephalitis of Strumpel rather 
than to meningeal disease. 

Diagnosis. — The diagnosis in a well-developed case of infantile cerebral 
paralysis is not difficult. The early development of the malady (after a hard 
labor it may be) , the marked arrest of normal development, and the epileptic 




Hemiplegia, with contractures. The patient 
had suffered since the age of two years. 
(Curschmann.) 



INFANTILE CEREBRAL PARALYSIS 929 

convulsions, with the spastic state of the muscles, all separate this form of 
infantile paralysis from those forms which depend for their existence upon 
lesions in the spinal cord, for in the latter the paralyzed parts are flaccid. 
There are, however, two forms of spinal spastic palsy of childhood with 
which this condition can be confused, one of which is the so-called " hered- 
itary spastic spinal paralysis," but in this disease the mental symptoms 
are lacking and the condition is progressive. The second state which 
resembles this disease is " amaurotic family idiocy," but in this malady the 
paralysis may be flaccid or spastic and blindness is an early symptom. 

Prognosis. — It must be evident that the prognosis as to complete recovery 
in severe cases is anything but good. In those cases in which the mental 
powers are feeble and convulsions frequently recur, the outlook is bad both 
as to recovery and a long duration of life. If they live they are hopeless imbe- 
ciles or idiots. When the affection is confined chiefly to one side of the brain 
— that is, when there is hemiplegia — adult years may be reached and ordinary 
mental pursuits followed in many cases. 

Some of these patients, moreover, can be materially improved by proper 
training, in which instance special senses which are not impaired, or intel- 
lectual centres which have escaped the wreck, may be developed to such an 
extent that a fair degree of comfort and intelligence may be attainable. 
The convulsions cannot be cured, as they depend upon faulty development, 
but they may be modified by skilful treatment, consisting in the administra- 
tion of nervous sedatives, the avoidance of all causes of nervous excitement 
and irritation, and the moderate employment of the bromides. As a rule, 
better results can be obtained from hygienic methods and from mental train- 
ing in an institution devoted to this purpose than can be obtained at home. 
At one time it was considered that operative interference might be of very 
great value in these cases, but we now know that little can be expected from 
such a plan of treatment. In those cases in which the skull has seemed to 
be abnormally small it was proposed that the skull should be cut, or bone 
should be removed, in such a way as to permit expansion of the brain. But 
the smallness of the skull is probably more dependent upon the size of the 
brain than is the size of the brain upon the condition of the skull. In some 
instances the parents prefer running the risk of the child's death as the 
result of such a grave operation rather than to have it continue a hopeless 
invalid, and in such cases, if there are distinct localizing symptoms, epileptic 
or otherwise, the question of cerebral localization and operation must be 
carefully considered. 

Little's Disease. — The name " Little's disease" has been applied by some 
writers to the cerebral palsies of childhood; but is probably best restricted 
to cases in which there is congenital spastic rigidity of the limbs, particu- 
larly of the legs, tending to improvement. In Little's disease, thus defined, 
there is normal mental capacity and no epilepsy or athetosis. The condi- 
tion is purely motor from defective development of the pyramidal system 
in the brain or, according to Dejerine, in the spinal cord. 



59 



930 DISEASES OF THE NERVOUS SYSTEM 



APHASIA. 

Definition and Symptoms. — Aphasia is a condition in which the function 
of speech becomes impaired or arrested as the result of disease involving 
those parts of the brain which are concerned with the expression of ideas 
in words. For the power of speech it is necessary that the individual shall 
have not alone the motor centres which will cause the proper muscular 
movements which give rise to certain sounds, but in addition there must 
be, in close association with these centres, others in which the conception of 
an idea must originate, and still others in which a sense of the appearance 
of words, or sounds of words, is stored. When a child is learning to talk, 
an object, such as a horse, is pointed out to him, and the word "horse" is 
frequently repeated at the same moment. He therefore learns to associate 
a certain shape and form with the word "horse." For him to do this it is 
necessary that his visual apparatus shall carry to his brain a certain form, 
and that his brain should store up that form as typifying a certain object. 
It is also necessary that his auditory apparatus shall carry to his brain a 
certain sound or sounds, and that his brain shall associate this sound with 
the form that he has seen. In addition it may be that he has touched or 
stroked the horse, and so his sense of touch has conveyed to his brain a cer- 
tain model, or form, which is associated with those received by means of 
his eyes and ears. When, therefore, he sees a horse a second time the mem- 
ories or imprints derived from these various sources are utilized, and he 
attempts to reproduce the word "horse" by a process which calls into play 
certain muscles which are necessary for making this sound. Speech is there- 
fore in one sense a complicated function, closely connected with the organs 
of special sense, of intellection, and with the motor neurones as well. This is 
perhaps made more clear by the following diagram: 



A 

o- 




A, pathways for receiving imprints or models ; B, centre for storage of models; C, centre for storage of 
motor memories ; D, concept centre ; E, motor centres for controlling muscles of speech at F. 

A visual impulse, an auditory impulse, a touch impulse, an olfactory 
impulse, or a taste impulse, or all of them together, pass to the centre B, 
where they are received and stored. From B these memories or imprints 
are transmitted, whenever they are needed, to those centres in the brain 
which are concerned with the power of the conception of an idea, or they 
may be transferred directly to C, which may transform them into speech 
by mimicry, without any idea or higher intellectual process than that con- 
cerned with imitation. If the child thinks of a horse at D, he receives 



APHASIA 931 

memories of the character of a horse from B and sends from D an impulse 
which cause C to send impulses to the organs of speech. It is evident, 
therefore, that if the sensory tracts are diseased before the centres for storing 
the character of external objects have received and retained models or 
impressions speech will be impossible, or if any part of the mechanism 
described in the diagram is undeveloped or damaged, the entire chain 
fails because one of its links is broken. 

This process may, however, be even more complicated than that described. 
Thus, there may be stored in the storage centre not only the model or imprint 
of a horse but also the additional memory of the appearance of the word 
" horse" when in type, and in addition there may be stored the memory of 
certain movements which are characteristic of a horse, so that the child can 
imitate its movements or perhaps draw an outline of its appearance. While 
pantomime and drawing are not speech, they are so nearly related to it as to 
really form part of it. Again, it is necessary that there should be stored at 
C the models or memories of those muscular movements which will give rise 
to the sound of the word horse, for this is part of learning how to talk. 

In certain cases in which the brain is diseased the patient may see and 
feel and hear a horse, and his concept centres may know perfectly that a 
horse is before him, or that the word " horse " is in print, but he cannot say 
the word "horse "'because the centres concerned with the storage of mem- 
ories of the muscular movements necessary to speak the word "horse" are 
destroyed. He may write the word " horse " or draw a horse, but he cannot 
say "horse." 1 To this form of motor aphasia the word aphemia is applied. 
If the centre in which the memories of how to write the word "horse" are 
destroyed the condition is called agraphia, and if those in which the muscular 
movements required to describe a horse by gesture are diseased it is said 
to be amimia. When the tracts that associate the storage centres for mem- 
ories of words are interfered with, the patient skips, or jumbles, or repeats 
his words, and this is called conduction aphasia; and if he speaks one word 
when he means another, it is called paraphasia. 

On the other hand, when the sensory portion of the speech mechanism 
is diseased the patient may be able to say the word "horse," but if he sees 
a horse he cannot say that he has seen it because he has lost the memories 
of the horse; or if he sees the word "horse " in print, he may be able to repro- 
duce the letters in writing, in their order, but he is entirely unable to read, 
for he has lost the memory of the significance of these letters when so joined. 
This is called alexia, or word blindness, an unfortunate term, as blindness 
would indicate failure of visual power, which does not exist. Again, in cer- 
tain cases there is loss of memory of sounds. The voice of a speaker may 
be heard and even imitated, but the patient understands nothing more than 
if an unknown language was spoken. It conveys no idea to his mind. This 
is called word deafness — another unfortunate term, because hearing in the 
ordinary sense of that word is perfect. Apraxia is still another nearly 
related state in which the patient fails to appreciate the purposes or uses 
of an object. He may see, hear, and touch a knife or a coin, but his mind 
cannot grasp its uses. 

1 As a matter of fact, these powers are usually lost. 



932 DISEASES OF THE NERVOUS SYSTEM 

When we come to study the lesions which produce these disturbances 
in the ability to express an idea, we find that when the patient has aphemia 
or motor aphasia the damage has been done to the third left frontal con- 
volution (Broca's convolution). In such a case he also cannot write either 
his own ideas or the words that he hears spoken, but he can copy. If the 
lesion is a severe one, his power of understanding words he sees written or 
hears spoken is usually impaired. In other words, he also suffers from 
word-blindness and word-deafness. When he has word-blindness or alexia, 
the lesion is at the angular gyrus. If there is a pure alexia the lesion is in 
the subcortical substance of the angular gyrus. Aphasia also develops 
when a lesion takes place from hemorrhage, embolism, or thrombosis in the 
knee of the internal capsule, for at this point the fibres which convey 
speech impulses are destroyed. 



TUMORS OF THE BRAIN AND ITS MEMBRANES. 

Intracranial tumors arise from the substance of the brain itself or from 
the membranes which surround it. A great variety of these growths have 
been recorded, but by far the most common are tubercle, gumma, glioma, 
and sarcoma. Cancer, fibroma, osteoma, neuroma, and vascular tumors 
also rarely occur. Echinococcus cysts may develop. 

Etiology and Frequency. — The causes of these morbid growths are not 
understood except in the case of tubercle and gumma. Sex seems to exercise 
a very distinct influence, for we find that males suffer very much more fre- 
quently than females. Gowers states that out of 650 cases of brain tumor 
440 occurred in males to 210 in females. Dana gives the figures at 644 to 
320, and Starr's figures are nearly identical in their proportions. This great 
preponderance in males is not explained by either syphilis or injury, for 
there is no greater frequency of gumma in men than in women. On the 
contrary, tubercle and glioma are the growths that are particularly fre- 
quent in men. Gowers has shown that after the first six months of life till 
old age all ages suffer about equally. Thus, the percentage in the first 
decade is 18.5, in the second 14, in the third 20, in the fourth decade 18.5, 
and in the fifth 14. Most of the growths in childhood are tuberculous, 
and indeed they form 53 per cent, of all growths at all ages, if gumma be 
excluded. 

Pathology and Morbid Anatomy. — Tumors of the brain affect its tissues 
in its different areas as follows, according to Gowers: In the hemispheres 
297, in the cerebellum 179, in the base of the brain 76, in the pons 59, in the 
central ganglia 48, in the medulla 31, in the corpora quadrigemina 13, and 
in the cms 10. 

Tuberculous tumors occur as solid, firm, round masses which are not 
rarely multiple. Their size varies from that of a pea to a hen's egg or even 
larger. The growth starts from the lymphoid sheaths of the vessels, and 
rapidly obliterates them. For this reason it is devoid of vessels and its tissue 
soon undergoes necrosis, so that on section it is cheesy and shows spots 
of softening. As the surface is soft, and the surrounding brain substance 



TUMORS OF THE BRAIN AND ITS MEMBRANES 933 

is also softened, the mass is clearly outlined, hence the name tuberculoma. 
Finally, the growth may become calcified or undergo suppuration. Tuber- 
culous growths are often found in the cerebellum, and they also occur in the 
pons and cerebrum. When in the cerebrum they are usually found along 
the great vessels in the interpeduncular space or in the fissure of Sylvius; 
not rarely the growth is near a Pacchionian body, but it may be found in 
the depths of the centrum ovale. 

Gummata of the brain rarely reach a size greater than that of a 
hickory-nut. They are also somewhat cheesy in appearance and have 
an irregular surface, which may be gelatinous, or indurated and hard, 
and enclosed in a fibrous capsule. These growths are thought to spring 
from the bloodvessels of the dura mater. 

Sarcoma occurs as round, oval, or spindle-cell tumors which destroy the 
tissues of the brain as they grow. When they are of the gliomatous type 
they differ greatly from all the growths so far described, for they are not 
round, but extend by a process of infiltration between the nerve cells. They 
may be soft and mucoid (myxoglioma), or firm and fibrous (fibroglioma). 
Gliomas of the soft variety are liable to hemorrhage. A cystic form of 
glioma due to softening is not rare. Gliomata are usually single. 

The secondary changes produced by these growths are of importance 
and depend chiefly upon the pressure of the tumor upon healthy tissues 
which in this way are destroyed. The very growth of the tumor inside the 
skull also increases intracranial pressure, and if it be so situated that it 
prevents the free passage of cerebrospinal fluid from the choroid plexus 
in the lateral ventricle through the third ventricle and the iter a tertio ad 
quartum ventriculum, then distention of the lateral ventricles or internal 
hydrocephalus develops. A tumor of the pons, of the corpora quadrigemina 
of the middle lobe of the cerebellum, or in the third ventricle may cause such 
obstruction. A third result of the intracranial tumor is irritation of the 
nerve cells of the brain and inflammation in them or in the meningeal 
membranes, and lastly it may cause actual thinning of the skull by the 
pressure induced. 

Symptoms. — By far the most common symptom of brain tumor is head- 
ache. This headache is usually severe and is characterized by sharp exacer- 
bations. In some instances it is dull and boring in character. In others 
it is sharp, stabbing, and tearing. By reason of its constancy it prevents 
sleep, and in its most severe paroxysms may produce temporary aberration of 
mind. The pain is widely diffused, and is particularly severe if it encroaches 
on the dura which is supplied with sensation by the fifth nerve. If the pain 
is localized it does not necessarily indicate that the growth is in that neigh- 
borhood, although in those cases in which the tumor is superficial the locality 
of the growth and of the pain is often identical. 

Next to headache in constancy as a symptom is vomiting. The expulsion 
of the stomach contents is usually spoken of as "projectile/' and in this 
respect it resembles the vomiting of certain forms of intestinal obstruction. 
Although the vomiting is severe, nausea is often absent. This symptom is 
supposed to be most frequent and severe when the growth is rapidly pro- 
gressing. Vertigo also occurs and varies in severity from slight dizziness to 



934 DISEASES OF THE NERVOUS SYSTEM 

a degree which causes the patient to fall. Not infrequently this vertigo 
causes the patient to walk in the direction in which it is not his intention to 
go. Vertiginous symptoms are more common in tumor of the cerebellum 
than in lesions elsewhere, and often the patient falls to one side. Another 
very important symptom of brain tumor is optic neuritis, which occurs in a 
large proportion of cases and which often enables us to make a diagnosis of 
brain tumor with the aid of the ophthalmoscope when the other symp- 
toms are so obscure that it is difficult to determine the nature of the 
patient's disease. 

Optic neuritis is usually most marked in cases of tumor of the cerebellum, 
of the midbrain, and of the great ganglia near the base. It occurs less fre- 
quently when the tumor is in the cortex or springs from one of these mem- 
branes, but the localizing value of neuritis is really not great. Nearly always 
both optic nerves are involved, although sometimes the lesion develops in 
one before it attacks the other. Gowers gives three reasons for this optic 
neuritis : First, irritation of the nerve fibres produced by the pressure which 
finally causes inflammation. Second, distention of the nerve sheaths and 
the lymphatic spaces of the papilla by subarachnoid fluid, which, perhaps, 
contains irritating poisons. The third cause is thought to be inflammation 
of the meninges, which is so frequently present, and which may extend to 
the optic nerve. 

Slowness of thought and gradual mental failure are not infrequently 
present. Sometimes aphasia develops. All these three symptoms are 
prone to occur when the tumor affects the frontal lobe, and the symp- 
tom of aphasia is, of course, most frequently developed when the left 
frontal lobe is involved. Epileptiform convulsions occur in about one- 
quarter of the cases of brain tumor, and are especially marked in those 
instances in which the growth directly or indirectly produces irritation of 
the cortex. So, too, there may be symptoms which for a time resemble the 
early stages of an apoplexy. Quite rarely actual rupture of a bloodvessel 
occurs, and so the symptoms are really apoplectic. 

Paralysis due to brain tumor may be unilateral or bilateral. When uni- 
lateral it may manifest itself as a monoplegia or as a hemiplegia. It is 
usually gradual in onset, and when hemiplegic in type is due to the presence 
of a growth in the upper part of the pons, in the crus, or in the internal cap- 
sule, or over a wide area in the cortex. Localized paralysis, such as mono- 
plegia, may be due to a growth involving the cortex or the subcortex before 
the fibres have come together so closely that even a small tumor must 
affect the whole bundle and produce widespread .paralysis. Such a mono- 
plegia involving the arm or leg is not infrequently associated with epilepti- 
form attacks, limited to the paralyzed part. If the growth is in the lower 
third of the pons the ordinary form of crossed paralysis may be present, the 
face being paralyzed on the side of the lesion, while the arm and leg are 
paralyzed on the opposite side. 

A rarer form of crossed paralysis (Weber's syndrome) may result from 
tumor of one crus involving the third nerve. The eyes are deviated to the 
side opposite the lesion and the pupil dilated on the side of the lesion, while the 
arm and leg, as in ordinary hemiplegia, are paralyzed upon the opposite side. 



TUMORS OF THE BRAIN AND ITS MEMBRANES 935 

Bilateral paralysis due to brain tumor can only occur when the growth 
is multiple and presses upon both sides of the brain, or when it is so situated 
that it can at once cut off fibres from both sides as they approach the middle 
area, as in the pons or in the medulla. Under these circumstances the legs 
are usually more affected than the arms, even though the face as well as 
the arms be included in the paralysis. Contractures, tonic spasms, or con- 
vulsions, either generalized or Jacksonian, may also occur. They usually 
indicate that the growth is situated somewhere near the cortex, where 
it produces other irritations. 

If the tumor is in the frontal area and grows forward it may cause 
protrusion of the eyeballs and paralysis of the extrinsic muscles of the 
eye, while if it grows backward it may cause spasms and epileptiform 
convulsions by the irritation of the motor area of the cortex. 

The development of a growth in the central region produces symptoms 
which are more definite than those which are found in association with 
growths elsewhere, because it is the motor area of the brain. Not infre- 
quently localized convulsions, or Jacksonian epilepsy, occur in such cases 
and paralysis limited to the same muscles may follow such an attack. The 
part in which the convulsion begins and the subsequent paralysis indicate 
the presence of the tumor in or beneath the centre supplying the centres 
controlling these muscles. Disorders of sensation in the affected limb may 
be present, consisting of numbness, tingling, and even hemianesthesia. 

When a tumor involves the parietal region the symptoms are not definite, 
but pertain chiefly to common sensation and " muscle sense." 

If the superior parietal lobule be invaded there is more or less loss of 
"muscle sense/' and often the symptom astereognosis is present. When 
the angular gyrus are involved, word blindness may be present. 

When that portion of the parietal area near the longitudinal fissure is 
invaded we not infrequently have spasms or convulsions in the lower 
extremities on the side opposite the lesion, because the growth begins to 
invade the part of the leg centre which is on the inner surface of the hemi- 
sphere. 

Tumors of the occipital lobe, if in the cuneus or otherwise near the cal- 
carine fissure, produce lateral homonymous hemianopsia. If the growth in the 
occipital lobe is sufficiently far forward to involve some of the parietal area, 
and so do damage to the angular gyrus, word -blindness and hemianopsia 
may develop, and if the invasion extends still farther, hemiataxia, hemi- 
anesthesia, and even some hemiplegia due to involvement of some of the 
fibres of the internal capsule may be present. 

In the first left temporal convolution brain tumor produces word-deafness, 
a form of sensory aphasia. Occasionally large tumors in the temporal 
area produce vertigo. 

Tumors of the corpus callosum are not only very unusual, but produce 
symptoms which are not very definite, being primarily those of mental 
failure and secondarily those due to encroachment upon neighboring parts. 
In addition to the general symptoms of brain tumor, the growth in this 
region produces hemiplegia, ultimately developing into paraplegia, great 
mental dulness, and finally coma. 



936 



DISEASES OF THE NERVOUS SYSTEM 




^O S P H E^ 

Showing the areas of the brain concerned with special functions. 1. Prefrontal area. 2. Central 
area. 3. Parietal area. 4. Occipital area. 5. Temporal area. (Modified from Fuller.) 



Fig. 122 




Corpus callosum. 7. Thalamus opticus. 10. Corpora quadrigemina. 11. Cms. 12. Pons. 
13. Medulla oblongata. 14. Cerebellum. 15. Fourth ventricle. (Modified from Reichert.) 



TCMORS OF THE BRAIN AND ITS MEMBRANES 



937 



When a tumor involves the great basal ganglia or the fibres of the internal 
capsule, hemiplegia is the most prominent symptom, and hemianesthesia 
and choreic movements may be present. 

If the posterior part (pulvinar) of the optic thalamus and nearby tissues, 
particularly one of the optic tracts, are involved by the growth, hemianopsia 
may be present, but this hemianopsia may be separated from that which 
is due to a lesion in the occipital lobe by the presence of Wernicke's sign 
(hemianopic pupillary inaction). 



Fig. 123 




10. Corpora quadrigemina. 



11. Crus. 12. Pons. 13. Medulla oblongata 
(Modified from Reichert.) 



14. Cerebellum. 



Having from these several symptoms determined that a brain tumor 
is present, it still remains for the physician to determine its locality, and 
this can only be done by his knowledge of cerebral localization. For this 
study the brain can best be divided into fifteen parts, most of which can be 
seen on the accompanying diagrams (Figs. 121, 122, and 123). 

The numbers in the text refer to the numbers in the figures and show 
where the growth would be situated. 



938 



DISEASES OF THE NERVOUS SYSTEM 



Tumors of the prefrontal area 
(See Fig. 121). 



Tumors of the central area , 
(See Fig. 121.) 



Tumors of the parietal area 
(See Fig. 121.) 



Tumors of the occipital lobe 
(See Fig, 121.) 



Tumors of temporal area 
(See Fig. 121.) 



Tumors of corpus callosum 
(Very rare.) 
(See Fig. 122.) 



7, 8, 9. 
Tumors of the great basal ganglia 

and capsule. 
(See Fig. 122, for 7 and Fig. 118 

for 8 and 9.) 



10. 
Tumor of the corpora quadri- 
gemina (vermis of the cerebel- 
lum) and pineal gland. 
Additional information as to 
these lesions can be had by study- 
ing Figs. 118 and 123. 



Table of Cerebral Localizing Symptoms. 



No symptoms, or 

Stupidity. 

Silliness. 

Emotionalism. 

Loss of smell on one side or both sides. 

Hemianopsia and optic neuritis. 

Protrusion of the eyeball. 

Paralysis of the extrinsic ocular muscles. 



Jacksonian epilepsy. 

Sensory disorders, tingling or hemiansesthesia. 

Impaired muscle sense. 

Motor aphasia and agraphia. 

Local palsy after spasm. 

No symptoms, or 

Loss of muscle sense if supramarginal gyrus is affected. 

Word -blindness if angular gyrus and inferior lobule are affected. 

Paralysis or spasm of the lower limbs if the upper margin of the 
cerebral area is invaded. 

Perhaps slight paralysis of the sixth nerve if the angular gyrus is 
affected. 

Homonymous hemianopsia if the cuneus or the neighborhood of the 
calcarine fissure and first occipital convolution are involved. 

Failure to grasp meaning of surrounding objects (mind-blindness) if 
cuneus escapes. 

Word-blindness and some hemianopsia if the angular gyrus is affected. 

Hemiataxia, hemiansesthesia, and partial hemiplegia if the internal 
capsule is slightly involved in the posterior part, and also homony- 
mous hemianopsia from involvement of the optic radiations. 

No symptoms if on right side. 

Word-deafness if the posterior part of the first and second temporal 

convolution is involved. 
Vertigo and forced movements, if the growth is low down, due to 

irritation of internal ear. 

Gradually developing hemiplegia followed by paraplegia. 

Dulness and other mental symptoms suggesting paresis. 

Stupor ) and various symptoms due to pressure upon neighboring 



Coma 
Death. 



structures. 



Progressive hemiplegia. 

Anaesthesia (?). 

Choreic movements if tumor involves optic thalamus (7) and nearby 
part of capsule (8). Starr thinks that these movements are cortical. 

No localizing symptoms if the tumor involves the caudate or lenticular 
nucleus (9). 

Hemianopsia and the hemiopic pupillary inaction of Wernicke, 2 
if the optic tract or its endings near the posterior part of the optic 
thalamus and adjacent tissues are involved. If this pupillary in- 
action of Wernicke is absent hemianopsia indicates a lesion in the 
occipital lobe involving the cortex or the optic radiations. 

Cerebellar inco-ordination. 

Forced movements. 

Ocular palsies, often symmetrical. 

Hemianopsia if primary optic centres of one side are destroyed; 
blindness if destroyed on both sides. 

Deafness or partial deafness if posterior tubercles of corpora quadri- 
gemina are affected. 



1 In the preparation of this table much use has been made of the facts stated by Dana in his work 
on Nervous Diseases. 

2 A ray of light thrown on the blind half of the retina will not produce reflex pupillary contraction, 
though the pupils react normally if the light strikes the other half of the retina. 



TUMORS OF THE BRAIN AND ITS MEMBRANES 



939 



Tumors of cms . . . 
(Very rare.) 



12. 
Tumors in the pons 



13. 
Tumors in medulla 



14. 
Cerebellar tumor 



15. 
Tumor in anterior fossa 



Hemiplegia. 
Hemiansesthesia (?). 

Paralysis of oculomotor nerve upon same side as tumor (crossed 
paralysis). 

Facial palsy on same side as tumor; hemiplegia on opposite side 

(crossed paralysis). 
Trifacial paralysis on same side as tumor if below middle of pons ; 

hemianesthesia on opposite side (crossed sensory paralysis). 
Hemiansesthesia and hemiplegia if tumor is large and above middle 

of the pons. 
Conjugate deviation of eyes away from the lesion. 
Hemiplegia and hemiansesthesia with hypoglossal paralysis or other 

cranial nerve palsy on side of lesion. Glycosuria and vasomotor 

disturbance. 
Symptoms of bulbar paralysis if growth is large. 
Headache ") 

Vomiting 
Vertigo 

Optic neuritis J 
Reeling gait if in middle lobe. 
Glycosuria and cranial nerve palsies if pressing upon or in middle 

lobe. 
Bulbar symptoms (i. e., cranial nerve palsies). 
Hydrocephalus if tumor presses on aqueduct of Sylvius. 
Same symptoms as prefrontal tumors. 
Loss of smell, sight, and oculomotor paralysis. Acromegaly, optic 

neuritis, and temporal hemianopsia if the tumor is in middle fossa 

and involves optic chiasm. 



unusually severe. 



Diagnosis. — As already stated, the important symptoms in the diagnosis 
of brain tumor are headache, vertigo, optic neuritis, convulsions, and par- 
alysis. It must be remembered, however, that these symptoms are none of 
them pathognomonic of brain tumor, and that each of them is often present 
in other maladies. It is the combination of symptoms rather than any one 
of them alone that indicates or establishes the diagnosis. Headache and 
vertigo are due to a host of causes, as convulsions and paralysis are 
common conditions; it is the localization of the convulsions and of the 
paralysis, pointing to a distinct focus,, that is significant. Hysteria may, 
however, cause localized palsies and localized anaesthesia. Sometimes, too, 
localized convulsions are not only due to tumor, but are symptomatic of a 
general condition such as poisoning, or of a widespread nervous disease 
such as paresis. The most valuable sign of brain tumor, optic neuritis, may 
be present in chronic contracted kidney, chronic lead poisoning, and severe 
anaemia, etc., but these conditions can be eliminated from the case by the 
absence of the other signs and symptoms of these maladies. 

Among the pathological states that may produce symptoms of brain 
tumor is to be mentioned localized meningitis due to tuberculosis or syphilis. 
(See Meningitis.) In tuberculosis the degree of optic neuritis is usually 
slight; there is a primary tuberculous focus existing elsewhere, and, as the case 
progresses, evidences of a general meningeal inflammation may develop. 
Syphilitic meningitis is usually diffuse, not localized, and when localized 
is to be considered as a gumma or tumor. Another cause of such symptoms 
is abscess. This may be differentiated by its rapid development and by the 
presence of a septic focus elsewhere, as in the ear or in other parts of the 
body. (See Brain Abscess.) 



940 DISEASES OF THE NERVOUS SYSTEM 

The question as to the character of the growth is determined by the fol- 
lowing facts in many cases. Tuberculous growths are frequently met with, 
particularly in children. The presence of tuberculous infection elsewhere 
also points to this form of tumor. So, too, the presence of a malignant 
growth in some other part of the body suggests that the lesion in the brain 
is of the same character. A history or the presence of the scars of syphilis 
will indicate the existence of a gumma. Gowers states that if the tumor 
be in the cerebellum or pons, there is some probability "of its being tubercle 
or glioma, and if it is in the cortex the probability that it is syphilitic is con- 
siderable." "A tumor outside the brain tissue is probably sarcoma." So, 
too, the disappearance of the symptoms under active antisyphilitic treatment 
point to syphilis as the cause. "A tumor which grows rapidly at the onset 
and then becomes stationary is probably tuberculous." 

Prognosis. — The prognosis in all forms of brain tumor is grave. It is 
least so in gumma and next best in tubercle, for in the former active treat- 
ment may cure, and in the second a long period of arrest may ensue. A 
growth in the pons or medulla is more dangerous as to life than one in the 
cortex, but the presence of severe symptoms of brain tumor, be the seat of 
the growth what it may, is always of grave omen. 

Treatment. — From what has been said of the etiology and pathology 
of brain tumor it must be evident that medicinal treatment can do nothing 
more than palliate the patient's suffering, unless the growth be syphilitic. 
For the relief of the headache the various coal-tar products, such as ace- 
tanilid, phenacetin, or antipyrin, may be employed, and their efficiency is 
usually much increased by giving simultaneously 1 or 2 grains of caffeine 
and 10 or 20 grains of one of the bromides, preferably the bromide of stron- 
tium or bromide of sodium. In those cases in which the headache becomes 
so severe as to be insupportable, hypodermic injections of morphine may be 
employed, but it is an interesting therapeutic fact that this drug gives less 
relief in the pain of brain tumor than in almost any other affection charac- 
terized by pain. Excessive vomiting is to be checked by administrations 
per rectum of 10 or 20 grains of chloral with 60 grains of bromide of sodium, 
to which may be added 30 to 60 minims of deodorized tincture of opium. 
So, too, epileptiform convulsions, if they are severe, may be prevented, at 
least in part, by the use of the bromides, or, if an aura is present, by 
inhalations of nitrite of amyl. 

In those cases in which there is the history of syphilis, the administration 
of mercury and the iodide of potassium is, of course, strongly indicated, 
and if a gumma is producing symptoms such as convulsions, which may 
in themselves endanger the patient's life, the mercury should be pushed as 
actively as possible, being given by the mouth, by inunction, by hypo- 
dermic injection — that is, by every avenue of entrance — in the hope that it 
may exercise its influence upon the syphilitic growth before a convulsion 
sufficiently violent to cause death ensues. In other instances, when there 
are no acute symptoms which demand immediate interference, protiodide 
of mercury may be alternated with iodide of potassium, iodide of sodium, 
or iodide of strontium. 

When the growth is due to tuberculosis the administration of cod-liver 



ABSCESS OF THE BRAIN 941 

oil, iron, and arsenic, and residence in a climate in which plenty of fresh 
air and sunshine can be constantly obtained, is essential. In such cases 
great improvement in the general health may do something toward arresting 
the local process. 

In those forms of brain tumor which are not tuberculous or syphilitic, 
the use of drugs, except to relieve pain, is practically useless, and opera- 
tive interference offers the patient the best chance of recovery. Surgical 
procedures can, however, only be resorted to in those cases in which a 
definite localization of the tumor can be made, and where that locality is 
so situated that the surgeon can reach it without doing damage to vital 
parts. The earlier the operation is performed the better is the outlook. 
M. Allen Starr has collected 400 cases of brain tumor which were operated 
upon. In 154 instances tumor of the cerebrum was successfully removed, 
and the patients recovered. In 52 cases the patients died. In 16 instances 
in which the tumor was in the cerebellum it was removed and the patients 
recovered. In 8 instances death followed removal. It is interesting to note 
that in 91 instances of supposed cerebral tumor the growth could not be 
found on operation. The same failure to discover a growth was met with 
in 22 instances of supposed cerebellar tumor. 

Of the cases which recovered 52 were sarcoma, 29 were cysts, 8 were 
gummata, 19 were tuberculous, and 15 were gliomas. 

For the measures which are to be pursued in the removal of brain tumor, 
the reader is referred to the modern works on surgery. 



ABSCESS OF THE BRAIN. 

Definition. — Abscess of the brain is a condition in which an accumulation 
of pus takes place in the cerebrum, or the cerebellum, or between these 
parts and their covering membranes. In the latter case the brain substance 
forms one wall of the abscess and the membranes the other wall. The 
latter type of abscess differs from purulent meningitis in that the inflam- 
matory process is primarily in the nervous tissues, and that it is limited to a 
comparatively small area. Abscess of the brain without involvement of 
the membranes is much the more common form, and the white matter suffers 
very much more frequently than the gray substance. Abscess rarely occurs 
in the central ganglia, the pons, the medulla, or the middle lobe of the cere- 
bellum. 

Etiology. — Abscess of the brain is always due to an infection by some 
pathogenic organism. In some instances the process is excited by an injury 
which affords a nidus in which the organism may develop; in other cases 
a septic embolus is carried from another part of the body in which there is 
an infected area; in still others the infection takes place more directly, as in 
those instances in which by fracture of the skull injury and infection both 
occur, or, as in the case of abscess of the middle ear and mastoid disease, 
the infection spreads by way of the sinus. 

Middle-ear disease is the cause in a great proportion of cases, about 45 
per cent, arising from this primary focus of infection and 25 per cent. 



942 DISEASES OF THE NERVOUS SYSTEM 

from injury. The remaining causes are infection of the other cranial bones 
than the mastoid or septic foci elsewhere. 

Males are affected far more frequently than females, in the proportion of 
3 to 1 . This is largely due to the fact that males are so much more exposed 
to injury than females. If the cases of abscess due to middle-ear disease 
are studied by themselves, the proportion is almost equal; but if those due 
to trauma are considered by themselves, the proportion is 5 of men to 1 of 
women. 

The disease is most frequent between the tenth and twentieth years of 
life. In the second decade ear disease is the common cause, and in the 
third decade ear disease and injury, or a distant focus of infection, are about 
equal in frequency as causes. 

Pathology and Morbid Anatomy.— -A majority of cases of brain abscess 
affect the right side of the brain. Out of 71 cases collected by Oppenheim 
55 were in the temporal lobe, 13 in the cerebellum, 2 in the pons, and 1 in 
the crus. 

The pathological process which results in abscess consists primarily of 
an encephalitis which speedily goes on to the stage of suppuration. This 
encephalitis may be due to any organism capable of causing an active 
inflammatory process. Thus, the Streptococcus pyogenes, the Staphylo- 
coccus pyogenes aureus, and the pneumococcus may be the provoking 
factors. In other cases the typhoid bacillus may be the cause, and even the 
streptothrix may produce such a lesion, as in a case seen by me in consulta- 
tion with Dr. J. H. Musser. The abscess is nearly always single, but two 
or more pockets of pus may be present. The size of the abscess varies 
greatly. In some cases it is so small as scarcely to be recognized, a small 
collection of pus being found in the centre of an area of softening ; whereas 
in other cases the quantity of pus may be very large, varying in quantity 
from a drachm to several ounces. 

The abscess may be surrounded by an inflammatory fibrous wall which 
serves to separate it from the neighboring white matter, or it may be con- 
tained in a cavity without any such well-defined margin, the walls of the 
abscess being composed of softened brain tissue. The latter form is prone 
to spread more rapidly than the abscess which has been walled off. On 
the other hand, the wall of the abscess may rupture and produce sudden 
death. Not rarely the extension of the inflammatory process produces a 
meningitis if the abscess is situated near the surface of the brain, and a 
septic thrombosis of the nearby vessels may occur. 

Symptoms. — It is of interest to note that cerebral abscess may occur 
without producing symptoms sufficiently typical to lead to an antemortem 
diagnosis. In the great proportion of cases, however, the symptoms of its 
existence are well developed. The most constant of these is headache, 
general or localized; it is excruciating when associated with middle- 
ear disease; next in constancy is mental disturbance, the patient being 
alternately irritable and dull, and often seeming to be exceedingly 
ill. The temperature, unlike that of septic processes elsewhere, is usually 
normal or subnormal, unless the abscess ruptures, when it may be hyper- 
pyretic. The surface of the skull is often hypersensitive, and in some cases 



ABSCESS OF THE BRAIN 943 

it has been possible to localize the abscess by the dulness on percussion 
produced by its presence. Optic neuritis is often present. None of these 
symptoms is in any sense pathognomonic, since all may occur in other 
states of disease; but when they are taken into consideration in connection 
with a history of middle-ear disease, injury, or the presence of a septic 
focus elsewhere, they possess great diagnostic value. The deafness due 
to destruction of the auditory centre is masked by the deafness due 
to the disease in the ear. Paralysis of one side of the face is not of 
much diagnostic value, since this symptom is often due to the inflam- 
mation about the facial nerve as it passes through the stylomastoid 
foramen. 

The value of localizing symptoms depends, of course, upon the part 
of the brain which happens to be affected. When the infection spreads 
from the mastoid bone after or during otitis media, and infects the temporal 
lobe, there are no localizing nervous symptoms because we are in the dark 
as to the function of the temporosphenoidal lobe. In a few cases a lesion 
in the left temporosphenoidal lobe has caused aphasia. When the occipital 
lobe is involved the patient may present the symptom called optical aphasia, 
for in this lobe is situated the memories of objects and of words seen. Starr 
has observed a case of this character. The patient knows an object when it 
is placed before him, but cannot name it. A lesion of the temporal lobe 
may also produce this symptom by pressure, and it may likewise cause 
hemiplegia or hemianesthesia by pressure upon the internal capsule. Hemi- 
anopsia may also be caused in this manner. 

When the abscess is in the cerebellum the symptoms are those charac- 
teristic of cerebellar tumor, viz., a staggering gait, vertigo, and, it may be, 
vomiting, diplopia, and nystagmus. In some instances the patient staggers 
toward the diseased side. If pressure is brought to bear by the abscess 
upon the crus or pons there may be paralysis of the oculomotor or facial 
nerves on the side of the lesion, with increase in the knee-jerks on the opposite 
side. 

Diagnosis. — The diagnosis of brain abscess is not difficult if the symp- 
toms just described have been preceded by a history of injury or of a septic 
process elsewhere, near or remote. There are two other states with which 
it may be confused, namely, meningitis and thrombosis of the lateral sinus. 
In the former condition the onset is usually more abrupt, the headache is 
prone to be more severe in the early stages, and a sharp febrile movement 
is usually present; whereas, as has already been pointed out, in cerebral 
abscess fever is often absent unless the abscess ruptures. The pressure of 
abscess produces a slow pulse like that of cerebral compression, but in 
meningitis the pulse is usually very rapid. Additional symptoms of menin- 
gitis, which are of great value, are the stiffness of the muscles of the neck, 
the muscular twitchings, the early development of squint, and, last of all, 
the presence of a pathological state of the cerebrospinal fluid obtained by 
lumbar puncture. (See Cerebrospinal Fever.) 

When thrombosis of a lateral sinus is present the febrile movement is sharp 
and severe, with marked remissions and exacerbations as in sepsis. There 
is swelling of the jugular vein on the affected side and of the conjunctiva 



944 DISEASES OF THE NERVOUS SYSTEM 

as well, associated, it may be, with exophthalmos. Swelling, cedema, 
and pain on pressure over the mastoid may also be present. The use of the 
ophthalmoscope also reveals choked disk in many cases as an early symptom. 

Prognosis. — This depends very largely upon the site of the abscess and 
the ability of the surgeon to evacuate and drain it. In all cases the prognosis 
is necessarily grave. That many patients may recover if promptly relieved 
is shown by recent statistics, which show that 60 per cent, of traumatic 
abscess recover after operation, and about 50 per cent, of abscess due to ear 
disease do likewise. 

Treatment. — The treatment is purely surgical, and for the necessary 
procedures reference must be had to surgical treatises. 



ACUTE CEREBRITIS OR ENCEPHALITIS. 

Definition. — Acute cerebritis, sometimes called " acute encephalitis/ ' is a 
condition in which there is an acute inflammation of the brain arising as a 
primary disease not secondary to meningitis. 

Etiology. — The cause of acute cerebritis is always an infection due to 
the entrance of a micro-organism into the body, and in most instances the 
condition arises as a complication of measles, scarlet fever, smallpox, or 
ulcerative endocarditis, or in the- convalescence from influenza. Acute 
alcoholism and other forms of poisoning may, by diminishing vital resist- 
ance in the brain, predispose to this condition. Possibly trauma may have 
a like result. Whatever may be the cause, this condition as a primary acute 
disease is very rare. 

Pathology and Morbid Anatomy. — The inflammatory process is not widely 
diffused, as a rule, but is found to exist chiefly in the distribution of one or 
more nearly related bloodvessels. At times it affects the same areas on both 
sides of the brain. In some instances only the cortex is involved, while in 
others the process chiefly affects the white matter. A limited form of this 
condition is the acute inflammation of the medulla, pons, or midbrain (polio- 
encephalitis inferior of Wernicke or acute bulbar paralysis). 

The changes found in the affected parts are those characteristic of acute 
inflammation in all the nervous tissues, and indeed in any acute inflamma- 
tion, namely, hyperamiia, out- wandering of blood cells, and minute hemor- 
rhagic extravasations, followed by the ordinary degenerative changes in the 
nerve cells produced by an interference with their normal blood supply and 
the effects of toxaemia. The nerve-cell body or ganglion cell itself suffers from 
cloudy swelling, loses its sharp outlines, and its nucleus becomes indistinct 
or disappears. The axones and dendrites also undergo a similar change. 
The interstitial tissues are at first filled with small cells, and ultimately there 
is an overgrowth of the neuroglia cells, so that patches of sclerosis are pro- 
duced. This last result is, of course, permanent, and if it takes place to 
any great extent may seriously impair the function of the brain. If the inflam- 
matory process is in the cortex, adhesions to the meninges may take place. 

Symptoms. — The symptoms of acute cerebritis depend to a large extent 
upon the portion of the brain which is chiefly affected, although the general 






ACUTE CEREBRI TIS 945 

manifestations of an acute inflammatory process in the brain are present 
in all cases. The patient is seized, after a few hours of general distress, with 
headache and dizziness, followed by a chill and, it may be, vomiting. These 
symptoms are in turn speedily followed by fever and rapidity of the pulse 
and respirations, and these in turn in some instances by delirium of a violent 
type. If the case is severe the patient may now pass into coma, and then 
gradually pass to death, or, after several days, or even weeks, of these symp- 
toms, consciousness gradually returns, the temperature falls, and recovery 
takes place, although, as already stated, permanent impairment of some 
of the cerebral functions may persist. 

The special symptoms which depend upon the areas of the brain which 
are affected consist in hemiplegia, monoplegia, aphasia, or in word-blind- 
ness and word-deafness, hemianopsia, or mutism. Any of these may become 
permanent. In still other cases the patient suffers from impairment of the 
intellectual powers or the changes in the motor cortex produce epileptic 
attacks, and in other instances the development of the sclerotic patches 
already named results in the production of a condition identical with 
disseminated sclerosis with nystagmus, tremor, and peculiar speech. The 
very rare condition called " polioencephalitis superior of Wernicke " is 
manifested by the presence of ptosis, strabismus, nystagmus, and even optic 
neuritis with vertigo and a staggering gait. In addition there may be difficult 
speech and facial paralysis. 

Diagnosis. — Acute encephalitis may be confused with brain tumor when 
epileptiform convulsions and paralyses are prominent, but the absence of 
choked disk and the rapid onset will distinguish the former. In its "coma- 
tose" and "epileptic" forms it may resemble apoplexy or epilepsy, and a 
close study of the entire clinical picture is necessary, with the history, to 
differentiate such cases. 

Prognosis. — That the prognosis in acute encephalitis in the early course 
of the malady must be uncertain is manifest when we consider the character 
of the lesions which are present. Even after the active stage of the disease 
is passed the outlook as to complete restoration to health is still clouded 
because it is not possible to tell what secondary changes may develop in the 
brain or its membranes. All cases of acute encephalitis are to be regarded 
as of much gravity. A high temperature, convulsions, profound and pro- 
longed coma are all very unfavorable symptoms. Even in the very grave 
cases a remarkable degree of recovery may occur. 

Treatment. — This consists in the application of an ice-bag to the head, 
and in the use of moderate doses of tincture of aconite if there is circulatory 
excitement. If the bowels are confined, an active saline purgative is useful 
to move them and to deplete the bloodvessels. A hot foot-bath may also be 
used. Phenacetin and acetanilid may be employed for the relief of pain, 
but they usually fail. On the other hand, the use of opium or morphine 
often makes the pain worse. Absolute rest in a darkened room is essential. 
After the acute process is over iodide of potassium may be given in the dose 
of 10 grains three times a day, with the hope that in this manner inflammatory 
exudates and adhesions may be absorbed. 

60 



9i6 DISEASES OF THE NERVOUS SYSTEM 



THROMBOSIS OF THE VENOUS SINUSES. 

Etiology. — Thrombosis of the venous sinuses is due, as are cases of throm- 
bosis elsewhere, to an inflammation of the endothelium which lines these 
vessels. This inflammation may be the result of a septic infection in remote 
or in neighboring tissues, as, for example, in suppurative otitis media. 
Where the cause is sepsis the thrombus usually contains micro-organisms. 
The vast majority of instances depend upon suppuration in the ear. 

Pathology and Morbid Anatomy. — The size of the thrombus varies very 
greatly. Beginning as a small clot in one sinus, it may gradually increase 
in size until the sinus is filled, and may even extend to adjacent sinuses and 
into neighboring veins. If septic in origin it may be purulent in character. 
The longitudinal sinus is very rarely affected. The lateral sinus is the one 
most commonly involved, and after it the cavernous sinus. 

Symptoms. — The symptoms of thrombosis of the lateral sinus are con- 
gestion of the veins in the neighborhood of the mastoid, with swelling of the 
tissues covering it. There is often pain and tenderness on pressure. Not 
rarely the cervical glands are enlarged from infection, and wryneck may 
be present. Choked disk is frequently present upon both sides. With the 
infection of the sinus there is usually a history of a rigor followed by high 
fever, with headache, vomiting, delirium, and finally coma. The fever not 
rarely follows a septic course, rising and falling sharply. Other evidences 
of septicaemia may also be present, such as sweating, diarrhaa, and the 
occurrence of infarctions in such organs as the lungs, spleen, and 
kidneys. 

In thrombosis of the cavernous sinus there is local swelling, congestion 
of the face about the eyes, epistaxis, and undue fulness of the retinal veins. 
Occasionally squint develops as a result of interference with the function 
of the oculomotor and abducens nerve. 

Thrombosis of the longitudinal sinus is manifested by intense venous 
congestion in the scalp, and indeed of the entire head. Choked disk may 
be present and epistaxis may occur. 

Prognosis. — This is unfavorable unless surgical interference gives relief, 
and surgical interference is practically limited to cases of disease of the lateral 
sinus. 

Treatment. — This is purely surgical, and consists in trephining or other- 
wise opening both the source of infection and the sinus and thus removing 
the focus and the clot. For details as to the method of operation, and as to 
the statistics of recovery following such operations, the reader is referred 
to books on surgery. 

CEREBRAL MENINGITIS. 

Definition and Etiology. — By meningitis is meant an inflammation of the 
membranes covering the brain or spinal cord. From an anatomical stand- 
point there are three of these — the dura mater, the arachnoid, and the pia 
mater — but from the standpoint of the clinician and pathologist these mem- 



CEREBRAL MENINGITIS 947 

branes may be divided into two parts, the dura mater on the one hand and 
the arachnoid and pia mater (pia-arachnoid) on the other, for the dura is 
often inflamed by itself, but the pia and arachnoid are always affected 
together. "When the dura is alone involved it is called pachymeningitis, and 
when the other membranes are affected it is called leptomeningitis. 

Pachymeningitis. — Pachymeningitis may occur in an internal form, when 
the smooth inner layer of this membrane is inflamed (pachymeningitis 
interna), and in an external form, in which the outer layer is chiefly affected 
where it is in contact with the bone (pachymeningitis externa). The latter 
is the most common type by far. 

Pachymeningitis externa is, in the greater proportion of cases, secondary 
to some traumatism or to disease of the bone. Thus, a blow on the head 
which fractures the skull, or necrosis of the skull, may so result. Very much 
more rarely an acute infection arises, as in an infectious and septic malady 
such as erysipelas. 

Pathology and Morbid Anatomy. — The inflammatory process resembles that 
seen in any inflammation, namely, hyperemia followed by swelling and 
cellular infiltration, and this in turn by the formation of pus which is found 
between the skull and the dura mater, or, in extraordinary cases, between 
the layers of this membrane. When the inflammatory process does not go 
on to suppuration, the external layer of the dura becomes thickened and 
adherent to the skull. If the inflammation is very severe the inner layer of 
the dura is affected, and the pia mater may become involved and adherent 
to it. 

Symptoms. — These consist in those characteristic of the cause, as the 
primary unconsciousness from a blow, or the pain of bone disease, and in 
the development, as direct symptoms, of headache, confusion of mind, 
delirium, and in severe cases convulsive seizures. Fever may or may not be 
present. If pus collects, symptoms of pressure on the brain may develop, 
and paralysis of the opposite side of the body may ensue (hemiplegia). 

Diagnosis. — The history of injury, of bone disease, or of some focus of 
infection makes the diagnosis possible. 

Prognosis. — This is bad in direct proportion to the severity of the inflam- 
matory process and the degree to which the pia mater is involved. External 
pachymeningitis is less grave than leptomeningitis. 

Treatment. — This consists in the use of saline purgatives to relieve cranial 
congestion, in applying an ice-cap to the head, rest in bed in a darkened 
room to secure perfect quiet, and in the employment of aconite as a cardio- 
vascular sedative if the pulse is excited. If symptoms of cerebral com- 
pression develop, as coma or paralysis, the fluid or pus must be evacuated 
by operation. 

Pachymeningitis Interna. — Pachymeningitis interna occurs in a purulent 
and in a hemorrhagic form, the purulent being very rare. To the hemor- 
rhagic type the terms " hemorrhagic internal pachymeningitis " or " hematoma 
of the dura mater " are sometimes applied. Even this type is rarely met with, 
and its existence is rarely recognizable before autopsy. It affects males far 
more commonly than females (4 to 1, Gowers), and is generally met with 
after the fiftieth year. It is also met with more commonly in the first twelve 



948 DISEASES OF THE NERVOUS SYSTEM 

months of life than in childhood or early manhood. As a rule, in adults it 
develops in the course of some form of chronic insanity, particularly in the 
course of general paralysis of the insane, or in cases of chronic inebriety. 
Very rarely it has complicated the course of one of the acute infectious dis- 
eases, such as typhoid fever or smallpox. In children it may complicate 
scurvy. 

Pathology and Morbid Anatomy. — The exact method or process by which 
the hemorrhagic extravasation takes place is not known. The autopsy 
reveals a bilateral, and rarely a unilateral, extravasation between the layers 
of the dura and between the dura and the arachnoid. Not only is a bloody 
fluid formed in these spaces, but a pseudomembrane is also present; it may 
be in several layers. These layers are at first red and later may be pallid, 
and, by adhering together at spots, form pockets in which the bloody fluid is 
found. When the condition has existed a long time this fluid may be decolor- 
ized and contain crystals of cholesterin. Very rarely suppuration takes 
place. 

Symptoms. — The symptoms are in many cases, if the disease complicates 
chronic insanity, so suppressed, or absent, that no suspicion of the state just 
described is harbored. In some cases the patient develops attacks which 
resemble those of apoplexy, which are supposed to be due to fresh extrav- 
asations of blood. In other instances there are signs of cerebral com- 
pression, as shown by stupor, or coma, or optic neuritis. Headache and 
vomiting may be present. Partial hemiplegia may develop. 

The prognosis is very unfavorable. Treatment is almost useless. Quiet 
and rest, with cold to the head, is all that can be done. In cases with 
strictly localized symptoms surgical intervention is justifiable. 

Leptomeningitis. — Leptomeningitis is the form of meningitis which com- 
plicates the course of all of the acute infections, notably pneumonia, erysip- 
elas, septicaemia, and less frequently variola, scarlet fever, typhoid fever, 
and measles. Measles produces it very commonly because this malady is 
often followed by otitis media, and because otitis media not rarely causes 
mastoid abscess, and, from this focus, infection involves the meninges or 
the lateral sinus. It is probable, too, that a very considerable proportion of 
cases of leptomeningitis are caused by infection which takes place through the 
nose. It can be readily understood that any infectious micro-organism which 
can gain access to the meninges through the openings in the skull or in the 
blood may cause such an inflammation, and, in addition, that the possibility, 
or probability, of infection is greatly increased by any disease which lowers 
vital resistance, such as nephritis. It must not be thought, however, that 
all cases of leptomeningitis due to the pneumococcus are complications of 
croupous pneumonia, for this micro-organism may produce a meningitis 
by direct infection, without the lung being affected in the least. It is prob- 
able, too, that the typhoid bacillus may, in a case which has long since con- 
valesced from the fever, act in a similar manner. (For the relationship of 
leptomeningitis to pneumonia and typhoid fever the reader is referred to 
the articles on those diseases. Also to that on cerebrospinal meningitis.) 

Meningitis is more common in children during the first decade of life 
than at any other period, but in these cases the inflammation usually involves 



CEREBRAL MENINGITIS 949 

the meninges at the base, whereas in adults that part of the meninges which 
covers the convexity is chiefly affected. 

Morbid Anatomy and Pathology. — The inflammatory process may involve 
the whole membrane or be quite limited. The limited cases are those which 
arise from direct infection from a nearby focus of disease. Thus, in cases 
which are secondary to middle-ear disease the lesion is often unilateral, 
whereas in those cases in which the pneumococcus is the infecting agent 
the entire convexity on both sides is usually affected. In the latter type of 
case the effusion which develops is often large in quantity and purulent. 
If the cause is tuberculous the base is usually affected. (See Tuberculous 
Meningitis.) The actual lesions found in the meninges in these cases are 
noteworthy. Beginning with hyperemia and congestion they pass on to 
cloudiness of the membranes affected, which is particularly well marked 
along the course of the bloodvessels because of the engorgement of the 
accompanying lymph vessels. Small spots of purulent material are dotted 
along these vessels which, as they increase in size, coalesce, and so consider- 
able areas are covered by pus. When the process is severe the dura mater 
and the cerebral cortex may be involved by the inflammatory changes. 

Symptoms. — In studying the symptoms of leptomeningitis it must be 
recalled that the manifestations of involvement of the cortical area are by 
no means pathognomonic. Every physician of experience has seen cases 
of typhoid fever or croupous pneumonia present evidences of meningitis, 
yet the autopsy has revealed no such lesion present. In other words, as 
pointed out when these diseases were discussed, toxins produced by the 
specific organisms may cause symptoms identical with those of meningeal 
inflammation. This is exceedingly common in the pneumonia of children. 

There are, however, certain symptoms of meningitis which are certainly 
indicative of either inflammation or irritation of the meninges, particularly 
if they are associated with a disease or an injury qualified to produce menin- 
geal involvement. These consist in fever, headache, vomiting, retraction of 
the head, and rarely convulsions. Grinding of the teeth, obstinate constipa- 
tion, and an excessive hyperesthesia of the skin of the arms and legs are also 
common symptoms. When the inflammatory process is basilar the symp- 
toms are much more definite and reliable. In addition to those just named 
we find that optic neuritis is present, and strabismus and ptosis, due to the 
pressure exercised upon the cranial nerves, develop. The pupils may be 
contracted in the early stages because of irritation of the oculomotor nerves, 
and later widely dilated by reason of paralysis of these nerves. Fever may 
or may not be present, and the pulse is usually slow even if the temperature 
is raised. Kernig's sign may be present. (See Cerebrospinal Meningitis.) 
A rapid loss of flesh takes place in nearly all cases. 

Diagnosis. — The symptoms of basilar leptomeningitis, whatever its cause, 
are usually unmistakable. A very useful aid to diagnosis is lumbar punc- 
ture, already described under Cerebrospinal Meningitis. If the cerebro- 
spinal fluid escapes with a spurt from the needle, it is indicative of the 
presence of tuberculous meningitis, but by no means positive of this condi- 
tion, for it sometimes happens that a similar high pressure exists in cases of 
purulent meningitis and of spinal tumor. If disintegrated blood is present 



950 DISEASES OF THE NERVOUS SYSTEM 

in the cerebrospinal fluid it is an indication of the presence of pachymenin- 
gitis or injury. Fresh blood, on the other hand, is probably due to the 
puncture. If the fluid is perfectly clear, every inflammatory affection of the 
meninges except tuberculosis may be excluded. In tuberculosis it may be 
clear, but is often cloudy, and toward the end of the case even purulent. 
The normal proportion of albumin in it is 0.02 to 0.04, and if more than 
0.05 is present an inflammatory process is probably going on. If the small 
quantity of sugar which is normally present is absent, this is a sign that 
inflammation is present. 

Treatment. — Aside from the employment of rest and cold to the head, if 
fever is present or pain is suffered, we can do little for this condition except 
we resort to lumbar puncture for the purpose of relieving pressure. 

The cerebrospinal fluid may also give us valuable information as to the 
presence or absence of meningitis, if it be examined microscopically and a 
quantitative estimation of its leukocytes is made. As a general rule, there 
is a marked increase in lymphocytes if the inflammatory process is tuber- 
culous, and of polymorphonuclear cells if it is non-tuberculous. Exceptions 
to this rule occur, and therefore the presence of either one of these forms of 
leukocytes in increased number is not pathognomonic. 

Microscopic examination of the cerebrospinal fluid may also be made 
for the purpose of discovering tubercle bacilli, or the diplococcus of pneu- 
monia, or other pathogenic micro-organisms. The fluid for this purpose 
should be kept on ice for not less than twelve hours, until a small clot is 
formed. The web-like fibres of this clot are transferred to a cover-glass, 
spread in as thin a film as possible, and stained by the methods commonly 
employed for staining the tubercle bacillus. Where the examination must 
be performed at once, the fluid may be put in a centrifuge, and the 
sediment examined by the staining methods already described. As with 
examinations of the sputum in suspected tuberculosis, the finding of tubercle 
bacilli is a positive sign of great value, but the failure to find them by no 
means proves that the disease is not tuberculous. Reference to the presence 
of the Diplococcus intercellularis meningitidis has already been made in the 
article upon Cerebrospinal Meningitis. Occasionally the streptococcus and 
staphylococcus are found. In African "sleeping sickness" trypanosomes 
have frequently been found in the cerebrospinal fluid. 



DEMENTIA PARALYTICA. 

Definition. — Dementia paralytica, often called "meningoencephalitis," 
"paresis," or "general paralysis of the insane," is a state characterized ana- 
tomically by a widely diffused process of degeneration in the central nervous 
system, particularly in the cerebral cortex, with morbid changes in the pia 
mater. The chief symptoms in the early stages are the development of 
great irritability of temper, forgetfulness, carelessness as to habits, and later 
delusions of grandeur. Clinically it is characterized by a progressive par- 
alysis of the body, associated with certain physical signs, and a progressive 
loss of mental power of a peculiar kind. The most striking symptom of this 
disease is the "delusion of grandeur." 



DEMENTIA PARALYTICA 951 

Etiology. — Without doubt syphilis is a provoking cause in a large propor- 
tion of cases (75 per cent.), but it is not present in all, and in no case is it to 
be regarded as a direct cause, in the sense that the syphilitic virus is active in 
a given instance. On the contrary, it is, like locomotor ataxia, a parasyphilitic 
affection, that is, a sequel of that malady, appearing from five to twenty 
years after the initial lesion. Alcoholism, excessive sexual indulgence, and, 
indeed, excesses of every kind, are also without doubt factors of importance. 
The disease is a common one among roues. Some cases seem to follow a 
sunstroke or severe injury. 

The disease is one of the middle period of life, between thirty and fifty 
years, but a number of cases have been recorded as occurring in children 
who have usually had hereditary syphilis. 

Pathology and Morbid Anatomy. — The primary change in cases of this dis- 
ease takes place in an increased blood supply to the pia mater and in the 
smaller vessels of the cerebral cortex, associated with degenerative changes 
in the bloodvessel walls. The progress of these degenerative changes results 
in the development of fusiform dilatations of the bloodvessels and the filling 
of the lymph spaces with serum. The exact cause of these changes is not 
understood, but Mott believes that they are due, in part at least, to the forma- 
tion of a toxic substance called choline, which is not only found in the lymph 
spaces, but diffused through the whole cerebrospinal fluid. This poison 
causes congestion of the veins of the brain, and affects chiefly those which 
empty into the longitudinal sinus. Ultimately the quantity of lymph present 
in the perivascular spaces is so great that a true cerebral oedema is produced. 
There is an overgrowth of the neuroglia about the vessels, and this newly 
formed connective tissue sends fibrils down between the cells of the cortex, 
with the result that a true sclerosis develops. Associated with these con- 
nective-tissue changes there are degenerative changes in the cerebral neurones. 
The body of the neurone undergoes hyaline and then fatty degeneration, 
pigmentation, and finally atrophy. When the disease has been present for 
a long time, autopsy reveals the presence of small cysts in the white and gray 
matter, and so marked a decrease in the size of the convolutions and of the 
entire brain that it is found to be much smaller than is normal. Its surface 
is harder than is natural, pigmented, and adherent to the pia mater, which 
is also found to be the site of overgrowth of connective tissue. The ventri- 
cles contain an excess of fluid, and their lining membrane, the ependyma, 
is thickened. It is noteworthy that the left hemisphere is usually more 
affected than the right, and that the changes already described affect the 
frontal lobes and the areas of the motor cortex before the rest of the brain 
is involved. 

In most cases of paresis degeneration is found in the spinal cord, so that 
spinal symptoms are added to the cerebral signs and form part of the clinical 
picture of the disease. The lateral and posterior tracts are usually affected, 
producing symptoms of ataxic paraplegia. Sometimes the posterior columns 
alone are degenerated, presenting symptoms of locomotor ataxia. Rarely 
disseminated sclerosis is found; and recently, in one case, the spinal cord 
in a case of paresis was found to be suffering from syringomyelia. In a 
few cases of locomotor ataxia (tabes dorsalis), fully developed and typical, 



952 DISEASES OF THE NERVOUS SYSTEM 

the cerebral signs of paresis came on, as if the disease had finally "risen" 
to the brain. These cases constitute the "ascending type" of paresis. 

Some authorities believe that paresis is identical in nature with tabes — that 
it is a "tabes of the brain." A clinical picture of paretic dementia with tabes 
is, therefore, met with. Rarely the spinal symptoms precede the cerebral 
symptoms in the development of the disease. So, too, symptoms of spastic 
paraplegia may develop. Sometimes autopsy reveals the fact that pachy- 
meningitis and hematoma have occurred as the result of the aneurysmal 
dilatations of the cerebral and pial vessels, already described, leaving behind 
them an organized membrane beneath the dura, or a mass of encysted 
blood clot. 

Symptoms. — When the symptoms of dementia paralytica are well devel- 
oped, they are so characteristic and obtrusive that there can be little difficulty 
in reaching a correct diagnosis in regard to the condition from which the 
patient is suffering. It is only when the disease is in its stage of onset, or in 
an atypical form, that any doubt can be present. 

As a rule, the early symptoms are recognized in retrospect rather than 
at the time at which they occur, unless, perchance, these symptoms are very 
strongly developed. It is noticed that the patient seems to be nervously 
fatigued or mentally fagged, and often this condition is ascribed to the 
excesses which have been committed in connection with venery, wine, 
and other forms of nervous stress. The temper is usually irritable, and 
the friends notice that the patient takes offence at remarks which ordinarily 
he would not notice. At times he is remarkably forgetful. Naturally tidy 
as to his habits and dress, he becomes careless and slovenly. Occasionally 
sleeplessness will be complained of. 

Although, before the onset of the symptoms, he may be apparently kind 
and faithful to his family, he begins to be brutal in his conduct toward his 
wife and children, and perhaps returns to the alcoholic and sexual excesses 
which laid the foundation for his disease many years before. The speech 
becomes indistinct, hesitating, and if the tongue is protruded a very fine 
tremor may be seen in it. There is also a very marked tremor of the 
hands. Ataxia of station (Romberg's sign) is a common symptom. The 
pupils are generally unequal and irregular, and the pupillary light reflex 
may be lost, while reaction to accommodation is maintained. In other 
words, the Argyll-Robertson pupil is present, for the same reason that it is 
present in cases of locomotor ataxia, because Meynert's decussation, or 
other fibres, involved in the light reflex arc are affected by the degener- 
ative process already described. The loss of consensual reflex is also fre- 
quently observed. 

The symptoms of onset are often prolonged over the period of many 
months, and sometimes for several years, depending upon the rapidity 
with which the pathological changes in the brain develop. The disease 
is progressive and ultimately the symptoms of the later stages are devel- 
oped. These symptoms may consist in delusions, which are usually com- 
posed of extravagant ideas. Thus, the patient may, on the one hand, 
believe that he is some great historical character, or that he is a ruling 
potentate, or, again, that he is possessed of fabulous riches. In one instance, 



DEMENTIA PARALYTICA 953 

for example, within the writer's knowledge, the patient took a room at a 
prominent hotel, after having provided himself with large sums of money, 
and from the balcony outside of the room showered the crowd beneath with 
coins of different values, with the idea that his wealth was limitless. In 
another instance, the manager of a small plant for making steel became 
imbued with the idea that his company had obtained and could fill con- 
tracts for the delivery of manufactured steel on a scale far beyond those ever 
attempted by any corporation, although as a matter of fact the business of 
the concern was at its last ebb, and his delusions aided in causing its final 
financial collapse, through its inability to carry out the agreements which he 
made with other concerns. In this instance the stress of business worry 
combined with previous excess was an active factor in producing the dis- 
ease. 

As the degenerative process in the brain continues, the patient's judg- 
ment becomes profoundly impaired. He rarely is capable of continuous 
thought, and no longer adheres for hours at a time to his delusions. He 
frequently becomes exceedingly emotional, and laughs and cries without 
adequate cause. At times he is excessively depressed; at other times 
exalted, and he may occasionally become frenzied with rage, during which 
time he may commit some crime. 

The handwriting is often characteristic. It may become illegible, either 
because the letters are badly formed or because important words are 
dropped out. Still later, loss of power occurs in the limbs until total 
paralysis may be present. Sensation is not so markedly disturbed, but areas 
of anaesthesia and analgesia may be found. The reflexes may be markedly 
increased or entirely lost. 

Naturally, there is an impairment of the general health with the progress 
of the disease. Epileptiform attacks or sudden periods of unconsciousness 
(apoplectiform attacks) develop, accompanied by paralysis of one limb, or 
by hemiplegia. Death usually ends the case by the end of the third to the 
sixth year, the patient dying of exhaustion or of some intercurrent disease, 
such as pneumonia, obstruction of the bowels, or of one of the epileptiform 
or apoplectiform attacks. 

Cases of paresis in which the delusion of grandeur is prominent are the 
earliest recognized, and constitute the classic form of the disease. There 
are many, however, in which depression simulating melancholia is present 
throughout; that is, the depressed form of paresis. But in a large proportion 
of all cases the mental symptoms are mainly those of progressive mental 
loss, without distinct delusions (the simple or demented form of paresis). 
An alternation of excitement and depression (circular form of paresis) is 
observed rarely; delusions similar to those of paranoia or of alcoholic 
insanity may mask the underlying condition. 

Diagnosis. — Dementia paralytica must be separated in its early stages from 
neurasthenia. The patient suffering from nervous exhaustion usually studies 
his own symptoms in the greatest detail, and usually considers that he is an ill 
man, while the paretic has a very much more optimistic view and often insists 
that he is more than usually well, when it is manifest that his ill health is 
extreme. So, too, the neurasthenic rarely has complete lapses of memory 



954 DISEASES OF THE NERVOUS SYSTEM 

and defects of speech. From cerebral syphilis paresis is separated by the fact 
that the former disease usually manifests severe pain in the head and true 
aphasia due to a syphilitic arteritis in the neighborhood of the speech centre. 
The fine tremor of the tongue and of the hand in paresis is absent in cere- 
bral syphilis. Optic neuritis is usually present in cerebral syphilis, but 
not very common in paresis. So, too, the mental state is one of constant 
depression in syphilis, and not that of excitation. From multiple sclerosis 
paresis is separated by the presence in sclerosis of nystagmus and intention 
tremor and by the absence of delusions. 

Prognosis. — This is absolutely unfavorable. No cases ever recover, 
although temporary, and it may be prolonged; remissions, which cause 
encouragement on the part of the friends, may occur. 

Treatment. — It must be evident, from the pathological condition already 
described, that treatment can do little. In paresis when there is a clear his- 
tory of syphilitic infection, the iodides and mercury may be freely used in 
connection with hot baths. But it must be remembered that this disease is 
the sequence of syphilis rather than the direct result of it, and therefore 
these remedies are in no sense specific. Their general tendency is favorable, 
and they may perhaps arrest for the time being the progress of the vascular 
changes, but they cannot cure those in existence. If the patient is difficult 
to control, it is far better both for himself and his friends that he should be 
committed to an asylum where he can be properly cared for, not only in the 
sense of being properly controlled, but of being well fed, as the maintenance 
of health and general nutrition is, of course, of importance. Sleeplessness 
may be treated by any one of the good hypnotics, of which chloral, trional, 
and sulphonal are the best. Occasionally, hyoscine may be used. Care 
must be taken that the carelessness of the patient in regard to his bowels 
does not result in obstinate constipation, which may be difficult to relieve. 
For this reason, active purgatives are often necessary. If outbreaks of 
excitement comes on, jfa of a grain of hyoscine may be given hypo- 
dermically. 

DISSEMINATED SCLEROSIS. 

Definition. — Disseminated sclerosis is characterized by the development 
of irregularly distributed patches of sclerosis in different parts of the brain 
and spinal cord. Similar changes also take place in the cranial nerves. 
It is sometimes called " insular sclerosis " or " multiple sclerosis." By the 
French it is called sclerose en plaques disseminees. It has only been 
recognized as a distinct disease for a little more than thirty years. 

Etiology. — The essential cause of multiple sclerosis is not known. It 
affects both sexes equally, and occurs at all ages, though very rarely in 
childhood. Its most common period of existence is, however, from the thir- 
tieth to the fortieth year. Occasionally it has been known to follow one of 
the acute infectious diseases, and has been regarded as a consequence of 
disseminated myelitis of infectious origin (Marie); but it is doubtful whether 
this malady has any direct productive effect in the case. Syphilis, that 
great cause of organic nervous disease, does not seem to be frequently 
present as an etiological factor. 



DISSEMIXATED SCLEROSIS 955 

Pathology and Morbid Anatomy. — The lesions of disseminated sclerosis 
consist, as already stated, in irregularly distributed patches in which the inter- 
stitial tissues have undergone sclerotic change. These patches are found 
chiefly in the white matter of the brain, being comparatively rare in the 
gray substance of the cortex. They are irregular in outline and vary in size. 
In appearance they are reddish-gray and translucent. The surface of a patch 
is usually even with the surrounding brain tissue, but it may be slightly 
depressed. A sharp line of demarcation separates the diseased area from 
the healthy tissues. When touched, the patches seem harder than normal 
gray matter, but they are not usually met with until section of the brain or 
cord is made, when they appear in strong contrast to the surrounding white 
tissue. They may be found in considerable number in the lateral ventricle, 
in the corpus callosum, crura, and pons. The patches in the spinal cord 
are not so reddish in hue as in the brain, but are more gray in color and 
extend vertically rather than transversely; but this rule is not absolute, and 
at times the transverse extension of a patch may embrace the entire thick- 
ness of the cord. When one of the cranial nerves is involved, it is found to 
be gray in color and sclerotic for a certain portion of its length. In some 
instances the entire thickness of the nerve is involved. The olfactory, optic, 
oculomotor, trifacial, and facial nerves are the ones which are most com- 
monly affected, and in the case of the optic nerve the favorite seat is the 
chiasm. 

The sclerotic process in this disease does not differ very materially from 
that met with in sclerotic processes occurring in other organs of the body; 
there is an overgrowth of the true neuroglia or connective tissue, and side 
by side with this overgrowth a corresponding atrophy or disappearance of 
the nerve cells and fibres themselves takes place. When the degenerative 
process is well advanced, we find scattered through the connective-tissue 
fatty granules and nerve cells which show evidence of degenerative 
change. In the nerve fibres the chief change takes place in the myelin, 
but after the disease is far advanced the axis cylinder also becomes 
affected and finally is completely destroyed. In the central nervous system 
it is usually found that secondary degeneration in the nerve fibres above or 
below the seat of the original sclerotic patch is only met with when the dis- 
ease has been sufficiently severe to destroy the axis cylinders. On this 
account secondary degenerations are not common in disseminated sclerosis, 
the axis cylinders surviving in the midst of fully developed sclerotic patches, 

Symptoms. — The symptoms of disseminated sclerosis depend almost 
entirely upon the areas of the nervous system which are chiefly affected by the 
pathological changes just described. Among the earliest symptoms in many 
cases is a loss of power in the extremities. In the legs the symptoms may be 
ataxic, but usually simulate those of spastic paraplegia in a striking degree. 
When spastic paraplegia is present, this indicates that the sclerotic process 
has involved the pyramidal tracts, and the knee-jerks are found to be exag- 
gerated. In other instances inco-ordination of the hands, or of one hand, 
may be the first manifestation of the malady, and in still others sensory 
disturbances in the legs or arms are first complained of by the patient. The 
inco-ordination of the muscles of the arms is often very marked indeed. 



956 DISEASES OF THE XERYOUS SYSTEM 

Often it is impossible for a patient to carry a glass of water to his lips without 
spilling it (intention tremor). The co-ordinated movements which are 
necessary in writing are impossible because of the quick or spasmodic 
contractions of the muscles employed for this purpose. The cause of 
these irregular movements is not known. According to some it is depend- 
ent upon the fact that certain fibres are affected, and impulses going along 
certain channels, particularly the motor, are delayed in passing through scle- 
rotic areas, or that those which pass along fibres still unaffected are made 
inadequate and, as it were, embarrassed. By others it is thought that the 
sclerotic patches have involved afferent fibres of the cerebellar system which 
are concerned with muscular sense. 

If sensory fibres in the dorsal columns are involved, areas of anesthesia 
or hemianesthesia, also ataxia of the extremities, will develop, the severity 
of these symptoms depending, of course, upon the area involved in the 
sclerotic process. The eye symptoms are usually well marked. One of 
the earliest and most constant of these is nystagmus. Eyesight fails 
through involvement of the optic nerve or because of a sclerotic patch at 
the optic chiasm. As the disease advances pallor of the optic disk, partic- 
ularly its temporal half, and sometimes optic atrophy can be recognized 
on ophthalmoscopic examination. One eye is often much more affected 
than the other, and loss of accommodation may occur. In other 
instances the pupillary reflex may be lost, yet the pupil will react to 
accommodation. In other words, the Argyll-Robertson pupil is present. 
The affection of the external ocular muscles, aside from the production of 
nystagmus, consists most frequently in a failure in convergence and in con- 
jugate deviation. More rarely a single muscle is affected and squint is pro- 
duced. When the facial nerve is affected, the symptoms in the early stages 
may consist in clonic spasm of the muscles of the face, followed eventually by 
paralysis. The lesions of the cranial nerves, which produce these results, 
may, as already pointed out, occur in the nerves themselves or involve their 
nuclei. 

Of all the symptoms of disseminated sclerosis perhaps the most character- 
istic and most frequent is the peculiar disorder of speech in which syllables 
are enunciated in a measured manner. To this mode of speech the term 
staccato or scanning is applied. The exact cause of this is not clear. It does 
not seem to be dependent entirely upon paralysis involving the tongue or 
the lips. 

The mental condition of the patient is usually not materially altered. 
The memory may be slightly impaired and the patient seem somewhat 
emotional. Very occasionally actual insanity develops. Paroxysmal attacks 
of vertigo and vomiting are occasionally met with, and in some cases the 
patient is seized with attacks which closely resemble an ordinary apoplexy. 
These attacks, it will be remembered, sometimes develop in patients who 
suffer from general paralysis of the insane, and they appear either as ordinary 
coma, as Jacksonian epilepsy, or as a hemiplegia which is fleeting in char- 
acter. All these symptoms of an apoplectiform type may recur frequently, 
and are usually recovered from, but occasionally death comes on during 
coma. It is a fact worthy of note that, notwithstanding the profound changes 



DISSEMINATED SCLEROSIS 957 

which take place in different portions of the nervous system, trophic changes 
in the muscles are rarely met with, even in advanced cases. 

Diagnosis. — The most characteristic symptoms of disseminated sclerosis, 
as just stated, consist in the intention tremor, the staccato speech, the 
nystagmus, the peculiar jerking, inco-ordinated movements of the muscles 
of the arms and sometimes of the legs, weakness of the legs, and the 
gradual involvement of the cranial nerves. 

The disease is to be separated from locomotor ataxia by the jerking character 
of the inco-ordinated movements; and by the exaggeration of the reflexes, 
which are in contrast to the absent reflexes of ataxia. From paralysis agitans 
it is separated by the fact that in the latter disease there is a finer tremor of the 
hand, or of the parts of the body which may be affected (the tremor is passive), 
by the peculiar attitude of the patient in paralysis agitans, and by the absence, 
as the disease progresses, of the characteristic symptoms just spoken of as 
peculiar to multiple sclerosis. General paralysis of the insane is distinguished 
by the presence, in the classic type of this disease, of delusions of grandeur, 
by the twitching of the muscles of the lips and tongue, which are more con- 
stant and severe than they are in multiple sclerosis, and by the other evidences 
of mental change. In a case of disseminated sclerosis, in which the lateral 
columns of the spinal cord are involved, it may be difficult to differentiate 
multiple sclerosis from spastic paraplegia, but as the disease progresses the 
development of the other symptoms of disseminated sclerosis makes the 
diagnosis easy. From hysteria disseminated sclerosis is to be separated by 
the fact that nystagmus does not appear in this functional nervous disorder, 
and by the inconstancy of the symptoms in many cases of hysteria. The 
other characteristic stigmata of hysteria may also be found. (See article on 
Hysteria.) 

Prognosis. — The prognosis in a case of disseminated sclerosis is absolutely 
unfavorable as to ultimate recovery. The disease is characterized by various 
remissions or periods of arrest, so that death is sometimes postponed for 
a considerable period of time. The prognosis as to duration of life is worse 
in those cases in which the lesions involve nervous tissues closely associated 
with vital functions, as when sclerotic changes take place in the pons, 
or, above all, when they occur in the medulla. It is noteworthy that 
pregnancy or trauma increases the rapidity with which the disease pro- 
gresses. 

Treatment. — Everywhere in this book, when we have considered the 
treatment of diseases depending upon sclerotic changes or overgrowth of 
connective tissue it has been pointed out that our therapeutic resources are 
inadequate. We do not know the causes of this connective-tissue over- 
growth, and so are unable to combat it, nor do we know why the cells degen- 
erate. Neither have we any reason to believe that in the future we will 
discover any remedy which will cause the absorption of connective tissue 
when it is once formed, and it is certain that fibres which have once degen- 
erated and have been destroyed cannot be regenerated by the action of any 
medicine. 



958 DISEASES OF THE NERVOUS SYSTEM 



DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN 

THE SPINAL CORD. 

LOCOMOTOR ATAXIA. 

Definition. — Locomotor ataxia is a disease characterized chiefly by inco- 
ordination of gait and station, loss of muscle sense, and loss of the deep 
reflexes. It is often accompanied by pain. The most noteworthy loss of 
reflexes is in the patellar tendon and iris. Pathologically, it is characterized 
by slow progressive lesions which affect chiefly the sensory nerve roots and 
the posterior or dorsal columns of the spinal cord. It is sometimes called 
tabes dorsalis, or posterior spinal sclerosis. 

History. — Cases of locomotor ataxia were recorded as a form of paralysis 
many years ago, but it was not till 1847 that Todd clearly separated this 
malady from other states of paralysis. In 1840 Stanley had recognized that 
the affection was associated with changes in the posterior columns of the 
spinal cord. In 1855 Reynolds first showed that the disease was essentially 
a state in which the symptoms were due to a loss of muscle sense, and not to 
loss of power in the motor nerves or muscles — a view confirmed by Turck, 
who made a microscopic demonstration of the site of the lesions. 

Etiology. — Males suffer more than females in the proportion of 10 to 1. 
In a large hospital experience of over twenty years I have never seen a case 
in a woman. Half the cases develop in the decade of life between thirty and 
forty years, and 80 per cent, between thirty and fifty years. Gowers states 
that it rarely develops after fifty years. 

By far the most common cause of the disease is acquired syphilis. Rarely 
the syphilis is hereditary. Some writers have gone so far as to state that 
locomotor ataxia is due to this cause in over 90 per cent, of the cases (Sachs). 
Gowers gives the rather moderate proportion of 77 per cent.; Starr 70 per 
cent. It is, however, important for the student to remember that locomotor 
ataxia is not syphilis of the nervous system, but rather a remote result of the 
syphilitic infection. In many instances the ataxic symptoms develop so many 
years after syphilitic infection that the patient cannot believe that the two 
maladies have any relationship of cause and effect, the more so as ataxia is more 
frequently met with in patients who have presented very mild secondary 
symptoms than in those who have had severe symptoms in the early stages. 
Rarely the ataxic symptoms develop within five years of the primary sore. 

Next to syphilis as a possible cause is traumatism. Severe falls, or blows 
upon the spine, have been followed, months or years later, by tabes dorsalis, 
but it is impossible to tell whether the trauma is the direct cause of the 
malady. Sometimes other diseases of the cord finally produce locomotor 
ataxia. 

Pathology and Morbid Anatomy. — In studying the morbid anatomy and 
pathology of locomotor ataxia it is important for the student to recall the 
fact that the primary lesion of the disease is in the posterior ganglia and 
posterior roots of the spinal cord, and in the ganglia of the cranial nerves, 
and not in the posterior columns of the spinal cord, as was thought at one 



PLATE VII. 



£~^\ Sensory 
3 Motor 

C__3 Association 




XIII 



The Cervical and Sacral Enlargements of the Spinal Cord in 
Cross-section— showing the various neurones in the gray matter, 
the direction of their axones, and the varieties of fibres in the 
different columns of the cord (Starr). Blue, motor-; red, sensory-; 
purple, association-neurones and axones. 

I. Ant. median column. II. Anterolateral column. • III. Gowers' anterolateral ascending column. 
IV. Marginal column. V. Lateral pyramidal column. VI. Direct cerebellar column. 'VII. Lissauer's 
tract. VIII. Ext. portion of column of Burdach. IX. Root zone of the column of Burdach. X. 
Descending comma-shaped bundle of Schultze. XI. Post, commissural tract. XII. Column of Goll. 
XIII. Septomarginal tract. 



LOCOMOTOR ATAXIA 959 

time. The sensory cells in the posterior ganglia, outside of the cord, are 
flask-shaped bodies, each of which has a process which divides into two 
axones. One of these goes by the posterior nerve root to the spinal cord, 
and the other goes to the afferent nerve, which extends to the peripheral 
portions of the body. (See Plate VII.) Degenerative changes take place 
in the proximal axone as well as in the peripheral portion of the distal axone. 
These changes are sclerotic and are carried into the cord, so to speak, by the 
proximal axone. Therefore, locomotor ataxia consists primarily in disease of 
the proximal axone, secondarily in disease of the distal axone, and finally 
in disease of those fibres in the posterior portion of the spinal cord which 
have their origin in the proximal axone just described. While it is true 
that the primary lesion is not in the cord, it is nevertheless a fact that the 
chief manifestations of the pathological process are to be found in this por- 
tion of the nervous system. Indeed, the changes in the spinal cord are so 
well developed in typical cases that the macroscopic examination suffices 
for the diagnosis at the autopsy. 

The affected portions of the cord are smaller than normal and more 
grayish in appearance. The distribution of those areas varies greatly. 
In some instances the disease is so moderate in degree and in distribu- 
tion as to be difficult of recognition, except by the microscope. In others, 
if the malady is far advanced, the whole length of the posterior columns 
may be affected. There are certain parts of the cord which are particu- 
larly prone to the development of the disease. Thus, the lesions are usually 
well developed in the posterior columns in the lumbar region, particularly 
in the neighborhood of the posterior root zones, and this accounts for the 
fact that the legs show the earliest and most severe symptoms. As we 
ascend the cord, however, the lesions are chiefly found in the postero- 
median columns. 

In instances in which the disease affects the arms as well as the legs and 
is well developed, the posteroexternal columns are affected even in the 
cervical region (Fig. 124). 

Under the microscope it is found that the connective tissue in the pos- 
terior columns of the cord has undergone hyperplasia or overgrowth. The 
fibrous sheath of the bloodvessels is particularly affected and is seen to be 
thickened and to project connective-tissue fibrils into nearby parts. The 
nerve fibres may have disappeared entirely or be represented by atrophied 
or wasted fibres. In some cases the vessels of the pia mater are also 
thickened, particularly in the part covering the posterior columns, and these 
vessels may also give off fibrils of connective tissue which add to the con- 
nective-tissue overgrowth in the superficial part of the cord. 

The changes which are found in the posterior nerve roots vary greatly in 
their degree. In some instances they are so slight that they can be recog- 
nized only by careful microscopic examination; in other instances they 
are so well marked that the naked eye can detect them. Under these circum- 
stances they appear atrophied and the connective-tissue elements may be 
somewhat increased. The root fibres in the cord are more affected than 
those outside of the cord. The ganglia are also affected by an overgrowth 
of connective tissue, and by an atrophy of their nerve cells. Beyond the 



960 



DISEASES OF THE NERVOUS SYSTEM 



Fig. 124 




ganglia pathological changes in the mixed nerve are rarely seen as a con- 
tinuation of the process found in the nerve roots, but it is a well-recog- 
nized fact that marked primary changes are to be found in the peripheral 
nerves, and especially in the cutaneous branches. These changes consist in 
anatrophy of the myelin sheath followed by degeneration and segmentation 
of the axis cylinder, and they occur at the distal extremity of the nerve in 

greater degree than higher up. The main 
nerve trunks are rarely affected. It is 
largely because of these neural lesions that 
sensation in the skin and in the joints and 
the muscular sense are lost. 

In certain cases the changes of locomotor 
ataxia may be well marked in the cord and 
slight in the nerve roots, and in others the 
nerves are chiefly involved. It is important 
that this fact be remembered because it 
serves to fix in the mind of the student the 
fact that locomotor ataxia is not solely a 
disease of the posterior columns of the cord. 
While locomotor ataxia chiefly affects the 
spinal cord and its nerve roots, it also at- 
tacks quite frequently the cranial nerves, 
and of these the optic nerve suffers most 
severely and most frequently. Its nerve 
fibres atrophy and its connective tissue 
undergoes proliferation. 

By no means rarely marked degenerative 
changes are found in the joints. The artic- 
ulating cartilages are eroded, the joint may 
become filled with fluid, and for these rea- 
sons dislocations may occur. Trophic 
changes also occur elsewhere. (See Symp- 
toms.) 

Symptoms. — In a case of locomotor ataxia 
which is typical in its course the following 
symptoms are present, and if they are well 
developed it is not difficult to make a diag- 
nosis : 
The patient often states that his feet feel " muffled," that is, as if he had on 
several pairs of thick socks. In other cases he notices that on arising at 
night he has difficulty in getting a proper "purchase'' with his feet on the 
floor, or the floor may feel as if its plane is at a different angle from that pic- 
tured in his mind. These awkward sensations are due to the interference with 
the sensory nerve fibres, that is, with conduction of sensation to the spinal 
cord. He also has difficulty in walking in the dark, not only because his 
tactile sense is disturbed, but because his muscle sense is also impaired, with 
the result that he is in doubt as to the position of his limbs and as to the 
relative tonicity of opposing muscles. This loss of muscle sense depends 



Sclerosis of the lateral and (in the ante- 
rior cervical region) pyramidal tracts, with 
slight degeneration of the anterior coruna. 
A, cervical ; B, dorsal; C, lumbar sections. 
(After Gowers.) 



LOCOMOTOR ATAXIA 961 

upon the fact that the sensory nerves supplying the joints, tendons, and 
fasciae are impaired in function and the tracts in the spinal cord which carry 
these impulses which reflexly co-ordinate movement are also involved. If 
the impulse passes this area of damage and reaches the cord it passes up 
the posteromedian columns without decussation, and probably goes directly 
to the cerebellum, which presides over balance. These columns are always 
diseased if the ataxia is marked, but cutaneous sensibility is often pre- 
served, proving that the muscular and cutaneous sensations are carried 
by different tracts. 

Closely related to the disorder of muscle sense is inco-ordination, which 
produces the peculiar gait. In the ataxic gait the foot is raised awkwardly 
and then thrown down in front of the other foot with a characteristic uncer- 
tain movement, the whole under surface of the foot striking the ground at 
once. This uncertainty of movement becomes still more marked if the 
surface over which the patient has to walk is uneven, or if a rug upon the 
floor requires that the feet shall be lifted slightly to clear it. In other cases 
the edge of the foot rests on the floor instead of the plantar surface, and 
in the effort to correct this position another clumsy movement is made. 
If the light is poor or if the patient closes his eyes, the difficulty in muscular 
co-ordination may be so great that he staggers and falls. As ,the involve- 
ment of the sensory pathways becomes more marked, support by means of 
a cane, nearby objects, or another person, is needful for locomotion, and 
finally all attempts at walking have to be given up. In cases in which the 
upper portions of the cord suffer, there is a similar inco-ordination of the 
arms, so that the patient cannot carry food to his mouth if the eyes are closed. 
In other instances, however, even when the legs are practically useless, the 
arms entirely escape. If either the arms or the legs are extended the muscles 
do not remain steady, but alternately contract and relax, as the patient 
vainly endeavors to maintain his balance. There is no actual loss of 
muscle strength until the disease has lasted so long that the muscles waste 
from disuse. 

The same cause that produces the difficulty in gait also causes a disturb- 
ance of "station." That is to say, the patient cannot stand steadily, but 
sways in the endeavor to keep his balance. If his eyes are closed or if he is 
blindfolded he sways so widely that there is danger of his falling, and he 
may actually fall if he cannot co-ordinate his muscles by the use of his eyes, 
which will give him a conception of the relative position of surrounding 
objects. This instability is often very marked when the patient attempts to 
suddenly assume the erect posture after sitting in a chair for some time. 
As Romberg first called attention to this loss of station, the term "Romberg's 
symptom" is applied to this manifestation of the malady. 

Still another indication of the disease in the sensory pathways in loco- 
motor ataxia is the diminution and final total loss of the knee-jerks when the 
patellar tendon is tapped. This is called "WestphaVs symptom." 

So far only those disorders of motion which result from the loss of muscle 
sense have been discussed. There yet remain to be considered the charac- 
teristic sensory symptoms themselves. These consist in pain and loss of 
sensibility. Pain is a very frequent and often a very early symptom, occur- 
61 



962 DISEASES OF THE NERVOUS SYSTEM 

ring in about 90 per cent, of all cases, and it may be very severe. It occurs 
chiefly in the legs as sharp dartings called "lightning pains." Unlike the 
motor symptoms, these pains are not confined to the legs and arms, but are 
often present in the body and even in the head, where other symptoms of 
this disease are rare, except in the eyes. The pains are often agonizing and 
occur chiefly at night. In most instances they occur in periodic attacks, then 
ceasing for weeks or even months. They may develop in different parts of 
the body at each attack. They rarely have their seat in large nerve trunks, 
but exist in the more minute fibres of the nerves. When they attack the 
stomach they are called ''gastric crises," a term also applied to severe 
attacks of vomiting in this disease. So, too, attacks of intense pain may 
suddenly develop in the bladder, "vesical crises," and in the rectum, 
"rectal crises." There may be marked "girdle sensations" in the trunk. 

The fains are described as darting, rending, or burning, and the patient 
may speak of "burning toes" as his most troublesome symptom. Intense 
hyperesthesia of the skin in the painful areas may also be present. These 
pains are to some extent affected by atmospheric states. I have more than 
once known them to be produced or exaggerated by constipation, probably 
because of the absorption of intestinal toxins. 

It is important to bear in mind the fact that pain may be one of the 
earliest signs of this malady, and may vary from tingling to an agony 
without any of the disorders of the gait being as yet present. On the other 
hand, very severe ataxia may be present without any pain. In addition 
to these painful disorders various other disturbances of sensation also 
develop, such as formication, tickling, pricking, creeping, sensations of heat 
and cold, or hyperesthesia. When the disease is well advanced, diminution 
of sensation in the skin or even complete anesthesia may appear. The sense 
of pain and of touch may both be impaired. The pain sense may be lost 
and the heat sense retained, or, again, the tactile sense may be interpreted 
by the patient as pain or heat. A very interesting perversion of the function 
of sensation is the delay in the transmission of the sensory impulses, so that 
a very appreciable interval occurs between the moment at which the foot is 
pricked and the moment at which the patient appreciates the fact that the 
injury has been sustained. Obersteiner has recorded a case in which the 
interval was twenty-five seconds. So, too, the patient is unable to readily 
indicate the part touched. He may even assert that it is the left foot when 
it is really the right one that is irritated. To this symptom the term alio- 
chiria is applied. All these tests must be made, of course, with the patient 
blindfolded. The deeper portions of the body may be as anaesthetic as the 
skin, and injury to a testicle, pleurisy, and severe muscular inflammation, 
as after a deep injection of mercury, may be painless. Sexual power may 
or may not be lost. 

The changes which take place in the eyes in locomotor ataxia are so con- 
stantly met with and are so valuable to us from a diagnostic standpoint, that 
they are worth remembering. In about 80 per cent, of the cases the Argyll- 
Robertson pupil is present, that is, the pupil reacts to accommodation, but 
not to light. This state depends upon a lesion, somewhere in the path of 
the light reflex, which includes the optic nerve on the one hand and the 



LOCOMOTOR ATAXIA 963 

oculomotor nerve and nucleus on the other, with a connection between 
these two nerves which is not known. Some have taught that Meynert's 
decussation, between the primary optic centres in which the optic nerve 
ends and the third nerve nucleus, forms this connection and is the seat of 
lesion determining the Argyll-Robertson pupil. Recent studies indicate 
that the fibres concerned pass from the optic tract to the third nerve nucleus 
before the former has reached the primary optic centres. 

There may be loss of accommodation in some cases. The pupils are 
usually myotic; they may be unequal and uneven, especially during con- 
traction; they may also be irregular in shape. 

The second important ocular symptoms are those which depend upon the 
nerve supply of the extrinsic muscles of the eye. Diplopia may develop as 
a fleeting or permanent symptom due to insufficiency of one of the ocular 
muscles, the external rectus muscle being the one most commonly affected, 
although there is diversity of opinion as to this point. So, too, single or double 
ptosis may develop and be transient or permanent. In some cases all the 
extraocular muscles become paralyzed so that a complete external ophthal- 
moplegia may be present. The third ocular sign of importance is atrophy 
of the optic nerve, which takes place in about 10 per cent, of all cases. It is 
often present before any difficulty of the gait develops, and for this reason 
the presence of the disease may be first recognized by the ophthalmologist 
rather than by the general practitioner. It is thought by some writers that 
this manifestation of locomotor ataxia is more prone to develop in the 
instances in which the arms are involved than in those cases in which the 
lower portions of the cord are affected. Not rarely the presence of optic 
nerve atrophy seems to be accompanied by an arrest of the sclerotic process 
elsewhere. The field of vision is primarily diminished, there may be loss of 
color vision, but sometimes the failure is marked, even from the onset, in the 
neighborhood of the macula. The impairment of vision which ensues may 
progress to total blindness or become arrested and consist in more or less 
severe impairment. Usually the process is slow, but occasionally it is so 
rapid that even a few days produce great changes in the visual acuity. As 
is easily understood, when we consider the nature of the lesions which are 
characteristic of the disease the loss of vision is not always unilateral. 

When the optic nerve is examined by the ophthalmoscope in such cases 
the disk is seen to be pale and shrunken, but at times the degree of blindness 
is in excess of the changes in the disk. Finally, the disk becomes a pale gray. 

Occasionally deafness gradually or suddenly developes. It may be tran- 
sient or fleeting. 

The bladder in locomotor ataxia is often greatly impaired in its functions. 
The urine is often imperfectly expelled and as a result residual urine pro- 
duces cystitis. More rarely retention of urine ensues. The sphincter ani 
is also weakened, and so control of the feces is diminished. 

There still remain to be considered two results of the disease which are 
of interest and diagnostic importance. The first of these is the so-called 
"Charcot joint," to which reference has already been made. Owing to the 
changes in the elbow, shoulder, hip, and knees the landmarks of these parts 
may be completely obliterated, and great swelling often is present. The 



964 



DISEASES OF THE NERVOUS SYSTEM 



Fig. 125 



second of these trophic changes is the so-called perforating ulcer of the foot, 
which may or may not be accompanied by ulcerations about the toe-nails. 
Diagnosis. — As already intimated, the most valuable diagnostic symptoms 
and signs of locomotor ataxia are the loss of the knee-jerk, the swaying 
station, the Argyll-Robertson pupil, the optic atrophy, and the lightning 
pains. No one of these, however, enables us to make a diagnosis because 
of its presence. The disease must be differentiated from peripheral 

neuritis due to alcohol, lead, and arsenic, and 
from that due to typhoid fever and diph- 
theria. In these conditions there is loss of knee- 
jerk, swaying station, and often severe pains or 
anaesthesia it may be, but the Argyll-Robertson 
pupil is absent and the history of the patient as 
to exposure to alcohol, lead, or arsenic aids us 
greatly in the differentiation. To these states the 
term pseudotabes has been well applied. 

Locomotor ataxia is separated from the various 
forms of paraplegia by the persistence of the 
knee-jerk, which is usually exaggerated, and by 
the actual loss of power in paraplegia. From 
the spastic paraplegia due to lateral sclerosis 
true locomotor ataxia is separated by the spastic 
state of the muscles and the greatly increased 
knee-jerk. 

From general paralysis of the insane loco- 
motor ataxia may be difficult of separatoin, for 
in this disease the Argyll-Robertson pupil and 
other physical signs of locomotor ataxia may be present. As the case 
advances the predominance of the cerebral symptoms over the spinal symp- 
toms becomes marked and so renders the diagnosis possible. (See Paretic 
Dementia.) 

The fact that in rare cases of locomotor ataxia severe pains are felt in 
the trunk should never be forgotten, for it has happened not infrequently 
that they have misled the physician into a belief that caries of the vertebrae 
was present. 

The staggering gait of cerebellar tumor can scarcely be mistaken for 
locomotor ataxia. If there is doubt as to its cause it can be dispelled by the 
absence of shooting pains, by the presence of headache and of nystagmus. 
Prognosis. — The prognosis of locomotor ataxia may be best considered in 
two parts. So far as recovery is concerned, this is out of the question. So 
far as rapidity of progress is concerned, we must always be guarded in 
expressing an opinion. In the great majority of cases the disease lasts for 
years and is characterized not only by periods of rest, but of actual improve- 
ment of a very marked character in some cases. If there is a syphilitic his- 
tory the use of the proper specific remedies may arrest the malady, but they 
cannot cure the damage already done. Cases which attack those young in 
years and progress rapidly are most unfavorable, but even these cases make 
remarkable "stops " in the advance of the affection. 




Perforating ulcer of the foot in loco- 
motor ataxia. (Obersteiner.) 



LOCOMOTOR ATAXIA 965 

Treatment. — There is probably no grave disease of the nervous system of 
an organic nature which, in some instances at least, yields such good results 
from treatment as does this one. 

As may be gathered from the discussion of the pathology of locomotor 
ataxia, it must be evident that the physician can only palliate the symptoms 
of this disease, and that a complete cure is practically impossible. The most 
that we can do is to attempt to eliminate from the system the causes which 
are primarily active in the production of the characteristic lesions and so 
prevent further progress of the malady. What these poisons are we do not 
know, for, as already pointed out, even in those cases in which there is a dis- 
tinct history of syphilis, it is probable that the cord disease develops rather 
as a parasyphilitic condition than one depending directly upon syphilis. 
Nevertheless, in a large proportion of cases, benefit is obtained by the pur- 
suance of a plan of treatment which consists largely in the administration of 
mercury and the iodide of potassium. If the specific infection is of com- 
paratively recent date, the mercury should be used, but in many instances 
this is not the case, and the iodide of potassium is the remedy of choice. 
The rule governing its administration, under these circumstances, is to give 
that quantity which the patient can take without seriously impairing his diges- 
tive functions and general health. It is a question of the effect produced 
rather than one of grains of drug administered. Some patients can take 
very large doses without symptoms of iodism; whereas, others are affected 
even by moderate doses. The drug should be given in ascending doses until 
its full physiological effects are manifested, and then the dose is to be cut 
down one-third or one-half, and continued for a number of months. Very 
often the best results are obtained if in addition inunctions with mercurial 
ointment are practised twice or thrice a week. 

While, on the one hand, it should be our endeavor to use these two 
specific remedies very freely, it must also be remembered that the patient's 
vitality must be kept at the highest possible level by every means in our 
power. Poor health and digestive disturbance produced by the unwise 
employment of mercury or iodine probably does the patient more harm 
than the drugs do him good. Often it is advisable to give iodide of potas- 
sium for three months, and then to use mercury for three months. Starr 
asserts that the use of mercury hastens the process of optic nerve atrophy, 
and in those cases in which this symptom is present mercurial treatment 
should not be resorted to. In those cases in which there is no syphilitic 
history, or in which the mercurials are badly borne, arsenic may be given 
as a nerve tonic. Nitrate of silver was at one time thought to be advan- 
tageous, but there is nothing in our knowledge of this drug or of the disease 
which makes its employment in any way rational. 

For the relief of the pains in the peripheral nerves, the coal-tar products 
are our best remedies, acetanilid, phenacetin, and antipyrin being commonly 
employed. In other instances the salicylates are useful. If the pain is 
excessive, morphine must be used. 

For the twitching of the limbs, the bromides, which quiet the sensory 
portions of the cord, may be employed in sufficiently large doses to pro- 
duce sedation. 



966 DISEASES OF THE NERVOUS SYSTEM 

A method of treating these cases which is of some value is that introduced 
by Fraenkel, of Berlin. This method is not curative in the sense that it is 
supposed to influence the lesions in the cord, but is employed with the 
object of training other nerve fibres than those originally used, so that the 
patient may to some extent regain his muscle sense. This plan consists 
in making him take certain exercises which require co-ordination. A 
chalk line is drawn upon the floor and he is required to follow it as closely 
as possible; or, a series of cup-like depressions are made in a plank, which is 
placed across the foot of the patient's bed. These depressions are num- 
bered from one to ten, and he is instructed by the nurse to raise his leg and 
then rest his heel in the cup which she names. In this way the patient in 
some instances is able to speedily respond to the order, and so is trained 
to carry out well co-ordinated movements. Still another method consists 
in supplying him with a small double flight of steps provided with railings 
so that he cannot fall. The patient is then required to mount a few steps on 
one side and then descend a few on the other, using his legs to lift himself 
up on each step, and not pulling himself up by his hands, which rest upon 
the rails. In other instances still, definite spaces are marked out on the 
floor, and he is directed to take a stride which will bring his heel on each 
mark. It can be readily seen that a large number of such exercises can 
easily be devised if a little ingenuity is exercised. Care should be taken that 
the exercises are not continued so long that the patient becomes in the 
slightest degree exhausted. For this reason they should rarely be continued 
more than five minutes at a time, although they may be resorted to several 
times a day. Additional methods of treatment consist in the employment 
of massage, which is designed to maintain the nutrition of the limbs and to 
keep in health the bloodvessels and lymphatic system, thereby to a certain 
extent compensating for the lack of exercise from which the patient inevitably 
suffers. 

The various forms of baths at home, or at health resorts, may be employed 
rather for the mental effect which they will exercise upon the patient than 
with any hope that they would be in any way curative. The great advantage 
in resorting to the various health resorts where baths can be obtained is that 
the patient goes away for the purpose of getting well and leaves his business 
cares behind him. The great difficulty with cool baths is that the patient 
usually has not sufficient power of reaction to stand them, and tepid and 
hot baths often seem to exercise an enervating effect. Where baths can be 
used with the object of aiding in the absorption of mercury and the iodides, 
and where they do not produce depression, they are valuable. 

So far as exercise is concerned, this should be governed entirely by the 
strength of the patient. Under no circumstances whatever should he be 
permitted to become exhausted. Not infrequently severe attacks of pains in 
the limbs are precipitated by exercise which is sufficiently severe or pro- 
longed to diminish the nervous vitality of the patient or to tire the nerves 
themselves. 

Electricity may be used in the form of the galvanic current, the positive 
pole of the galvanic battery being placed at the nape of the neck and the 
negative pole at the sacrum and at the soles of the feet. The electrodes 



FRIEDREICH'S ATAXIA 967 

should be large so that the current will be well diffused. As a matter of fact 
the condition of the spinal cord and the nerve trunks is such that little real 
benefit can be expected from this plan of treatment except for its sedative 
influence. 

Some years ago a method of treating locomotor ataxia by suspension was 
introduced. A harness was attached to the patient's head and shoulders, 
and by this means he was gently swung free from the chair in which he was 
sitting. Under these circumstances, the weight of the lower portion of his 
body produced some extension of the spine, and it was claimed that in this 
manner marked benefits were produced. Hundreds of cases were treated 
by this method, but it is worthy of note that it has now gone out of fashion, 
proving that it does not possess the value which at first was credited to it. 



FRIEDREICH'S ATAXIA. 

Definition. — Under this name a disease of the nervous system is rarely 
met with which is hereditary and which depends for its clinical manifesta- 
tions upon lesions in the posterior and lateral columns of the spinal cord. 
It is, therefore, an ataxic paraplegia which is peculiar in that it develops in 
early life. Friedreich's ataxia is also called " hereditary ataxic paraplegia," 
" hereditary ataxia," " Friedreich's disease," and " family ataxia." 

History. — The malady was first described by Friedreich in 1861 and 
again in 1876. In the United States the most noteworthy study is that of 
Everett Smith in 1885. Schultze showed in 1877 that the disease was due 
to a congenital defect in the cord. 

Etiology. — The exact cause is unknown. Occasionally there is a distinct 
family history of the disease, but often no more than one child in a family 
is affected. Sometimes the symptoms develop after one of the acute infec- 
tious diseases of childhood, and it is then supposed to be due to development 
of the evidences of imperfect growth or to damage to poorly vitalized cells 
which have never become well developed. In some cases the parents have 
an alcoholic history; in others there is a history of syphilis. Neither of these 
facts are, however, of real etiological importance. The influence of age is 
uncertain. Rarely the malady manifests itself in infancy; more commonly 
it develops about the sixth or eighth year; if not at this period, then at 
puberty, and if not at puberty, then at about twenty-one years of age. The 
two sexes suffer about equally. It has been shown that defective develop- 
ment of the cerebellum may be a part of the pathological findings in this 
disease. Marie, however, believes that spinal cord atrophy in these areas, 
when due to cerebellar disease, is a separate malady, and the symptoms due 
to agenesis of the cerebellum are sufficiently distinctive to constitute a sepa- 
rate type of hereditary ataxia. 

Pathology and Morbid Anatomy. — As already stated, the lesions of Fried- 
reich's ataxia are chiefly found in the posterior and lateral tracts of the 
spinal cord, and the disease may therefore be considered as a combination 
of two maladies so far as the lesions and symptoms are concerned. 

When the spinal cord is removed from such a case at autopsy it is usually 



968 DISEASES OF THE NERVOUS SYSTEM 

seen to be smaller than normal, and the pia mater is commonly thickened, 
particularly over its posterior surface. 

If the cord is examined under the microscope with suitable staining (Fig. 
126), it is found that the posterior dorsal columns, particularly those of Goll, 
the lateral pyramidal tracts, and the direct cerebellar tracts all show degen- 
erative changes. These changes are not chiefly limited to one portion of the 
cord, as they are in most cases of locomotor ataxia, but extend up into the 
cervical region as well as in the lumbar region. The lesions are not only 
posterior and lateral, but anterior as well, for the direct pyramidal tract 
on either side of the anterior median fissure is affected. There is also 
atrophy of the cells in the anterior and posterior horns of the gray matter. 
The anterior and posterior nerve roots are also atrophied. The cells in the 
column of Clarke are markedly degenerated, and round-cell infiltration is 
present about the central canal of the cord. In this disease, as in other 

Fig. 126 




The lesion of Friedreich's hereditary ataxia. Maldevelopment and sclerosis of the lateral and 
posterior columns. (Schultze.) 

maladies, the loss of nervous tissue is followed by overgrowth of the neuroglia 
in the affected parts. 

Symptoms. — As Friedreich's ataxia consists, pathologically, in lesions in 
the posterior and lateral columns of the cord, it necessarily follows that the 
symptoms are closely allied to locomotor ataxia and lateral sclerosis. The 
onset of the disease is characterized by gradual loss of co-ordination, affecting 
the legs before it affects the arms, which causes unsteadiness in station, so 
that the feet, when the patient is standing, are placed far apart to maintain 
the balance of the body. In some instances the first symptom is that the 
child falls over objects which hitherto have not been obstacles in its path. 
When the child walks its gait is tottering, and if it closes its eyes the lack of 
co-ordination and consequent instability is so great that it may fall. The 
muscles of the legs are often strongly contracted in an endeavor to maintain 
the upright posture, and this condition of muscular rigidity is increased by 



FRIEDREICH'S ATAXIA 969 

the disease in the lateral tracts. The child if stripped and left standing is 
seen to be continually writhing in an endeavor to adjust opposing muscles 
in order to maintain its equilibrium. The knee-jerks are lost, but cases are 
occasionally met with in which the reflexes are exaggerated. These cases 
closely approximate the group called hereditary cerebellar ataxia. (See 
below.) 

Loss of power is not as early a symptom as is inco-ordination. It affects 
the legs far more severely than the arms. The extensors suffer less than 
the flexors, and this may place the feet in a posture like that of talipes 
equinus or varus. This deformity may also be caused not only by one 
group of muscles overcoming others by reason of their loss of power, but by 
the fact that if the lesions in the lateral columns of the cord predominate, 
a spastic paraplegia develops which may result in contractures as in ordinary 
ataxic paraplegia. In those instances in which the muscles of the trunk 
become affected curvature of the spine may develop. 

The mind is not affected by the disease, but nevertheless the patient 
rarely develops mentally as does the normal child. 

When the disease is well advanced, the movements of the lower and upper 
limbs become not only irregular from inco-ordination, but jerking in charac- 
ter, and this jerking movement may extend to the he'ad and be accompanied 
by tremor. Speech becomes impaired, the words are blurred because of imper- 
fect articulation, and the utterance may be sudden or explosive. The dis- 
order of speech is a late symptom of the malady, and may not appear for 
some years after the ataxic manifestations appear. When the eyes are 
moved laterally or upward nystagmus may be present, and it is peculiar 
in that it is absent when the eyeballs are at rest. The extraocular muscles 
are rarely paralyzed, and the optic nerves always escape. In these respects, 
therefore, the disease differs very distinctly from locomotor ataxia, in w T hich 
malady these parts are commonly involved. Occasionally, cases are met 
with in which the pupillary reflex is lost. In these cases, how r ever, syphilis 
is the cause, and the case is probably one of tabes with Argyll-Robertson 
pupils. 

The disease is usually characterized by an absence of all disturbances 
of sensation save that cramp-like contractions of the muscles in the early 
stages may cause the patient some suffering. In rare instances severe darting 
pains have been met with, or the patient has experienced numbness in the 
limbs. The symptoms of ataxia are usually made worse by prolonged rest. 

Diagnosis. — The development of the characteristic symptoms just enu- 
merated during the period of childhood renders the diagnosis easy, for the 
maladies which resemble Friedreich's ataxia are all of them affections of 
adult life, save multiple neuritis, which may cause, of course, pseudotabes 
and a disturbance of station and gait. From Marie's cerebellar hereditary 
ataxia Friedreich's ataxia can be separated by a study of the symptoms of 
that affection described below. 

It must be recalled, however, that cases of Friedreich's ataxia develop 
which present symptoms which do not follow characteristic lines. Thus, 
in some cases great muscular atrophy has occurred. Nystagmus may not 
appear. Diplopia may be present. 



970 DISEASES OF THE NERVOUS SYSTEM 

Prognosis. — The prognosis is, of course, hopeless. The only thing favor- 
able which can be said is that the disease often develops very slowly and 
has long periods of arrest. The child, if attacked early in life, rarely reaches 
adult years. 

Treatment. — Treatment, aside from that devoted to the maintenance of 
good nutrition, is of little avail, for obvious reasons. 

Marie's Cerebellar Hereditary Ataxia. — Under this name a form of 
hereditary ataxia has been described by Marie in which he has shown that 
a congenital defect exists in the cerebellum. The condition is characterized 
by ataxia, difficulty in speech, and nystagmus, and in these points resembles 
Friedreich's ataxia. It differs, however, in the presence of defective pupil- 
lary reaction and various ocular palsies with optic atrophy and exaggeration 
of the knee-jerks. Further, it develops in the third decade of life, whereas 
Friedreich's ataxia nearly always appears before the fourteenth year. 

L. F Barker has recently put the matter thus: The direct cerebellar 
tracts of the cord which are degenerated in Friedreich's disease end in the 
middle lobe of the cerebellum, which is defective in Marie's type. The 
ataxia of both these diseases therefore results from lesions of different parts 
of one system. In Barker's nomenclature the spinal part of the poste- 
rior spinocerebellar system is affected in Friedreich's ataxia, while the 
cerebellar part of it is involved in Marie's type. An analysis of the symp- 
toms in all the reported cases of Marie's disease has led H. T. Patrick to 
say that increase of knee-jerk is its sole distinguishing feature from Fried- 
reich's ataxia. Probably the most advanced view is that the two conditions 
are phases of one disease. 



ACUTE ANTERIOR POLIOMYELITIS. 

Definition. — This disease is sometimes called infantile spinal paralysis, 
acute infantile palsy, and acute atrophic paralysis. It is characterized by 
sudden loss of power in one or more of the limbs, most commonly the lower 
extremities. As a rule, the loss of power is complete, but occasionally it is 
localized in certain groups of muscles. Immediately after the development 
of the paralysis wasting of the muscles begins to take place and may be 
extreme. There is no disturbance of sensation. 

Etiology. — Within recent years it has become more and more evident that 
acute anterior poliomyelitis is due to an infection. That the disease at times 
occurs in epidemic form was noted by Colmar more than sixty years ago. 
Since his time a large number of such epidemics have been recorded in this 
country and Europe. Caverly has recorded 144 cases in one epidemic near 
Rutland, Vermont, and in 1905 Ham reported an epidemic of 131 cases in 
Queensland. These epidemics are often associated with outbreaks of 
.croupous pneumonia and influenza. The organism, if it be one, has not 
been isolated. Cases also occur which seem to be non-infectious. The 
most severe case I have ever seen followed a mother's attempt to punish 
a child for urinary incontinence by placing its naked back under a hydrant 
in midwinter. Within twenty-four hours the disease was present in full vigor. 



ACUTE ANTERIOR POLIOMYELITIS 



971 



The disease is distinctly one of early child life, the greatest number of 
cases developing in the first three years of life, it being very rare indeed 
after the tenth year. It is far more apt to develop in the summer than in 
winter, and has its greatest incidence in July and August. After this season 
it is most frequent in September and in June. 

Pathology and Morbid Anatomy. — The essential lesion of this disease is an 
acute inflammatory process in the anterior cornua of the spinal cord, with 
associated hypersemia of the membranes covering the anterior surface of 
the cord. The branches of the anterior spinal artery (Fig. 127) bear the 
brunt of the attack and are intensely engorged. Their finer branches are 
ruptured so that extravasations of blood take place into the gray matter. 
As a result of these changes the typical picture of tissues suffering from an 



Fig. 127 



ant 




a. spin post. 



Scheme to show the course and distribution of the terminal branches of the arterial plexus of the pia 
mater: a. spin, post., posterior spinal arteries: a. spin, ant, anterior spinal arteries* a. sil., anterior 
median fissure ; rec. ant., anterior root arteries. (Van Gehuchten.) 

acute inflammatory process is presented, for serum, leukocytes, and red 
cells crowd the nervous protoplasm. The ganglion cells of the gray matter 
in the anterior horns undergo marked degenerative changes. They undergo 
cloudy swelling and the nuclei become granular, or if the change is still more 
severe the nuclei disappear and the neurones lose their dendrites and become 
vacuolated. As a final stage the cell undergoes shrinkage, becomes a small, 
granular mass, and finally disappears. The damaged areas, in old cases, 
are occupied by connective tissue and are much shrunken, so that the affected 
gray horn is much smaller than its fellow. The anterior nerve fibres, which 
have their origin in this part of the cord, also atrophy. Associated with 
these changes in the anterior cornua of the cord there is often some involve- 
ment of fibres in the anterolateral tracts, because, it will be recalled, some 



972 DISEASES OF THE NERVOUS SYSTEM 

of the fibres, or axones, which leave the anterior horns pass upward and 
downward in these columns to enter the anterior horns above and below 
to associate their function, and it is also due to the inflammatory process 
extending into the white columns. 

The degree of the inflammatory process in the gray matter varies very 
greatly in different cases and may involve the cells of but a few muscles. 
It may affect chiefly that part of the gray matter which is most anterior or 
that nearer the commissure. In rare cases it would seem probable that no 
true inflammatory process develops in the cord, but that simple degenerative 
changes occur in the neurones in the anterior horns. 

Symptoms. — The symptoms of acute poliomyelitis usually take the fol- 
lowing course : A child in good health has a restless and feverish night, and 
seems on the next day to be somewhat out-of -sorts. In the course of twenty- 
four or forty-eight hours it not infrequently happens that the parents con- 
sider the child recovered from its acute illness, and it may be some days or 
weeks before the mother notices that one or both of the lower limbs are 
lacking in power. Not rarely it is found, as the child sits in its mother's lap, 
that one leg moves while the other hangs like a flail, or the mother notices 
that the child is unable to push its leg into its clothing as efficiently as it 
could do before it was taken ill. These may be considered as the symptoms 
of a comparatively moderate case. 

In instances in which the onset and course of the malady is more 
severe, we find that fever is quite marked, often rising as high as 102.5°, and 
continuing at this point for several days. Occasionally, at onset, it may 
reach as high as 105°, and with this febrile movement there may be headache, 
loss of appetite, and vomiting. Sometimes diarrhoea occurs. In these 
instances the manifestation of loss of power is usually so marked that its 
presence is recognized within a few hours of its onset. Even in these cases, 
however, it not infrequently happens that the child is supposed to have 
suffered from an attack of acute gastric catarrh or indigestion until its 
inability to make certain movements calls attention to the palsy. 

There is still a third type of cases in which convulsions appear at the time 
of onset. These convulsions may be cerebral or epileptiform in character, 
may be followed by deep coma lasting for many hours, and the symp- 
toms may resemble an attack of cerebrospinal meningitis. Occasionally 
pain is a symptom of some importance, if, as already pointed out, the 
lesions in the anterior horns extend sufficiently backward to involve some 
of the sensory fibres beyond the commissures. These pains are usually felt 
about the joints. In some cases they come on not as a symptom of onset, 
but as a sequel, and seem to be due to an associated neuritis. The degree 
of the paralysis varies greatly in different cases. In some instances only one 
or two muscles seems to be affected. In others, the whole limb may be 
paralyzed, or both lower limbs and one upper limb may manifest loss of 
power. Even when the paralysis is quite widespread, it is rare for the cranial 
nerves to be affected, and equally rare for the sphincter muscles to lose 
power. 

In some instances the disease seems to be progressive in its type, the full 
degree of paralysis not developing at once, but beginning in one part and 



ACUTE ANTERIOR POLIOMYELITIS 973 

then spreading to adjacent parts. Rarely one attack speedily follows another, 
involving a different set of muscles. 

In very rare instances the paralysis may develop without any history of 
the symptoms of onset alreaay described. Cases are on record in which 
the paralysis has been almost universal, but it is a noteworthy fact, in regard 
to the paralysis of acute poliomyelitis, that it is far more widespread in its 
early stages than later on, this being due to the fact that as the inflammation 
subsides certain cells which have not been irreparably damaged regain part 
or all of their functions, and so adequately supply the muscles under their 
control, or collateral muscles supply the power needed. On the other hand, 
it is a fact worthy of note that complete recovery of power in all the muscles 
affected practically never occurs. The result is, that impaired muscles may 
exist without great loss of power. 

The period of recovery usually extends from one to three months. The 
muscles which fail to recover soon lose their contractility to faradism and 
then to galvanic electricity. The loss of faradic responses may be present 
as early as the eighth or ninth day, but in other instances some response is 
maintained, for a number of weeks. At the end of a few weeks the reactions of 
degeneration are observed. As would be expected from the lesions already 
mentioned and described when discussing the pathology of the affection, 
sensation is usually unimpaired. Reflex activity is, of course, diminished 
or lost because of the spinal lesions and the atrophy of the muscles. As" 
secondary lesions to the paralysis we find shortening of the muscles with 
consequent contractures and deformities. 

The legs are affected more frequently than the arms in the proportion 
of 3 to 1. The muscles below the knee suffer more frequently than those 
above the knee, and the tibial and peroneal muscles suffer more frequently 
than those of the calf. In the forearms the supinators usually escape, but 
the deltoids suffer more frequently than any other muscles in the upper 
extremity. 

Diagnosis. — The acute poliomyelitis of childhood is readily diagnosed. 
Care must be taken that the muscular pains when they occur are not thought 
to be due to rheumatism. None of the other spinal lesions of childhood have 
such a characteristic onset. Cerebral palsies are usually unilateral and spastic. 
Pseudohypertrophic paralysis develops very gradually. The characteristic 
feature of the palsy in anterior poliomyelitis is the placidity. 

Prognosis. — This is usually good so far as life is concerned, although if 
the attack has been severe vital resistance may be so diminished that other 
affections may readily cause the death of the child. The degree of ultimate 
paralysis can only be determined after two or three weeks of careful obser- 
vation, when some idea as to the number of muscles which may recover can 
be obtained, particularly if electricity is used to determine the electrical 
contractility of the affected muscles. 

Treatment. — In the treatment of acute poliomyelitis little can be done in 
the way of directly combating the disease. The child should be put at 
absolute rest in a quiet and darkened room. Sweet spirit of nitre and citrate 
of potassium should be given in small and frequent doses to diminish fever 
and to cause mild perspiration. It has usually been held that the adminis- 



974 DISEASES OF THE NERVOUS SYSTEM 

tration of the salicylates, particularly salicin, is of advantage. This 
may be true with children who have a rheumatic or gouty heredity, but 
there is no reason to suppose that they exercise any specific influence upon 
the lesions in the cord. So, too, hot applications have been recommended 
to be applied to the back. It is difficult to understand how they can be of 
much value. Some mild counterirritant over the spine, such as a spice 
plaster, or a pepper plaster, may be advantageous. The whole object of the 
physician must be to produce nervous quiet and aid in diminishing the inflam- 
matory process in the cord by avoiding excitement of the nervous system. 

After the acute stage of onset is past, and the paralysis is present, that is 
to say, after sufficient time has elapsed for the acute stage of the inflamma- 
tion to have passed by, or, in other words, in three or four weeks after onset, 
moderately large doses of strychnine may be given, but care must be taken 
that the doses are not so large as to produce twitching or great nervous 
irritability. At this time, too, the slowly interrupted faradic current may be 
applied to the paralyzed muscles, and particularly to those which are semi- 
paralyzed, in the hope that in this way their nutrition may be maintained. 
It must not be forgotten, however, that the greatest care must be exercised 
that the muscles are not overfatigued, since if they are exhausted they will 
more rapidly atrophy than if no electricity was employed. If electricity is 
used before the spinal cord has recovered from the acute stage of the inflam- 
'mation, it will make the condition worse. In many instances it is advisable 
to use electricity on one day and careful, gentle massage on the next. The 
electrical current should never be employed in such strength as to give the 
child pain or distress. 

As general tonics for the nervous system the hypophosphites, glycero- 
phosphates, cod-liver oil, and iron may be used. 

Should any tendency to deformity take place, this must be treated by the 
methods commonly resorted to by orthopedic surgeons. Rapid recovery 
should not be expected in these cases. Careful treatment for months is 
necessary to get the best results. 



CHRONIC ANTERIOR POLIOMYELITIS. 

Definition. — It is evident from its name that this disease closely resembles 
acute anterior poliomyelitis. A very important difference lies in the fact 
that in the acute form the damage takes place suddenly, and then ceases to 
progress, some improvement occurring in most instances, whereas in the 
chronic form the atrophic process is slow in onset and progressive and so 
the symptoms get worse rather than better. When the symptoms develop 
during a period of from two weeks to a month the term subacute is applied, 
and when they come on even more slowly, so that several months are con- 
sumed in their advance, the term chronic is used. The dominant symptoms 
are muscular wasting with paralysis. Chronic anterior poliomyelitis is some- 
times called " chronic atrophic spinal paralysis " or " progressive muscular 
atrophy." 



CHRONIC ANTERIOR POLIOMYELITIS 975 

Etiology. — This is unknown. Exposure to cold and wet has been thought 
to be a cause in some cases. 

Pathology and Morbid Anatomy. — The lesions of chronic anterior polio- 
myelitis consist in atrophy of the nervous tissues of the anterior horns of 
the gray matter of the cord. Not only the cell bodies but their axones and 
dendrites all undergo degenerative change. There is no acute inflammatory 
process present as in the acute form of the disease, and no hemorrhages into 
the tissues about the vessels. The dominant change is a simple atrophy 
or wasting. The anterior nerve roots also suffer atrophic changes, and the 
so-called association fibres of the cord and the cells which give rise to them 
also atrophy. As these association fibres pass to the anterior lateral columns 
of the cord the degenerative process extends to them as well, and this, com- 
bined with the wasting of the anterior nerve roots, produces a shrinkage in 
the size of these columns, which is, however, not great enough to be recog- 
nized by the unaided eye. The atrophic process extends down these tracts 
and involves the motor nerve fibres all the way to the nerve plates in the 
muscles, which in turn undergo atrophy, the muscular fibres losing their 
striae and showing fatty globules inside the sarcolemma. 

Symptoms. — The symptoms of this malady vary somewhat with the por- 
tion of the spinal cord which is chiefly affected. Most commonly the earliest 
manifestations of the disease appear in the upper extremities, and this is 
usually called the " Aran-Duchenne type of the disease." It first manifests 
itself in the adductor muscles of one thumb. From these it extends to all 
the small muscles of the hand, which rapidly become wasted. Flexion of 
the fingers upon the hand is impossible, and as the interossei which flex the 
first phalanges are paralyzed, the long flexor and extensor muscles of 
the forearms are unopposed. As a result we find that the long flexors flex 
the second and third phalanges and the long extensors extend the first 
phalanges, giving the so-called "claw-hand" deformity. This effect is 
increased by the prominence of the extensor tendons, caused in part by the 
wasting of the smaller muscles of the hand. The hand or the shoulder on 
the opposite side soon suffers. Finally, all the upper arm and shoulder 
muscles atrophy, and later those of the upper thorax as well. Still later 
the lower extremities become involved. Often portions of the latissimus 
dorsi, the trapezius, the triceps, the pectoralis major, or other muscles 
escape. When the cervical muscles fail the head cannot be held erect, and 
when the costal muscles are atrophied the act of respiration may be solely 
diaphragmatic. Finally, symptoms of bulbar paralysis may ensue. 

In that type in which the disease first affects the lumbosacral portion of 
the cord the peroneal muscles in one leg undergo paralysis and wasting. 
This condition then develops in the muscles of the other leg. A little later 
the anterior tibial muscles are affected, first on one side and then on the 
other. At this time there is " drop-foot " and the patient has to use his 
thigh muscles to raise the leg so that the toes will not strike obstructions 
and cause stumbling. As the pathological process in the cord advances the 
adductor muscles in the thighs and the gluteal muscles are paralyzed. 

In still another type, sometimes called "Duchenne's type of ascending- 
paralysis, " the paralysis and wasting extend upward from the legs and 



976 DISEASES OF THE NERVOUS SYSTEM 

speedily affect the muscles of the trunk, the arms, the forearms, and the 
hands so that an almost total paralysis ensues and death comes from involve- 
ment of the centres in the medulla or by reason of some intercurrent disease 
such as pneumonia. Sensation is not disturbed, but in a few cases a sense 
of discomfort may be complained of in the legs. The reaction of degener- 
ation develops quite early in the affected parts and finally response to 
electrical stimulation is completely lost. The muscles present fibrillary con- 
tractions if irritated, but the bladder and rectum are not paralyzed. The 
paralysis is due to the wasting. The reflexes are diminished or lost in 
the affected muscles. 

Diagnosis. — It is important to remember that chronic muscular atrophy 
may arise from other diseases than chronic anterior poliomyelitis, such as 
amyotrophic lateral sclerosis, the muscular dystrophies, peripheral neuritis, 
and syringomyelia. 

From amyotrophic lateral sclerosis (which see) it is distinguished by the 
absence of spastic symptoms and lack of the exaggerated knee-jerk and of 
Babinski's reflex. 

From muscular dystrophy by the absence of fibrillary tremor and of the 
reaction of degeneration in the latter condition, and by the fact that the 
spinal form is a disease of adult life. From syringomyelia this condition 
is separated by the absence of the dissociated anaesthesia and of trophic 
lesions in the skin. 

In neuritis the distribution of the paralysis is usually symmetrical; 
whereas, in chronic poliomyelitis the paralyzed parts are irregularly dis- 
tributed. Unless the neuritis be purely motor in character there are sensory 
disturbances and tenderness on pressure over the nerve trunks and in the 
bellies of the muscles. Moreover, in neuritis there is commonly a toxic 
cause recognizable. 

The Charcot-Marie-Tooth type of muscular atrophy may be confused with 
certain forms of progressive muscular atrophy. The first of these, however, 
is a disease of early life, and the paralysis in the legs does not extend above 
the knees or above the elbows, as a rule. Further sensation is usually 
disturbed or impaired in the Charcot-Marie-Tooth type and preserved in 
this chronic muscular atrophy. 

Prognosis. — The prognosis is grave. The future of the case can be deter- 
mined somewhat by the rapidity of the development of the symptoms, for 
in the rapidly advancing cases the outlook is of course worse than in others. 
When the symptoms follow injury to the spine the prognosis is better than in 
the idiopathic cases. 

Treatment. — The rapid type of cases should be treated as we treat acute 
poliomyelitis. The chronic forms should be cared for in a manner practically 
identical with that of the advanced stages of acute poliomyelitis. The 
treatment, therefore, consists in hygienic surroundings, nutritious food, and 
an abundance of fresh air and sunshine. Care should be taken that the 
paralyzed muscles are not exhausted by too much rubbing or exercise. 
Strychnine may be given in moderate doses three times a day for several 
weeks at a time. Fowler's solution, in moderate dose, is also useful as a 
tonic, Therapeutic measures, however., cannot promise much in this disease. 



BULBAR PARALYSIS 977 



BULBAR PARALYSIS. 

Bulbar paralysis is a term applied to a group of symptoms referable to 
lesions of cranial nerve nuclei in the medulla oblongata or " bulb," which 
affect the tongue, lips, and larynx in peculiar association, so that the con- 
dition is called " glosso-labio-laryngeal paralysis." The lesions may impli- 
cate the cranial nerve nuclei in the pons and crus, and the gray matter of 
the spinal cord, but atrophy of the tongue and lips is the main feature of the 
disease which is centred in the medulla. 

Etiology. — The cause of this disease is unknown. It occurs most fre- 
quently between the thirtieth and fiftieth years. 

Pathology and Morbid Anatomy. — The lesions of this malady consist in 
degenerative changes in the nuclei of the motor nerves which supply the 
tongue, lips, larynx, and pharynx. As the disease advances, additional 
nuclei of the cranial nerves become involved so that the pneumogastric, 
the facial, the motor fibres of the trifacial, and more rarely the abducens 
and oculomotor nerves are affected. Occasionally, it occurs as part of 
amyotrophic lateral sclerosis. If the reader has a clear conception of the 
pathology of chronic anterior poliomyelitis he will understand the pathology 
of this affection as well. 

Symptoms. — The symptoms of chronic bulbar paralysis usually begin 
with difficulty in moving the tongue in speech so that the patient is unable 
to use easily letters like v, n, r, /, and I. The speech becomes nasal, 
swallowing becomes difficult, and when the muscles of the lips become 
affected labial sounds become imperfect, letters like b and p being difficult 
to pronounce. When the laryngeal muscles become paralyzed speech is lost 
completely. Chewing becomes difficult, owing to the paralysis of the tongue 
and lrps. There is difficulty in swallowing, and the food not infrequently 
finds its way into the larynx, from which it may descend and cause septic 
pneumonia. Owing to the paralysis of the facial nerves, the expression of 
the lower portion of the face becomes altered, the lips sag, and saliva may 
flow over the chin. Fibrillary contractions of the affected muscles also occur, 
and the tongue lies relaxed and powerless in the floor of the mouth. 

Diagnosis. — True bulbar paralysis must be separated from that still more 
rare affection known as myasthenia gravis. In this condition the general 
muscular system also suffers from feebleness, but degeneration does not 
take place in the affected muscles, and they do not undergo material wasting. 
Furthermore, the condition in myasthenia gravis is often characterized by 
periods of remission or partial recovery. Autopsy in those cases of myas- 
thenia gravis which have come to a fatal termination has always failed 
to reveal the lesions which have been described as characteristic of true 
bulbar paralysis. 

Prognosis. — This form of paralysis is invariably fatal. 

Treatment. — The treatment of bulbar paralysis consists in the adminis- 
tration of tonics, and in an endeavor to maintain the patient's general health 
at the best possible level. Do what we will, the disease cannot be affected 
by any plan of treatment yet devised. 
62 



978 DISEASES OF THE NERVOUS SYSTEM 



LATERAL SCLEROSIS. 

Definition. — Lateral sclerosis, also called " spastic paraplegia," is a con- 
dition in which the patient suffers from stiffness or spasticity of the mus- 
cles of the lower extremities, with loss of power which ultimately amounts 
to distinct paralysis. The condition is characterized by great reflex irri- 
tability. There are no sensory disturbances. 

History. — Tiirck described sclerosis of the lateral columns of the cord in 
1856, and Charcot made further contributions as to the symptoms in 1865. 
Seguin described it still further in 1873 as " tetanoid paraplegia," an excellent 
term, but it remained for Erb in 1875 and 1877 to make a full exposition of 
the disease. 

Etiology. — In many cases the cause of lateral sclerosis cannot be dis- 
covered. Syphilis may be a cause, or, to speak more correctly, the malady 
may be a sequel of syphilis. In some instances injuries to the back are fol- 
lowed by these symptoms. In one case in my experience a horse reared 
and fell backward on his rider, who at once found his legs paraplegic. This 
passed away in a few moments, but after a few months lateral sclerosis 
gradually developed. In another case under my care a man stood in very 
cold water washing sheep, and dated the beginning of his malady to that 
exposure. In both of these cases, however, it is quite probable that a pachy- 
meningitis or a hemorrhage into the cord or a myelitis was the cause of the 
symptoms rather than a true primary lateral sclerosis. In other cases pro- 
longed marches have seemed to produce it. It is a disease of the third and 
fourth decades of life. In some instances the disease seems to depend upon 
an hereditary defect in the lateral columns of the cord (Strumpell's family 
type of lateral sclerosis). 

Pathology and Morbid Anatomy. — The lesions of lateral sclerosis are clear 
and definite. As the name of the disease implies, they are situated in the 
lateral or crossed pyramidal tracts of the spinal cord, and they develop 
chiefly in their lower portions in the early stages of the disease. The axones 
progressively atrophy from below upward, and this is associated with dis- 
appearance of the myelin and an overgrowth of the connective tissue. 

When the disease invades the cervical region the anteromedian columns of 
the cord may be affected as well. 

Symptoms. — In studying the symptoms of primary lateral sclerosis it must 
not be forgotten that they may be simulated by secondary lateral sclerosis 
following lesions higher up in the cerebrospinal system. Thus, it is a well- 
known fact that a large number of lesions in the brain or cord may result 
in degenerative changes in these motor pathways, and so cause spastic para- 
plegia. Those in the brain are hemorrhage, abscess, tumor, and softening, 
which, affecting the motor cortex or the motor pathways, induce a descending 
degeneration in the pyramidal tracts. In these cases the symptoms are 
usually limited to one side, but in the cerebral palsies of childhood the 
lesions are often bilateral. (See Infantile Cerebral Palsy.) Any lesion in 
the spinal cord which cuts off the fibres in the lateral tracts from their trophic 
cells in the brain, also results in lateral sclerosis. Thus, a transverse myelitis, 



LATERAL SCLEROSIS 979 

disseminated sclerosis, hemorrhage into the cord, and syringomyelia may 
so result. Lateral sclerosis is not rarely a part of the pathology of paresis. 
Lesions outside the cord, such as tumors, disease of the spinal column, or 
thickening of the membranes may sometimes cause these symptoms. 

The symptoms upon which we base the diagnosis of lateral sclerosis are 
the peculiar spastic contractions of the muscles of the legs, so that they are in 
a state of extension as soon as the patient attempts to move them. The 
attitude of the legs is that of a person with ankylosis of both knees, and the 
foot is apt to be extended. When the patient walks he has difficulty in bend- 
ing the knees and the ankles, and still greater difficulty in raising the toes 
as the foot is brought forward for another step. For this reason he is prone 
to trip over small obstructions and to have bad falls, because his muscles 
are so stiff that he cannot catch himself as he loses his balance. The stress 
and strain of walking are therefore very great, and the muscles may become 
so fatigued that they ache, but this is the only sensory symptom. Crossing 
the legs when sitting becomes impossible, and if the patient is recumbent the 
knees may be approximated owing to the greater strength of the adductor 
muscles. This adduction of the knees also interferes with walking. If the 
patient's muscles are grasped they are found to be hard and tense. On 
further physical examination it will be found that the reflexes are all increased. 
Ankle clonus is marked, and the Babinski reflex is soon manifested. The 
reactions of degeneration do not appear and the muscles do not atrophy 
until the disease has lasted several years, when they may w^aste from disuse. 

Finally, when the malady has continued for a very great length of time 
the position of the lower extremities in stiff extension may be changed to 
that of contracture so that they are sharply flexed at the knees and fixed in 
this position. 

The upper extremities nearly always escape, but in the rare instances in 
which they are involved the extensor muscles suffer first and suffer most. 

Diagnosis. — As already pointed out, the diagnosis of this disease should 
not be made till the causes capable of producing secondary lateral sclerosis 
are excluded. Occasionally hysteria may produce symptoms very like it. 
A typical picture of such a case will be found in my book on Practical 
Diagnosis. In such an instance the sex of the patient and the other signs of 
hysteria should be carefully considered before a diagnosis of lateral sclerosis 
is made. When spastic paraplegia is combined with muscular atrophy the 
condition is one of amyotrophic lateral sclerosis (which see). 

Prognosis. — This is bad as to recovery, but its unfavorable character is 
modified by the fact that the progress is usually very slow. Often the dis- 
ease lasts twenty-five years or more. 

Treatment. — Unfortunately the results which may be obtained from the 
treatment of lateral sclerosis are not brilliant. The suggestion that nux 
vomica or strychnine be employed does not seem to be based on very rational 
views of the physiological action of this drug. Excitation of the motor tracts 
of the spinal cord is already present, and strychnine rather tends to increase 
this condition and to exaggerate the spastic condition of the lower extremities. 
In some instances full doses of the extract of conium are advantageous. In 
others large doses of chloral or one of the bromides may be employed. The 



980 DISEASES OF THE NERVOUS SYSTEM 

gentle forms of massage may also relieve the sensation of tension and aching 
in the limbs. Care should be taken that the patient does not walk far 
enough to exhaust himself. In some instances a hot pack will give relief, 
particularly if it is taken at bedtime, although of course it exercises no 
curative influence upon the progress of the disease. Electricity is useless. 

Syphilitic Spastic Spinal Paralysis.— Under the name of syphilitic spastic 
spinal paralysis Erb has described a form of lateral sclerosis developing 
within five years of the primary sore, but differing from ordinary lateral 
sclerosis by the presence of some lack of rectal and vesical control and mild 
disorders of sensation. This so-called syphilitic spinal spastic paralysis of 
Erb is due to a specific endarteritis, which produces embolism or thrombosis 
of the vessels of the spinal cord and a true myelomalacia, although some 
clinicians have considered it a meningomyelitis. 



AMYOTROPHIC LATERAL SCLEROSIS. 

Definition. — Amyotrophic lateral sclerosis is a progressive form of chronic 
spinal paralysis characterized by advancing muscular atrophy associated 
with spastic paraplegia, or, in other words, the symptoms of lateral 
sclerosis are present. Although the symptoms are largely spinal, modern 
research has shown that the motor pathway is affected throughout in 
advanced cases, from the beginning of its upper segment in the motor cortex 
to the endings of the lower segment in the peripheral nerves. The cardinal 
symptoms depend, however, upon degeneration of the contiguous parts of 
these segments, namely, the pyramidal tracts and the anterior horns of the 
gray matter; and the disease may be regarded as a combination of lateral 
sclerosis with chronic poliomyelitis. Not rarely the disease invades the 
medulla, and symptoms of progressive bulbar paralysis are added to the 
clinical picture. 

Etiology. — Amyotrophic lateral sclerosis is usually met with in persons 
between thirty and fifty years of age. In some instances there is a history of 
exposure to cold or of violent exertion. In still others, it is found that the 
patient has been an artisan employed in the handling of such metallic 
poisons as mercury, lead, or arsenic, or that he has been addicted to the 
excessive use of alcohol. In some instances, too, the disease has apparently 
followed severe injuries, but in no instance has it been proved that there is 
actual relationship between any of these causes and the development of the 
disease. In all probability, these factors only become active in those cases 
in which there is a defective development in the central nervous system, 
which renders its motor elements peculiarly susceptible to damage or disease. 

Pathology. — The pathological conditions in amyotrophic lateral sclerosis 
may be considered in three parts. The first and most important is the 
advancing atrophy which involves the motor neurones in the anterior horns 
of the gray matter of the spinal cord. Indeed, the condition is very similar 
to that which occurs in chronic anterior poliomyelitis or even identical with 
it. As a rule, the alterations take place chiefly in the cervical portions of the 
cord, but in some instances, particularly if the disease lasts a long time, the 



AMYOTROPHIC LATERAL SCLEROSIS 981 

anterior portion of the gray matter in the lumbar region is also affected. 
Similar atrophic changes take place in the motor nuclei of the cranial nerves 
in the pons and medulla. Next in importance to these alterations in the 
trophic portions of the spinal cord is the atrophy and degeneration of 
the fibres in the lateral columns and the anterior median columns. These 
changes extend to the motor cells of the brain and are not limited to the 
lateral columns, the cortex being involved secondarily by " retrograde" 
degeneration from the cord and medulla upward through the pons, crura, 
capsule, and corona radiata. In other words, the degeneration does not 
begin in the motor cortex, but in the spinal cord. Following the wasting of 
the nervous elements of the spinal cord, there is an overgrowth of connective 
tissue which not only involves the lateral columns and the anterior median 
columns, but also the association fibres which are closely connected with the 
anterior horns of the gray matter. 

Symptoms. — The symptoms of amyotrophic lateral sclerosis are quite 
characteristic, and depend in their development to some extent upon the 
portion of the nervous system which is first affected by the disease. In those 
instances in which the lesion first affects the cervical portion of the cord and 
the anterior horns of the gray matter the arms are first affected. These 
extremities manifest some stiffness in the muscles, and their reflex excitability, 
is increased. Almost simultaneously with these symptoms there is wasting 
of the muscles of one or both hands, with associated loss of power. From the 
hand the paralysis extends to the forearms, or it passes directly to the muscles 
of the shoulder and affects those of the forearms afterward. Fibrillary con- 
tractions develop very early, and may be produced by tapping the muscles or 
by exposing them to cold. The fingers are often in semi-flexion, and if the 
physician endeavors to straighten them, it is found that the muscles are rigid 
and resistant, even though the patient has lost power in them. 

When the disease develops chiefly in the pyramidal tracts of the motor 
columns of the cord, the evidences of spastic paralysis are the first things to 
impress themselves upon the observer, and it may be impossible in the early 
stages of the disease to separate the malady from ordinary lateral sclerosis, 
since the legs are stiff and move with difficulty, the knee-jerks are exaggerated, 
and ankle clonus and the Babinski reflex are usually present. When the 
patient walks the toe is dragged along the ground, the whole leg is stiff, and 
one foot is often placed awkwardly in front of the other, through the contrac- 
tion of the adductor muscles. 

Whether the disease first begins in the arms or in the legs, it is worthy of 
remembrance that it is often very much more marked upon one side than 
upon the other. 

As the disease advances it sometimes happens that evidences of bulbar 
paralysis develops, the speech becoming affected, as in ordinary bulbar par- 
alysis. Swallowing may also become difficult. Owing to paralysis of the 
uvula and palate, choking often takes place, and fluids when taken into the 
mouth escape through the nose. Indeed, all the symptoms of bulbar 
paralysis may be present, and inequality of the pupils may be noted. Tap- 
ping the affected muscles in any portion of the body usually produces marked 
contractions in the muscle tapped and in neighboring groups of muscles. 



982 DISEASES OF THE NERVOUS SYSTEM 

When contractures occur the hands may become greatly deformed, and the 
feet may be distorted into any of the forms of talipes. 

In the advanced forms of the disease the muscles of the trunk and neck 
become atrophied, so that it is impossible for the patient to sit up, and the 
head falls to either side or forward. The muscles develop the reactions 0} 
degeneration and lose their electrical excitability. There is no loss of intelli- 
gence, but sometimes in advanced cases a mild dementia appears. When 
the bulbar symptoms are marked, palpitation of the heart is often present. 

Diagnosis. — From bulbar paralysis amyotrophic lateral sclerosis is sepa- 
rated by the fact that lateral sclerosis presents marked spinal symptoms 
with paralysis of the upper extremities and spastic paraplegia of the lower 
extremities. If in a case of supposed bulbar paralysis these symptoms 
develop later it proves that the bulbar palsy has been due to the oncoming 
of amyotrophic lateral sclerosis. If the symptoms are due to the presence 
of a meningitis in the cervical portion of the cord, there is stiffness and loss 
of power in the arms, and there will also be pain of a severe character. So, 
too, injury or pressure upon the spinal cord in the dorsal and lumbar regions, 
producing a spastic paraplegia, will also produce sensory disturbances and 
involve the functions of the bladder and rectum. 

From syringomyelia amyotrophic lateral sclerosis is separated by the pres- 
ence in the former of analgesia and the rapid trophic changes which take 
place not only in the muscles, but in the bones, the skin, and its appendages. 
In many instances it is almost impossible to differentiate between amyotrophic 
lateral sclerosis and ordinary lateral sclerosis, and it is only by the develop- 
ment of the symptoms which arise from involvement of the gray matter of 
the cervical portion of the spinal cord and the medulla that the separation 
can be made. 

Prognosis. — The prognosis in a case of amyotrophic lateral sclerosis is 
absolutely unfavorable so far as recovery is concerned. The duration of life 
depends upon the rapidity with which the vital centres in the medulla become 
involved. In some instances death comes within two years after the onset of 
the malady, whereas in others it lasts for a decade or even longer. The pro- 
longed cases are usually those in which the involvement of the lateral columns 
seems to be the first stage of the disease. As a rule, death does not occur as 
the direct result of the disease, but from complications which are produced 
by it; as, for example, the inhalation of particles of food into the respiratory 
passages because of the bulbar paralysis. Rarely there is heart failure due 
to involvement of the cardiac centres. 

Treatment. — There is no form of treatment which can be considered cura- 
tive. Gentle massage and the use of electricity, with the hope that the wast- 
ing of the muscles may be diminished, has been tried by some clinicians, but 
it is manifest that this plan of treatment must be used with great caution, 
since if the trophic centres are destroyed, the muscles must necessarily 
undergo wasting more rapidly if they are exercised than if they are not 
used. If bulbar symptoms are present the patient should be fed by means 
of a stomach tube. The employment of nervous stimulants, such as strych- 
nine, is inadvisable, because it exaggerates the spastic condition of the 
lower extremities. 



MYELITIS 983 



MYELITIS. 



Definition. — Myelitis is a term which at one time was loosely applied to 
all inflammatory processes in the spinal cord. Its application is becoming 
limited as our conception of the diseases in this part of the body becomes more 
definite, but it is still used to describe an inflammatory process in the cord, 
which is general or widely diffused or disseminated. A myelitis may be acute, 
subacute, or chronic. If it extends across a given segment of the cord it is 
called a "transverse myelitis;" if it is distributed in several foci through the 
cord, it is called " disseminated myelitis," and if it extends upward or down- 
ward, it is called an " ascending or descending myelitis." 

The term " acute myelitis " is applied to those cases of sudden onset taking 
but a fortnight to develop. The term subacute is applied to those which con- 
sume from two to six weeks in onset, and the term chronic to those which 
develop so slowly that a longer time elapses before the disease is marked. 

When the gray matter of the spinal cord is affected, it is called "polio- 
myelitis," from the Greek word rzoho^, meaning gray. 

When the brain and cord are involved it is called " encephalomyelitis," 
and when the gray matter about the central canal in the cord is affected 
it is called a "central myelitis." 

Acute and Subacute Myelitis. Etiology. — The chief cause of this condi- 
tion is without doubt an intoxication, due to the action of toxins developed 
during the course of acute infectious diseases. At one time it was thought 
that exposure, sexual excess, and severe toil were causes, but we now know 
that at the most they are but predisposing factors in that they diminish vital 
resistance. In addition to the ordinary infectious fevers, myelitis may be 
caused by gonorrhoea and malaria. Occasionally severe vesical infection 
produces acute myelitis. Myelitis has also been said to follow concussion of 
the spine and other injuries, but they probably act solely as predisposing 
agencies. 

Pathology and Morbid Anatomy. — If we take transverse myelitis as a type 
of the various forms of this disease, we will find on opening the spinal canal 
that the pia mater at the level of the lesion is hyperaemic and reddened. The 
cord is also reddened and somewhat swollen, and its bloodvessels engorged 
On section of the cord the lines of demarcation between the white and gray 
matter are to a great degree obliterated. The cord is softened and its texture 
may be actually diffluent, this very soft state being, however, at least in part 
a postmortem change. If this part of the cord is placed under the micro- 
scope it is seen to be filled with granular cells, the bloodvessels are sur- 
rounded by extravasated leukocytes, and bacteria may be found. Small 
extravasations of blood into the tissue of the cord may be present from rup- 
ture of the vessels. The nerve cells are found to have undergone granular 
degeneration, and their axones and dendrites have also been destroyed. 
The axis cvlinder of the nerve fibres is greatly swollen and has evidently 
undergone segmentation. Fatty degeneration of the myelin is found. The 
connective-tissue cells are swollen, and if any time has elapsed, an over- 
growth of the neuroglia is present. 



984 DISEASES OF THE NERVOUS SYSTEM 

For a clear understanding of the cause of the symptoms met with in acute 
myelitis, myelomalacia, and chronic myelitis it must be remembered that 
the presence of a lesion in the spinal cord in the motor tracts produces a 
descending degeneration in that tract, because the nerve fibre is cut off from 
its nerve cell or neurone. If the lesion be in the sensory tracts the degenera- 
tion is ascending. The ultimate symptoms, therefore, consist not only in 
those which arise from the primary focus or lesion, but in those which develop 
as the result of these secondary changes. These changes are demonstrable 
within a few days after the injury, and rapidly progress so that at the end 
of three weeks the degeneration of the affected fibres is at its height. The 
overgrowth of the connective tissue is not marked until a later period. Thus, 
we find that the chief degenerative change below the lesion is in the anterior 
and lateral pyramidal tracts, and above the lesion in the dorsal columns 
of Goll and Burdach, in the direct cerebellar tracts, and in the columns of 
Gowers, In addition to these chief secondary changes, there is also, for a 
short distance below the primary lesion, descending degeneration in the 
anterior and anterolateral colums, and in certain small " fields" of the 
dorsal columns (oval field of Flechsig, etc.), which contain the so-called 
association fibres. 

The ascending degeneration which takes place after a transverse lesion 
affects chiefly Goll's and Gowers' columns, and the higher the primary lesion 
the greater the degree of the degenerative process. The column of Burdach, 
on the other hand, while markedly degenerated near the site of the lesion, is 
less and less affected higher up in the cord. 

Symptoms. — The symptoms of myelitis vary somewhat with the portion 
of the cord which is affected and with the extent of the pathological process. 

When there is a transverse myelitis of the dorsal portion of the spinal cord 
the symptoms in the stage of onset consist in wretchedness and moderate fever. 
There may be fain in the back and numbness and tingling in the lower 
extremities. Twitchings or cramp-like contractions of the muscles in the legs 
may occur, and, very rarely in adults, a convulsion may develop. Sometimes, 
however, these prodromata are absent, and the first symptom complained of 
is loss of power in the lower limbs, which speedily develops into a complete 
paraplegia. Paraplegia may become complete in a few minutes or a few 
hours. In other instances of the subacute type the onset is so slow that 
days and even weeks may elapse before the loss of power is complete. 

The paraplegia arising from a transverse myelitis in the dorsal region is 
usually spastic, and the deep reflexes are increased. The legs are outstretched, 
as in ordinary paraplegia, unless degenerative or irritative lesions arise in 
the lateral pyramidal tracts below the site of the transverse lesion, when they 
may become flexed by the spastic state of the muscles of the thighs. In other 
instances these muscles suffer from twitchings and temporary contractions, 
which may be strong enough to prevent the examiner from eliciting any signs 
of exaggeration of the deep reflexes. There is always paralysis of the bladder 
and rectum in transverse myelitis, and retention or incontinence of urine and 
feces may be present. Partly because of pressure and unavoidable unclean- 
liness, but chiefly because of trophic disorders and abnormal blood supply, 
bed-sores are prone to develop on the sacrum and buttocks. The muscles in 



MYELITIS 985 

the legs do not rapidly atrophy, because they receive trophic impulses from 
the cells in the anterior cornua of a lower level of the cord than that of the 
lesions. The skin of the legs and of the body below the level of the lesion 
is anaesthetic to all forms of irritation, and at the upper margin of this 
anaesthetic area there is a girdle sensation, and, it may be, a band of 
hyperesthesia. 

When the myelitis affects the lumbar cord the paraplegia is not only abso- 
lute as to voluntary movement, but as to reflex action as well, all reflexes being 
lost. A similar condition also occurs in some cases when the injury is at a 
higher level, provided that the cord is completely severed or the injury so 
severe that severance is practically complete. 

If the lesion is in the cervical cord the arms are not only paralyzed, but 
undergo atrophy and are flaccid, the legs suffer from a spastic paraplegia, 
and the arms, legs, and body are anaesthetic. There may also be dilatation 
or contraction of the pupils. If the lesion is high up in the cervical area, 
then the paralysis of the arms may be spastic instead of flaccid, and 
they do not undergo atrophy. In such a case respiration is very difficult, 
because of the loss of power in the diaphragm and in the other respiratory 
muscles. 

Prognosis. — While it is a fact that the prognosis in transverse myelitis is 
always grave, it is also a fact that partial recovery sometimes takes place. 
Thus, Oppenheim states that that form following gonorrhoea always gets 
better under good treatment, and that that form due to the acute infectious 
fevers -has good chances for recovery. On the other hand the outlook in 
syphilitic cases is not good, and in septicaemia, tuberculosis, or puerperal 
sepsis it is bad. Again, the prognosis varies with the severity of the symp- 
toms and the lesion, for manifestly it must be worse in complete transverse 
myelitis than in that form in which the destruction of the cord is not so com- 
plete. The cause of death is usually bed-sores, with exhaustion and septic 
cystitis. 

Treatment. — An understanding of the lesions of this disease makes it evi- 
dent that treatment of a curative nature is useless. Careful feeding with 
easily digested food, the maintenance of perfect cleanliness in the parts pressed 
upon in the dorsal position, and the cautious use of the catheter should be 
resorted to. Hyoscine may be given to stop the annoying twitchings of the 
muscles. 

Chronic Myelitis. Definition and Etiology. — Chronic myelitis is, as its 
name implies, a chronic form of inflammatory process in the cord which 
develops as a result of a large number of causes. Not only may the causes 
of acute myelitis set up a process which may become slow and chronic in its 
progression, but other factors may produce it, of which the most important 
are impairment of its blood supply resulting from degenerative changes in 
the bloodvessels from atheroma or syphilitic arteritis. Chronic myelitis may 
also arise as a result of pernicious anaemia. In some cases, too, the primary 
cause lies in a meningitis of the membrane surrounding the cord, whether 
this meningitis be due to an infection or to injury followed by infection. 
When syphilis is the cause, it not rarely happens that the inflammatory 
process is limited to one or more parts of the spinal cord, so that the symp- 



986 DISEASES OF THE NERVOUS SYSTEM 

toms of spastic paraplegia due to disease of the lateral pyramidal tracts 
develops, or in other instances the symptoms of locomotor ataxia are present, 
because the posterior tracts in the cord are affected. Rarely but one side 
of the cord may be affected, producing a crossed paralysis of motion and 
sensation (Brown-Sequard syndrome). 

Finally, the physician must recall the fact that most of the forms of chronic 
disease of the spinal cord, such as disseminated sclerosis, amyotrophic lateral 
sclerosis, and the various forms of poliomyelitis, may, in their advanced stages, 
resemble what has been called chronic myelitis. Indeed, it is so rare to meet 
with a case of chronic myelitis which cannot be placed under one of these 
headings that many neurologists are inclined to deny the existence of chronic 
myelitis as a separate malady. (See below.) 

Pathology and Morbid Anatomy. — The changes in the spinal cord which 
are found in cases of so-called chronic myelitis are not so manifest as in the 
acute form when the cord is studied by the naked eye. In one class of cases 
the appearance is quite like that of disseminated sclerosis in that areas of 
overgrowth of connective tissue are found in both the white and gray matter 
of the cord. This overgrowth of the neuroglia is situated chiefly around the 
bloodvessels, the walls of which are also thickened and their lumen nar- 
rowed. When as a result of the degenerative process an axis cylinder has 
become distended or swollen, a small cavity is formed, and if many of these 
are present they may give the section of the cord a cribriform appearance. 
The pia mater is often found adherent to the cord. 

In the other type of case a microscopic study of the cord reveals changes 
which are evidently the result of the several diseases of the cord already 
named, and which are really the cause of the symptoms presented by the 
patient rather than that a true primary chronic myelitis has been present. 
Thus, it is found that as a result of a lesion in the pyramidal tracts, a descend- 
ing degeneration of the fibres in that tract takes place, or if the lesion has been 
in the posterior columns, an ascending degeneration ensues. 

Symptoms. — When the condition of chronic myelitis follows acute myelitis, 
the symptoms of that state persist with gradually increasing severity until 
death by exhaustion or some intercurrent malady ensues. If, however, the 
process is of the slow or chronic type from the time of onset, the 'primary 
feeling of weariness and weakness on exertion passes gradually into a state of 
paralysis, more or less complete. Owing to the degenerative changes in the 
lateral tracts, the paralysis is usually spastic. There is often an exaggeration 
of the deep reflexes, with ankle clonus. In other instances the character of the 
response to reflex stimulation is entirely dependent upon the portion of the cord 
which is involved. The muscles may gradually waste and give the reactions 
of degeneration. Not rarely the loss of power extends gradually to the trunk 
and arms. Sensory disturbances are common. There may be patches of 
anaesthesia and paresthesia, and occasionally moderately severe pains may 
be felt in the nerves in the extremities. Vasomotor disorders in localized 
areas of the skin may be present, one part being very pallid and another 
hypersemic. Bed-sores finally develop, as in the acute form of the disease. 

Diagnosis. — Chronic myelitis as a separate disease is so rare that a diag- 
nosis of its presence should be made only after a most careful study of a case. 



MYELOMALACIA 987 

From disseminated sclerosis it is separated by the absence of evidence of 
lesions in the brain and lower cephalic centres, such as nystagmus, intention 
tremor, and scanning speech. From lateral sclerosis it is separated by the 
absence of vesical and rectal paralysis in that disease. Then, too, lateral 
sclerosis is not characterized by loss of sensation. Paralysis due to polio- 
myelitis is separated also by the absence of anaesthesia, and the fact that the 
paralysis of the muscles is not, as a rule, so general. 

Prognosis. — Recovery does not occur. Life may be prolonged for years 
if the process is not progressive and no intercurrent disease attacks the 
ienfeebled sufferer. 

Treatment. — This is, of course, concerned entirely with the maintenance 
of good health, with the hope that a terminal infection may not occur. If 
there is a clear history of syphilis the iodides and mercury may be used, but 
they are rarely of much value in this state. 



SENILE PARAPLEGIA. 

Under this unsatisfactory clinical title may be described a condition 
occasionally met with in old persons, and probably depending upon impaired 
blood supply to the cord, resulting from degenerative changes in the vessels 
which are not severe enough to result in myelomalacia. 

Symptoms. — The symptoms consist in a moderate degree of loss of power 
in the lower limbs so that it is difficult for the patient to move about. The 
legs may be shuffled along the floor instead of lifted clear of it. "When the 
malady develops rapidly and is severe it may be impossible for a time to 
separate it from true myelitis. 

Treatment. — The treatment consists in rest in bed, massage, and hydro- 
therapy. Internally, the iodides and circulatory stimulants, such as strych- 
nine and digitalis, should be used. 



MYELOMALACIA. 

This term is applied to a state of the spinal cord in which it undergoes 
softening because of embolism or thrombosis of its bloodvessels, with 
the result that its blood supply is impaired. The degenerative changes 
consist in those which we would expect to find when necrosis of these parts 
occurs, namely, extravasated red and white blood cells, fat-globules, and 
broken axones. When the patient lives for a considerable length of time 
after this accident to the circulation occurs, a microscopic examination of 
the cord will reveal an overgrowth of connective tissue. The essential 
difference between this state and one of acute myelitis is that in this 
condition the process is necrotic; whereas, in the latter it is primarily 
inflammatory, and diapedesis of white and red cells takes place as a part 
of a vital process. 



988 DISEASES OF THE NERVOUS SYSTEM 



SYRINGOMYELIA. 

Definition. — Syringomyelia is a condition of the spinal cord characterized 
by the formation of a cavity or cavities in its substance; by loss of pain 
sense and temperature sense, with preservation of tactile sense; by the devel- 
opment of progressive muscular atrophy and paralysis, and by nutritional 
changes in the skin, muscles, bones, and joints. 

History. — Although a very rare disease, it was described before many 
other very common maladies, the state of the spinal cord having been first 
noted in 1546 by Etienne and given its name by Ollivier in 1824. We are, 
however, able to diagnosticate the affection by reason of researches of 
Schultze and other later investigators. 

Etiology. — This is unknown. In some cases it is probably dependent 
upon a congenital defect. In other instances it has been thought to be due 
to disease of the spinal arteries, and in some cases Van Gieson has shown 
that it has developed from a perforating hemorrhage into the cord itself. 

Pathology and Morbid Anatomy. — When the spinal cord in a case of syringo- 
myelia is examined macroscopically, the membranes are found to be normal, 
but the surface of the cord may be irregular and portions of it protrude, while 
at other places retraction of its surface seems to be present. A closer exami- 
nation of the areas of bulging may reveal fluctuation, and from such areas, 
if they be punctured, a clear serous fluid may run quite freely. This cystic 
state may extend very considerable distances up and down the cord, and 
may extend so far transversely as almost to cut the cord in two. The cavity 
is usually largest in the cervical and upper dorsal regions of the cord, but it 
may be confined to the lower part of the cord. On the other hand, as just 
stated, it may extend from the end of the cord even to the pons. The cavity 
may have large dimensions as to length and be so wide as to convert 
the cord into a thin-walled tube. 

It is because of these extraordinary changes that the Greek words syrinx, 
a tube, and myelon, marrow of the spine, is applied to it. So complete 
may be the excavating process that when the cord is severed from the 
medulla the fluid may escape and the cord flatten out like a ribbon. In 
some cases there are several cavities superimposed. On cross-section the 
cavity is usually found to be just back of the central canal in the gray com- 
missure and in the posterior cornua, or it may be present where the central 
canal should be. Occasionally it affects the anterior horns or the lateral or 
posterior white columns. 

The wall of the cavity consists in a well-developed mass of neuroglia 
(gliomatosis), which in its growth encroaches upon surrounding tissues and 
may cause definite symptoms before its centre becomes broken down. Some 
neurologists, on that account, prefer to call this disease, at least in its 
earliest stages, spinal gliomatosis, or gliosis. 

The loss of pain sense and temperature sense which is so characteristic 
has been ascribed to pressure by the neuroglia mass upon the fibers conduct- 
ing these sensations as they cross in the central gray matter on their way to 
the column of Gowers. This is at least a good working hypothesis. 



SYRINGOM YELIA 989 

Around the margin of the connective-tissue boundary just described there 
is usually an abnormal development of bloodvessels which are numerous, 
distorted, and larger than normal. 

Dilatation of the central canal by serous fluid is called hydromyelia, and 
is ordinarily associated with hydrocephalus. 

Symptoms. — The symptoms of syringomyelia consist in loss of pain sense 
and of temperature sense, so that the patient may be cut or burnt without 
feeling pain, although his sense of touch in the affected part is still preserved. 
In some cases the temperature sense may be preserved, or the sense of heat 
is lost and that of cold preserved, or vice versa. The areas in which the loss 
of pain sense exists are not symmetrical, but are irregularly distributed 
over the body. The fact that the lesion usually affects the cervical portion 
of the cord explains why it is that the areas of analgesia are usually found 
in the upper extremities. Associated with this impairment of pain sense 
there develop, as the disease advances, nutritional changes in the bones, 
muscles, and skin, and a progressive paralysis due to the muscle changes. 

The outward evidences of trophic disturbance are usually first noticed in 
connection with some injury which fails to heal and, becoming infected, 
forces a recognition of its presence upon the patient, not by pain, but by his 
observation with his eyes that healing does not take place. In some instances, 
however, nutritional changes occur without any history of injury. Felons 
may develop. When they are accompanied by severe necrosis the condition 
is usually called "Morvan's disease." In still other cases the finger-nails 
become deformed, or superficial gangrene of the skin develops. The shoulder-, 
elbow-, and wrist- joints become swollen, filled with fluid, and absorption of 
the articulating surfaces takes place, the condition in the upper extremities 
in this disease being practically identical with that seen in the joints of the 
lower extremities in certain cases of locomotor ataxia. 

The shafts of the long bones often suffer fracture, but these fractures 
are painless and only enforce attention because of the incapacity pro- 
duced. Painless dislocations may be caused by insignificant traumata. 
Curvature of the spine may also occur, due to muscular atrophy, and per- 
haps to changes in the vertebra?. Secondary contractures may take place 
and produce great deformity of the hands, which, added to the progressive 
muscular atrophy and the paralysis, impairs the use of the upper extremi- 
ties very much. In addition to these symptoms several special symptoms, 
dependent upon the site of the lesion, must be considered. Thus, if the 
lower part of the spinal cord is affected there may be vesical or rectal par- 
alysis; whereas, if the upper cervical cord is affected there may be unilateral 
retraction of the eyeball, narrowing of the palpebral opening, and a slow 
pupillary reaction because of involvement of the spinal centre of the cervical 
sympathetic. When anaesthesia is found on the face it is ascribed to impli- 
cation of the spinal root of the fifth nerve in the cervical region. 

Diagnosis. — As already stated, the loss of pain sense with preservation of 
tactile sense, the trophic changes, and the muscular atrophy all form a 
picture which reveals syringomyelia. Before all these symptoms develop 
the presence of a slowly increasing muscular atrophy may mislead the 
physician into the diagnosis of chronic poliomyelitis or progressive muscular 



990 DISEASES OF THE NERVOUS SYSTEM 

atrophy. Indeed, in its commonest type, syringomyelia presents the picture 
of progressive muscular atrophy when it is advanced, including the " claw- 
hand. " Less frequently the white columns of the cord are pressed upon 
by the central mass and symptoms of locomotor ataxia or of lateral sclerosis 
are found. The true condition is recognized by the dissociated anaesthesia 
already described. Tumor in the cord usually produces so much pressure 
that the symptoms of paraplegia are more marked than in syringomyelia, 
and a tumor is usually associated with severe pain. The dactylitis of 
syringomyelia bears a resemblance to leprosy, which, however, does not 
reveal the more general signs of disease in the cord. 

Prognosis. — The chance of recovery is of course nil, but as the disease 
progresses very slowly indeed, life may be prolonged for years. 

Treatment. — There is no treatment for syringomyelia. The affected 
extremities should be carefully protected from injury. 



HEMORRHAGE INTO THE SPINAL CORD. 

Definition and Etiology. — Spontaneous hemorrhage into the spinal cord 
is a very rare accident, so rare that some writers have denied its existence 
except when it has arisen from a direct traumatism. Minute hemorrhages, 
of course, occur in severe forms of acute myelitis. The most common period 
of life for this accident to occur is between the twentieth and fortieth years, 
but it may occur in infants. Hemorrhage due to injury may, of course, 
develop at any time. Gowers cites a case of hemorrhage occurring appar- 
ently as the result of repeated sexual intercourse. Occasionally hemorrhage 
into the cord ensues in cases of asphyxia, as in coal-gas poisoning, and cases 
have been reported in which haemophilia produced this lesion. The clot is 
usually found in these cases chiefly in the gray matter of the cord. Some- 
times it is single; in other instances there are multiple clots. If the escape 
of blood has been copious the blood may perforate the white matter and 
find its way to the pia. 

When the clot is of any size and the cord is examined shortly after the 
accident, changes resembling those due to hemorrhage into the brain are 
present. The cord is softened and infiltrated with small round cells and 
with red and white corpuscles which are seen to be undergoing granular 
change. The tissues are also stained by blood-coloring matter. If the patient 
lives for some weeks and then at death the cord is studied, there is found 
fatty degeneration of the neighboring tissues or a cicatrix of connective tis- 
sue which occupies the site of the hemorrhage. Secondary descending and 
ascending degenerations may ensue as in myelitis. 

Symptoms. — The symptoms of hemorrhage into the spinal cord vary, of 
course, with the level at which the lesion takes place. The general symp- 
toms are paraplegia with loss of sensation in the paralyzed limbs, and loss 
of control of the bladder and rectum. These symptoms are those of acute 
myelitis as well. In addition quite severe pain may be felt in the spine or 
be referred to the front of the thorax or to the epigastric region, and even to 
the legs. 



HEMORRHAGE INTO THE SPINAL MEMBRANES 991 

When the hemorrhage is in the cervical cord there is paralysis of the arms 
as well as the legs. The reflexes are usually lost at first because of shock, 
but ^oon reappear and are usually exaggerated unless the cervical or the 
lumbar enlargement of the cord is affected, when they are permanently 
absent in the arms or in the legs. Spastic contractions may develop later 
from descending changes in the crossed pyramidal tracts, as in myelitis. 
The muscles may undergo degenerative changes very rapidly because of 
damage to the cells in the anterior horns of the gray matter at the level of 
the lesion. 

Not rarely, if the hemorrhage has been at all large, a stage of secondary 
irritation and inflammation develops as a result of the extravasation of 
blood, and this may not only greatly increase the gravity of the symptoms, 
but destroy life. On the other hand, it not infrequently happens that the 
hemorrhage in the gray matter may not only destroy this part of the cord, 
but by pressure abrogate the function of the white matter. 

After the acute process is over, the paraplegia is greatly decreased as the 
pressure is decreased, but complete recovery does not ensue because the 
cord is permanently damaged, and so atrophy of the muscles, governed by 
that part of the gray matter which has been damaged, ultimately develops 
as in acute poliomyelitis. Some degree of spasticity persists through loss 
of fibres in the pyramidal tracts, and various sensory defects if the dorsal 
columns have not completely recovered. 

Diagnosis. — The diagnosis of hemorrhage in the cord is not to be made 
until the symptoms are so well defined that there can be little doubt as to 
their cause. The onset of the symptoms must be sudden, that is, almost 
instantaneous. If several hours are passed in their development it is prob- 
ably a case of acute myelitis. Pain is also an important symptom, for, if it 
is present, it points to hemorrhage. 

Prognosis. — This depends upon the severity of the symptoms and upon 
the site of the lesion. If it is in the cervical or lumbar enlargements, the 
prognosis is more grave than if it is in the dorsal cord. If bed-sores speedily 
develop the outlook is correspondingly bad not only because their presence 
shows grave lesions in the cord, but also because their existence is a menace 
to the patient's life. 

Treatment. — Absolute rest in bed is essential. An ice-bag should be kept 
over the spine, and small doses of aconite and the bromides used to allay 
circulatory excitement. The use of ergot in such cases as commended by 
Gowers does not seem to be based upon a correct conception of the physio- 
logical action of this drug. Some time after the hemorrhage the iodides 
may be used to aid in clearing up the inflammatory exudate. 

HEMORRHAGE INTO THE SPINAL MEMBRANES. 

Definition and Etiology. — A hemorrhage about the spinal cord may be 
outside the dura mater (extrameningeal or extradural), or inside the dura 
mater (intrameningeal). If it is between the dura mater and the arachnoid 
it is called subdural, and if it is between the arachnoid and pia mater it is 
called subarachnoid. 



992 DISEASES OF THE NERVOUS SYSTEM 

Rupture of a vessel in the spinal meninges occurs usually in adult life, 
and more frequently in males than females. Its most common cause is 
injury to the spine. It has been known to follow violent convulsions and as 
a sequel to those infections which result in purpura. In newborn infants 
the blood found between the spinal membranes has its origin in the meninges 
of the brain, and follows the cord downward. Sometimes, in cases of very 
severe inflammation of the spinal meninges, small extravasations of blood 
take place. 

In extradural hemorrhage the blood comes from the veins which lie between 
the dura and the bony canal. The quantity of blood which is poured out 
varies greatly. In some instances it reaches the full length of the cord. In 
other instances but a small area is covered by a clot. The most common 
seat for the hemorrhage is the cervical portion of the cord. The cord may 
or may not be compressed. 

Subdural hemorrhage, that is, the escape of blood between the dura and 
the arachnoid, also varies greatly in quantity. In subarachnoid hemorrhage 
the blood comes from the vessels of the pia mater, and the clot may surround 
the cord for a few inches or extend throughout the whole subarachnoid 
space. In very rare instances it may actually force its way into the cerebral 
ventricles. 

In all cases of hemorrhage into the spinal membranes, save the extra- 
dural type, the cerebrospinal fluid is blood-stained. This may be a valu- 
able diagnostic point, since lumbar puncture may reveal the presence of 
blood in this fluid. 

Symptoms. — No symptoms may be present unless the hemorrhage is 
extensive enough to cause compression, or unless a secondary meningeal 
inflammation develops. When the effusion of blood is considerable there 
is sudden severe pain in the back, usually about the level of the hemorrhage, 
which extends into the loins, and it may be to the anterior surface of the 
body. There may also be some muscular spasm in the parts involved by 
those nerves, the roots of which are pressed upon after leaving the spinal 
cord. These spasms may be severe enough to produce a convulsion, local- 
ized or general. Immediately after these symptoms evidences of loss of 
power develop and the symptoms resemble the early stages of acute myelitis, 
or of hemorrhage into the cord itself, save that it is rare for the paralysis 
of either sensation or motion to be as complete as it is in those conditions. 

If the hemorrhage is in the cervical region, the pain is felt in the neck and 
arms. There is difficulty of swallowing and of breathing, and, it may be, 
dilatation of the pupils. When it is in the dorsal region the pain is in the 
chest and abdomen, and when in the lumbar region it is chiefly felt in the legs. 
Consciousness is preserved unless it be lost through shock. Some hours or 
days after the hemorrhage a secondary reaction with febrile movement may 
develop. In fatal cases death usually comes on within a few hours. 

From a medicolegal standpoint it is interesting to note that at least 
one case of meningeal hemorrhage in the spine very closely resembled 
strychnine poisoning. If the symptoms are severe, death is very likely to 
occur within a few hours, If the patient survives the first few days, partial 
recovery from the paralysis may occur. 



COMPRESSION OF THE SPINAL CORD 993 

Prognosis. — The prognosis as to life is worse when the hemorrhage is 
high up in the meninges than when it is low down. 

Treatment. — The treatment of this condition consists in absolute rest, 
the employment of small doses of the bromides and aconite as nervous and 
circulatory sedatives, and counterirritation over the back in the shape of 
dry cups ,or leeches. The patient should be made to lie on his side or on 
his face rather than on his back, in order to prevent the accumulation of 
extravasated blood at the posterior portion of the cord. Where the quantity 
of blood which is poured out is very large, and the symptoms so severe that 
death is threatened, it may be advisable to call upon a skilful surgeon to 
relieve pressure by operation. 



COMPRESSION OF THE SPINAL CORD. 

Definition and Etiology. — Compression of the spinal cord occurs as the 
result of disease of the vertebra?, of growths in the vertebra? or the meninges; 
of growths occurring within the spinal canal, inside or outside of the dura 
mater; of aneurysm of the aorta, which, by pressure on the vertebra?, cause 
their absorption; as the result of syphilitic inflammatory processes in the 
spinal canal, or by the development of a pachymeningitis, which may involve 
the cervical or lumbar portions of the cord, and which is characterized by a 
thickening of the parts involved. The result of pressure exercised by any of 
these causes interferes with the nutrition of the spinal cord and with the 
transmission of impulses along its tracts, and the symptoms which arise vary 
in their character and severity with the degree of pressure and the alterations 
caused by it. 

Disease of the vertebrce is most commonly the result of tuberculous infec- 
tion, particularly in children. As a result of this process, the bones become 
softened, give way under the pressure which is exerted upon them, and as 
they do so pressure upon the cord results. In other instances a suppurative 
process results in the development of so much pus that pressure is produced 
by it, and not uncommonly a carious process in the vertebra? is associated 
with an inflammation of the dura mater, with consequent thickening of this 
membrane, so that pressure is produced. Again, the caseous masses which 
are formed , or the overgrowth of connective tissue which takes place, may cause 
pressure. In some instances the dura mater suffers from tuberculous infec- 
tion, and tubercles are found upon its inner surface, and both the arachnoid 
and pia mater may be involved. As a result the nutrition of the spinal 
cord at this point is impaired through interference with the circulation in 
its bloodvessels and probably also because of the obstruction to the circu- 
lation of lymph as well. The cord, in the majority of instances, is in- 
volved. If, however, the pressure is severe, there is apt to be an overgrowth 
of connective tissue whereby a sclerotic process is developed. The axis 
cylinders become swollen, and fatty globules can be found in the myelin 
sheaths. If the pressure is severe and is long continued, the cord may be 
markedly atrophied and the overgrowth of connective tissue be very great. 
In some instances there may be nothing left of the cord but a band of con- 
63 



994 DISEASES OF THE NERVOUS SYSTEM 

nective tissue. If the damage done to the cord is of a more severe type, 
ascending and descending degenerative changes occur. 

The symptoms produced by these lesions consist in pain in the 
spine and in the distribution of the nerves supplying the trunk and limbs. 
Not infrequently pain will be felt in the abdominal wall or in the neighbor- 
hood of the sternum because of the irritation of the nerve trunks as they make 
their exit from the spinal cord, according to the well-known law that pain is 
frequently referred to the peripheral ends of the nerve affected. Any jarring of 
the body by a misstep or a sudden movement or even a gentle blow upon the 
spinal column may cause the patient suffering. The muscles of the back are 
usually fixed, in order to protect the spinal column as much as possible. 
This fixation is partly voluntary and partly involuntary. In some instances 
a girdle sensation is felt in the nerves which make their exit from the area 
which is diseased. 

When the lesions are high in the cord there may be painful sensations in 
the arms, and if the lateral tracts are compressed there is an exaggera- 
tion of the reflexes, with a tendency to spasticity of the muscles. In other 
instances the patient may present all the symptoms of transverse mye- 
litis and develop bed-sores. The rapidity with which these symptoms 
develop in different cases varies very much, depending entirely upon the 
activity of the pathological process in the spinal column. In some instances 
years are consumed in the development of the advanced stage of the malady. 
In others paralysis of the lower extremities may be produced in a few 
months. 

The diagnosis of these cases is not difficult if the physician will carefully 
examine the spine. 

The prognosis is, of course, not very favorable, but it is a noteworthy 
fact that in those stages in which the process in the spinal column becomes 
arrested a very marked degree of recovery may take place. On the other 
hand, it sometimes happens that spinal disease in infancy results in later 
life in the development of lateral sclerosis or other diseases of the spinal 
cord. Much depends in the way of prognosis upon what the surgeon is able 
to do for the spinal disease. The nervous symptoms are to be considered 
purely secondary, and every effort made to modify the pathological process 
in the spine. 

The treatment of compression of the spinal cord due to disease of the 
vertebra is entirely in the hands of the orthopedic surgeon, who, by means 
of proper apparatus, can often do much good. The medicinal plan of 
treatment consists in the use of cod-liver oil, iron, and arsenic, the following 
of a perfectly healthy mode of life, and the use of good food. Pain is to 
be relieved, if necessary, by opiates, and the nervous twitchings by sedatives, 
like bromide and chloral. In some cases hydrotherapeutic measures are 
advantageous. 

Malignant growths of the vertebras, such as carcinoma and sarcoma, are 
rare. They are usually rapid in their growth and produce symptoms of 
spinal compression as soon as they invade the spinal canal. These 
malignant growths soon penetrate the dura, the arachnoid, and the pia, and 
speedily infiltrate the spinal cord itself, although the dura mater is usually 



COMPRESSION OF THE SPINAL CORD 995 

capable of protecting the spinal cord from direct infection when the disease is 
tuberculous. 

When a tumor of the spinal cord develops it is in the great majority of 
instances due to sarcoma. Tumor of the spinal cord is, however, exceed- 
ingly rare. Schlesinger found only 147 spinal tumors in 35,000 autopsies, 
and Starr states that the ratio of tumors of the spinal cord to tumors of the 
brain is 1 to 13. 

Here, again, the symptoms consist, as a rule, in intense neuralgic pain 
of a shooting or stabbing character caused by pressure upon the nerves 
as they leave the spinal canal. These pains are more severe than those 
produced by any other form of spinal disease, and they are felt in 
different portions of the body, according to the portion of the spinal 
cord which is involved. If the lower cervical portion of the cord is affected, 
the pain may be felt in one or both hands and forearms. If the growth 
is in the upper cervical region, they are felt in the shoulder or neck; if it 
occurs as low as the sixth dorsal segment the pain is felt in the chest, 
near the nipple; in the tenth dorsal segment it is felt in the abdomen and groin. 
When a tumor compresses the cord in its entire thickness degenerations 
ensue, descending in the lateral columns, ascending in the dorsal and other 
sensory columns, just as they arise in cases of marked caries of the vertebra?. 
Under these conditions the symptoms are those of a transverse myelitis. The 
level at w T hich the tumor is growing can largely be determined by localizing 
the symptoms, and the fact that tumor is present may be pointed to by 
the presence of growths elsewhere in the body. If the tumor is of the 
malignant type its growth is usually exceedingy rapid. 

Spinal symptoms due to new-growth differ from those due to caries of the 
spine by the fact that the stillness of the muscles of the back and tendons 
on jarring the spine is not so marked in growths as it is in tuberculous disease. 
In the latter case, also, there may be found a primary tuberculous focus. 

When compression is due to tumor the treatment is operative. In many 
instances it is possible to give the patient some relief by this means. Starr 
has collected 58 cases of tumor of the spinal cord in which an operation was 
attempted. In all his cases the tumor was found, and in 16 of them the 
patients recovered If the growth is malignant the possibility of doing 
much good by operation is, of course, remote. Pain may, however, be 
temporarily relieved by the removal of the pressure. 

The compression of the spinal cord produced by gummatous growths or by 
syphilitic exudations about the spinal cord present symptoms which also 
depend upon the area which is involved, particularly upon the level of the 
lesion. The condition may arise either in acquired or in hereditary syphilis, 
and the diagnosis is made by the history of the patient and the presence of 
pressure symptoms. The treatment is antisyphilitic. 

When an aneurysm of the aorta grows in such a manner that it erodes the 
vertebrse, it may produce symptoms of compression of the spinal cord. Thus, 
paraplegia may be developed, or severe pain may be felt in those parts of the 
body which are supplied by the nerve trunks which have their origin in that 
portion of the spinal cord which is affected. If the physical signs of the 
presence of aneurysm are demonstrable the diagnosis is not difficult, but if 



996 DISEASES OF THE NERVOUS SYSTEM 

the growth is in a backward direction it may present no symptoms which 
indicate its presence. An examination of the patient's back may not only 
reveal signs of vertebral disease, but a bruit or a transmitted pulsation 
and a history of syphilis and of trauma, if added to a discovery that 
the bloodvessels are sclerotic, will aid in discovering this cause of the 
symptoms. 

A sixth cause of compression of the spinal cord is hypertrophic cervical 
pachymeningitis, the pachymeningitis cervicalis hypertrophica of Charcot. 
This disease consists in a thickening of the dura mater to such a degree that 
the spinal cord and the spinal nerves as they pass through the dura are pressed 
upon. As a result the spinal cord suffers from meningomyelitis, and the dura 
mater becomes adherent to the pia mater. Sometimes hemorrhagic extrav- 
asations occur under the dura, and there is usually an overgrowth of con- 
nective tissue about the bloodvessels, both in and about the cord. 

The symptoms of this form of meningomyelitis are identical with those 
already described as occurring in cases in which the cord is compressed by 
other causes in the cervical region, but they have certain peculiarities which 
may aid in the diagnosis of the condition. There is pain in the back of the 
head and neck, with a certain degree of stiffness and difficidty in movement. 
The pain radiates down into the hands and arms, and is often exceedingly 
severe and neuralgic in type. Patches of anaesthesia or paresthesia may be 
present and localized muscular spasms may occur, followed by loss of power 
and the development of reactions of degeneration, when the disease has 
lasted long enough to interfere with the transmission of trophic impulses 
from the cord to the muscles affected. Finally, if the pressure becomes 
great enough to seriously impair the nutrition of the spinal cord, there will 
develop symptoms of spastic paraplegia due to descending degenerative 
changes in the lateral tracts. If the muscles supplied by the ulnar and 
median nerves are chiefly affected, the disease is present in the lower part 
of the enlargement; but if those muscles supplied by the musculospiral nerve 
lose power, the upper part of the cervical enlargement is involved. Loss 
of power in the triceps, anconeus, supinator longus, extensor carpi radialis 
longior, and the brachialis anticus, therefore indicate disease of the upper 
segment; whereas, a loss of power in the flexor carpi ulnaris and flexor 
profundus digitorum (ulnar nerve) and all the muscles of the front part of 
the forearm and thumb (median nerve) indicates disease in the lower 
segment. In some cases myosis from paralysis of the cervical sympathetic 
may be present. 

Treatment of cervical pachymeningitis promises more than would be sup- 
posed from the character of the lesions, probably because the condition is 
so often due to syphilis. Active counterirritation of the back of the neck 
by the electrocautery and the free use of the protiodide of mercury, alter- 
nating with large doses of iodide of potassium, should always be resorted 
to. Pain is to be relieved by the use of acetanilid or phenacetin, and if 
these drugs fail to give relief they must be combined with morphine. 



SPINAL MENINGITIS 997 



SPINAL MENINGITIS. 

Definition and Etiology. — A condition of inflammation of the membranes 
covering the spinal cord is practically always secondary to some lesion at 
another part of the body. In some instances the specific micro-organism of 
croupous pneumonia, of enteric fever, of acute articular rheumatism, or 
septicaemia finds its way to these parts and causes the pathological process. 
In other instances tuberculosis is the cause, whether it be primarily present 
in distant parts of the body or in the vertebral column. In some instances an 
injury affords a means of entrance to the body for micro-organisms, which 
attack the spinal meninges, particularly if the vital resistance has been low- 
ered by an accident. Spinal meningitis may also arise from cerebral men- 
ingitis by direct extension of an infection. 

Pathology and Morbid Anatomy. — Following the stage of acute hyperemia 
present in all acute inflammatory processes, there is an excess of serous fluid 
poured out between the dura mater and the pia, which fluid may, at autopsy, 
be found to be purulent. Patches of fibrinous exudate are found on the sur- 
face of the pia mater, the bloodvessels of which are engorged with blood and 
often suffer from small hemorrhagic extravasations. The spinal cord, the 
pia and the dura mater are often adherent. After the inflammatory process 
has been present for some time, the pia mater becomes much thickened by 
the development of connective tissue. The secondary changes which ensue 
consist in an inflammatory process which affects the superficial parts of the 
spinal cord and causes degenerative changes in the spinal nerve roots, the 
axis cylinders of which become swollen. Fatty globules appear in the myelin 
sheath. The changes in the spinal cord are most marked in the posterior 
and lateral columns, and in subacute or chronic cases these areas are affected 
by an overgrowth of connective tissue, which ultimately produces sclerotic 
patches. 

Symptoms. — The onset of acute spinal meningitis develops, as do most acute 
inflammations of serous membranes, with pain, chill, fever, and general 
wretchedness. The pain is felt in the back and limbs, and is greatly increased 
by movements. There is also a state of hyperesthesia of all the spinal nerves, 
so that touching the patient may cause great suffering. It is soon noticed 
that the patient is stiff and more or less fixed by muscular rigidity, which is, 
in part, due to the pain produced by movement and to the irritation of the 
nerves as they pass from the spinal cord. The stiffness of the muscles of the 
back and of the neck is the most marked. At this time " Kernig's sign" is 
developed, which consists in an inability of the physician to straighten the 
patient's leg at the knee after the thigh has been flexed to a right angle 
with the trunk. This state is due to spasm of the flexor muscles induced by 
the irritation at the point of exit of the nerve trunks. There is often soon 
developed an increase in the reflexes, chiefly in the legs, and this in turn is 
succeeded by paralysis and final loss of reflexes if the process is severe and 
prolonged. Along with these symptoms there speedily develops a paralysis 
of the bladder and rectum, so that there is retention or incontinence of urine 
and incontinence of feces. There may also be paralytic incontinence. 



998 DISEASES OF THE NERVOUS SYSTEM 

Because of the lesions produced in the nerve roots and in the spinal nerves 
as they pierce the meninges, trophic changes in the skin may develop, as 
shown by localized areas of pallor and congestion and the speedy develop- 
ment of bed-sores. 

If the disease is severe and the inflammatory process spreads until the 
upper portions of the cord are involved, death may ensue by reason of the 
inflammation reaching the level of the medulla and causing fatal disturbance 
of the function of respiration or of the heart. In such cases Cheyne-Stokes 
breathing and irregularity of the pulse may be the symptoms of impending 
dissolution. Not rarely the development of paralysis of the cranial nerves 
with convulsions and coma precede death. Death may come within a few 
days of onset or after several weeks. In the severe cases which recover the 
patient often permanently suffers from localized palsies, anaesthesias, and 
atrophic lesions in the skin and muscles. 

Diagnosis. — Aside from the character of the symptoms just described, 
which points strongly to meningitis, we may resort to lumbar puncture for 
the purpose of making the diagnosis more certain. A strong, hollow needle 
attached to a syringe, so that it may be easily handled, or a small trocar and 
cannula are passed into the spinal canal between the third and fourth lumbar 
vertebras, on a line drawn between the crests of the ilia. The direction of 
the needle should be slightly to one side and upward. (For further details 
as to this method see Cerebrospinal Fever.) As soon as it enters the 
spinal canal the cerebrospinal fluid will escape, drop by drop, or with a 
squirt, if the pressure is great. This fluid should be examined for bacteria 
to determine the nature of the infection. If the fluid contains disintegrated 
blood, the cause of the affection is a pachymeningitis or an injury. If fresh 
blood is present, the blood is probably due to the puncture. If the fluid is 
clear there is probably no true meningitis present. In cases of tuberculosis 
of the meninges it is usually quite cloudy. If it contains pus a purulent 
meningitis is present. If inflammation of the meninges is present no sugar 
will be found in the fluid. A study of the leukocytes in the cerebrospinal 
fluid may throw light upon the case. They are much increased in number 
in acute inflammatory processes. In chronic conditions the mononuclear 
cells are particularly increased. 

Prognosis. — Tuberculous meningitis is, of course, a state giving a hopeless 
prognosis. Septic cases are also grave. Those types due to pneumonia 
and typhoid fever sometimes recover. (See Pneumonia and Typhoid 
Fever.) 

Treatment. — The treatment of spinal meningitis consists in absolute rest, 
the patient being placed upon a soft bed. In some instances if there is any 
sign of bed-sores it is essential that an air-bed or water-bed should be used. 
The application of blisters or the actual cautery has been recommended, 
but in view of the possibility of bed-sores developing, it is questionable 
whether their use is safe. The same objection holds in regard to such 
forms of counterirritation as cupping and leeching. Twitchings or cramps 
of the muscles are to be relieved by the administration of sedatives to the 
spinal cord, such as bromide and chloral, and if the pain is very severe 
morphine must be used. At one time it was believed that full doses of 



CHRONIC SPINAL MENINGITIS 999 

calomel combined with opium were exceedingly valuable in the treatment of 
acute inflammation of all serous membranes, particularly those covering the 
brain and spinal cord. At the present time this method of treatment has 
almost entirely ceased, but in certain instances it would seem advisable to 
have recourse to it. The object is to give enough mercurial to exercise its 
so-called antiphlogistic influence, and to use the opium not only for the relief 
of pain, but for the purpose of preventing the calomel from purging the 
patient. The mercurial may be pushed until slight tenderness of the gums is 
manifested. 

Chronic Spinal Meningitis. Etiology.— Chronic spinal meningitis is 
said to occasionally have its origin in an acute inflammation of the meninges 
of the spinal cord. In all probability, however, such an origin is exceed- 
ingly rare, and in the majority of instances it is the result of syphilitic infection, 
whereby there is a thickening of the dura and the formation of an abnormal 
quantity of serum and connective tissue under it. As the result of the chronic 
inflammatory process in the membrane, a somewhat similar one is set up in 
the spinal cord near its surface, producing a meningomyelitis, which is in its 
nature clcfsely allied to the acute form of meningitis just considered. There 
is always present a thickening of the bloodvessels, a small-cell infiltration 
about their walls, and, if the process is severe, an obliterating endarteritis. 
Sometimes gummatous masses are formed. In most of these cases there is 
also present cerebral meningitis as well. 

Symptoms. — The symptoms of chronic spinal meningitis consist in stiff- 
ness of the back and extremities, with pains and cramps. There are also 
disturbances in sensibility, some portions of the skin being hypersesthetic, 
others anaesthetic. Motor power is also impaired, and if the inflammation is 
in the lower portion of the spinal cord there may be interference with the 
function of the bladder or rectum. 

Diagnosis. — Chronic spinal meningitis is to be recognized by the presence 
of the symptoms just described and by the use of lumbar puncture, which, 
if meningitis is present, will show an increased quantity of cerebrospinal 
fluid, which is usually under pressure, and which will, therefore, escape from 
the needle with a spurt. Care must be taken that ordinary lumbago with 
spasm of the muscles of the back and fixation and pain is not confused with 
this condition. Myelitis is to be separated by the absence of severe pain and 
of cramps in the extremities, and by the presence of paraplegia. 

Treatment. — The treatment of chronic meningitis consists, as must be evi- 
dent from its cause, namely, late syphilis, in the free use of protiodide of 
mercury and the iodide of potassium, given until a full physiological effect is 
produced. In other words, it is not a question of grains administered, but 
effects obtained. These cases are usually much benefited by going to the 
various hot springs, because, in addition to the use of mercurials by the 
mouth, they permit the simultaneous use of hot baths and mercurial inunc- 
tions. Everything should be done to keep the general condition of the 
patient at the highest possible level approaching that of health. 



1000 DISEASES OF THE NERVOUS SYSTEM 



ACUTE ASCENDING PARALYSIS (LANDRY'S PARALYSIS). 

Definition. — This is an acute ascending paralysis beginning in the lower 
extremities and rapidly passing upward until it involves the muscles of the 
trunk and upper extremities, finally causing death by failure of respiration. 
The condition is a very rare one. It must be clearly separated from those 
forms of acute ascending paralysis due to an acute ascending myelitis, or to a 
hemorrhage into the spinal membranes, and from ascending peripheral neuritis. 
It is a symptom-complex which results from a lesion of the lower segment 
of the motor pathway, either in the cord and bulb or in the peripheral nerves. 
It is sometimes called acute progressive paralysis, or Landry's paralysis, 
having been first described by Landry in 1859. Rare cases have been 
recorded in which the disease has begun in the arms and passed to the legs. 

Etiology. — The exact etiological causes of this malady are not understood. 
The disease occurs more frequently in males than in females, and its most 
common period of occurrence is between twenty and forty years of age. In 
all probability every case is due to an infection of the peripheral nerves and 
spinal cord, for it sometimes follows an acute illness due to a micro-organism, 
as, for example, influenza, smallpox, erysipelas, typhoid fever, and pelvic peri- 
tonitis. The excessive use of alcohol has seemed in some cases to be a 
powerful predisposing cause, and cases have been recorded in which, in the 
presence of a history of syphilis, the malady has been arrested by the use 
of specific remedies. 

Pathology and Morbid Anatomy. — The lesions found at autopsy in a case 
of Landry's paralysis are by no means constant in all cases. In some 
instances the chief lesions have been found in the spinal cord, in others in 
the peripheral nerves and nerve roots. In the spinal cord the lesions described 
in some cases have been practically identical with those of acute dissemi- 
nated myelitis, and in others they have been identical with those met with 
in severe peripheral neuritis. In every case, however, it is evident that the 
peripheral motor neurones are the portions of the nervous system most 
affected. 

Symptoms. — In some cases of acute ascending paralysis the onset of the 
paralytic symptoms is preceded for a few hours by a sense of general wretched- 
ness, with tingling or pain in the limbs or back. This is followed by a rapidly 
increasing weakness in the lower limbs, which may amount to a complete loss 
of power in from a few hours to several days. The muscles of the lower part 
of the trunk are next involved, and finally the muscles of the arms and of 
the upper thorax fall victims to the rapidly spreading malady. The respira- 
tion becomes difficult, the speech indistinct, and dysphagia may be present. 
Sensation in the paralyzed parts may be impaired, but it is not lost. The 
reflexes are decreased, and perhaps lost, but they may be restored later on 
and ultimately become excessive. Muscular atrophy does not develop 
even when the patient survives for weeks, and the sphincters usually, but 
not always, retain their power. Bed-sores do not develop. The mind nearly 
always remains clear, and the temperature is usually not elevated. Very 
rare cases have been reported in which the paralysis has been of the acute 



CAISSON DISEASE 1001 

descending type, the arms being the parts first affected. In such cases fatal 
bulbar paralysis may occur before the lower parts of the body are affected. 

Diagnosis. — Acute ascending paralysis is to be separated from acute 
poliomyelitis by the absence of rapid atrophy. From the paralysis due to 
an acute hemorrhage into the spinal meninges it is separated by the absence 
of pain and of spasm. From an acute ascending myelitis it is separated by 
the fact that there is no loss of sensation, that the sphincters are unaffected, 
and that the paralysis progresses more rapidly. 

Prognosis. — The prognosis depends upon the state of the respiratory cen- 
tre and the lungs, and upon the condition of the centres governing cardiac 
action. If these parts are involved, death, of course, speedily ends the case. 
Death may come in a few hours or days, or not for several weeks. Cerebral 
and bulbar symptoms are always grave. A fatal ending usually occurs, 
but cases sometimes improve and recovery may occur. 

Treatment. — The treatment of a patient suffering from Landry's paralysis 
should be almost identical with that advised in cases of acute myelitis. A 
warm bath may be given to draw the blood to the surface, and moderate 
counterirritation should be applied over the vertebrae. It is absolutely essen- 
tial that perfect rest be obtained, and that the patient shall lie upon the side 
rather than upon his back, since the dorsal position may increase the ten- 
dency to congestion of the cord. As the disease is probably dependent upon 
infection and toxaemia, the skin should be kept active by mild diaphoretics, 
and the kidneys should be stimulated to activity by the use of the vegetable 
salts of potash or other mild diuretics. Some writers recommend the admin- 
istration of salicylate of sodium, although they do not seem to be able to 
explain how it can do good. Gowers speaks highly of the use of ergotin, 
and mentions the case of a man of fifty-seven who developed symptoms of 
Landry's paralysis after exposure to cold and wet. To this patient ergotin 
was given every hour till 20 grains had been taken, when the symptoms 
became markedly improved and the patient speedily recovered, so that by 
the end of a week he was well. One can not help feeling that in all probability 
the ergotin had little to do with this remarkable recovery, as it is hard to 
see how this drug could be useful in combating an infection which was 
so severe in its nervous effects. When there is a history of syphilis the 
protiodide of mercury should be administered freely. 



CAISSON DISEASE. 

Caisson disease is a condition met with in persons who have been exposed 
to high atmospheric pressures for a number of hours, and is particularly 
prone to develop if severe toil has been maintained during the exposure. 
The disease is usually met with in artisans, or laborers, who are engaged in 
the building of piers or foundations many feet under water, where it is 
necessary to have a pressure of several atmospheres in order to keep the 
caisson dry. In some instances the pressure is as great as ninety pounds to 
the square inch. The atmosphere in the caisson often has a high proportion 
of humidity, and the temperature may also be quite high. The symptoms 



1002 DISEASES OF THE NERVOUS SYSTEM 

develop when the workman leaves the caisson and is exposed to normal 
atmospheric pressure. In mild cases nothing more than a feeling of dizziness 
and vertigo develop, associated, it may be, with neuralgic pains in the head. 
In severe cases the neuralgic pains become excruciating, so that the patient 
feels as if his muscles were being stripped from his bones, and this pain is 
followed by a loss of both motion and sensation in the lower limbs, although 
the patient still complains of the pain. Often nausea and vomiting are 
present, accompanied by violent epigastric paroxysms of pain. Occasionally, 
there is loss of power in the sphincters. In some instances pain is absent, 
but paralysis is present, paralysis being the more constant symptom. In still 
more severe cases coma develops, in which case death invariably results. 
The prognosis is generally favorable unless the symptoms of paralysis and 
pain are unusually severe. The mildest cases rarely last over twelve hours, 
and sometimes only three or four; but in severe cases, recovery may not take 
place for days or weeks. 

The pathology of this curious condition is not well understood. (A dis- 
cussion of many of the views concerning it will be found in the author's 
Fiske Fund Prize Essay for 1886. 1 ) It would seem probable that the symp- 
toms are largely dependent upon disorder of the circulation in the central 
nervous system. Air emboli were found in the small arteries of the postero- 
lateral tracts of the spinal cord, also secondary softening was observed. 
Those who have had the most experience with the disease in this country are 
Jaminet, Bauer, and Woodward, who made many observations during the 
building of the St. Louis Bridge, and A. H. Smith, of New York, who studied 
it during the building of the Brooklyn Bridge. 

Treatment. — The treatment is both prophylactic and palliative. The 
prophylaxis consists in having superimposed air chambers, each one having 
a different pressure so that the workmen may pass by degrees from the high- 
pressure caisson to the pressure of atmospheric air. It is also advisable to 
have the workmen brought to the surface with as little muscular effort 
as possible. In the building of the St. Louis Bridge, thirteen of the men 
who were employed in the building of the east pier, which was sunk 127 feet 
below high-water mark, died; but in building the east abutment, which was 
sunk five feet deeper, only one man died. In the latter case the workmen 
were lifted to the surface by an elevator instead of having to climb a 
ladder. 

When the symptoms come on, morphine should be given hypodermic- 
ally in adequate dose. A. H. Smith considered that ergot is of value. 
Hot compresses should be wrung out and applied to the feet and spine. 
Jaminet recommends a draught of a strong alcoholic stimulant, with ginger. 

The whole object of the physician should be to re-establish and equalize 
the circulation. If the pulse is full and the heart laboring, venesection 
should be freely employed. Sometimes relief can be obtained by returning 
the patient to the caisson. In some instances a small caisson for the resus- 
citation of workmen has been built on the surface, with advantageous results. 

1 New and Altered Forms of Disease due to the Advance of Civilization in the Last Half Century. 



NEURITIS 1003 



DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE 

IN THE NERVES. 

NEURITIS. 

Definition. — Neuritis is an inflammation of a nerve. When the in- 
flammatory process chiefly involves the perineurium it is called " perineu- 
ritis;" if the tissues surrounding the nerve bundles and between the nerve 
fibres are affected, it is an " interstitial neuritis," and if the nerve fibres them- 
selves are primarily affected, it is said to be a "parenchymatous neuritis." 
The latter condition is usually a subacute or chronic process and is charac- 
terized by' degenerative changes in the nerve fibres. The distinction, how- 
ever, between these different forms is theoretical rather than clinical, because 
it is not possible to draw a definite line between them in most cases. 

Etiology, — The causes of neuritis are very numerous. Any injury to a 
nerve trunk, as by a blow, stretching, or a wound, may give rise to the inflam- 
matory process, as may also tumors, which by pressure cause irritation. 
Sometimes the use of a tool or a crutch may, by constant pressure on a nerve, 
produce neuritis. Various infectious diseases and the abuse of alcohol may 
produce it, as may also many of the metallic poisons. In those cases, how- 
ever, in which the malady arises as the result of a poison, the neuritis is 
usually a multiple neuritis and does not affect one nerve alone. (See Multiple 
Neuritis.) Gout, and lithsemic states, also cause it. 

Pathology and Morbid Anatomy. — The nerve, which is acutely inflamed, 
is found on examination to be red and swollen and lacking its usual lustre; 
the bloodvessels supplying it are hypersemic or congested. If the process 
has been present for some time the nerve may be marked by swellings due 
to overgrowth of connective tissue and its endoneurium may be infiltrated 
by small cells. At this time one of three processes develops. Either the 
results of the acute inflammatory process undergo resolution or the inflam- 
mation becomes so severe that the nerve is destroyed, or if the process is 
more moderate, but continued, there is an overgrowth of connective tissue 
and gradual atrophy and loss of function. Microscopically, the inflamed 
nerve presents additional changes which serve to separate the parenchyma- 
tous form of the disease from that in which the perineurium and interstitial 
tissues are chiefly affected. In the parenchymatous type the myelin is 
opaque and swollen and soon undergoes segmentation with granular material 
between the segments. The axis cylinder may be continuous or broken into 
segments corresponding to the breaks in the myelin. Finally, the myelin 
and cylinder entirely disappear and only the nerve sheath containing a little 
granular matter is left. This last state may also arise as a result of the 
interstitial form of neuritis, but in this form the nerve is, in the early stage 
of the inflammation, more swollen and congested and the sheath filled with 
serum or purulent exudate. 



1004 DISEASES OF THE NERVOUS SYSTEM 

Symptoms. — The symptoms of neuritis vary over a wide range in severity. 
When the inflammatory process is very mild so that the normal function is 
but slightly perverted, as from moderate pressure, a tingling sensation is 
felt or, in its place, a sense of numbness is experienced. This is called par- 
cesthesia and can scarcely be said to be due to any real change in the nutri- 
tion of the nerve. 

When the change in the nerve is more severe the symptoms are more 
definite. Tingling or pricking sensations may be present not only at the 
site of the lesion, but at the peripheral part of the nerve. If the damage is 
the result of pressure there is rarely any pain, and motor paralysis, more or 
less complete, is present instead. If, on the other hand, the lesion is asso- 
ciated with any wound, and an infection of the nerve has taken place, 
then pain is usually present and is often severe. Pressure upon the inflamed 
nerve trunk by the finger-tips also increases the pain not only at the point 
of pressure, but at the end of the nerve as well. After the process in the 
nerve is so advanced that its function is greatly impaired, trophic changes 
occur in the muscles and skin, the former wasting and the skin becoming 
glossy. The muscles cease to respond to faradic electricity and later fail to 
respond to galvanic electricity, the reactions of degeneration being first 
developed. Injuries to parts supplied by the nerve affected may result in 
sloughing, but sores rarely develop unless an injury is suffered. 

When recovery begins the electrical contractility to galvanic stimulation 
first returns in part and later the power of voluntary movement. 

Diagnosis. — The diagnosis of neuritis involving a single nerve, or several 
nerves in nearly related parts, is not difficult, for the pain is limited to the area 
of the nerve, as is also the anaesthesia or hyperesthesia and loss of power. The 
condition is also pointed to by the history of injury or of some diathetic state 
which produces the affection. Pressure on the nerve trunk will elicit pain. 

Prognosis. — The outlook for recovery in most cases of neuritis is quite 
good because of the extraordinary power of regeneration possessed by nerves. 
Even if the damage to the nerve has been so severe that its function is 
abolished by the division of all its conducting fibres, the function can be 
restored by the surgeon, who, by excising the destroyed portion and joining 
the distal and proximal ends together, may re-establish the pathway for 
both sensory and motor impulses. So rapid is the regeneration that if a nerve 
is severed by accident, and immediately sewed together, power may return 
in two weeks. When the damage has been done by pressure or inflamma- 
tion the recovery rarely ensues in less than six weeks, and even eight months 
or a year may be consumed in the regenerative process. When recovery 
fails to occur and it is believed that only a small part of the nerve is diseased 
surgical procedures are necessary, but if there is reason to believe that 
permanent damage to a large part of a nerve has taken place, then the prog- 
nosis is hopeless. Sometimes the mere exposure of the nerve and the break- 
ing up of adhesions or exudates that cause pressure is sufficient to produce 
recovery. 

Treatment. — The treatment of neuritis may be divided into two parts, 
that devoted to the relief of pain and that to the abatement of the inflam- 
mation and to the regeneration of normal function. For the relief of pain the 



NEURITIS 1005 

part affected may be wrapped in lint, which is heavily smeared with equal 
parts of an ointment of ichthyol and lanolin, outside of which is placed 
some oil-silk to retain moisture. In some instances a hot poultice of flaxseed 
or hot compresses may be used in the earlier stages to diminish the activity 
of the inflammatory process. If the pain is so severe that sleep is interfered 
with, the various coal-tar products may be employed, of which the most 
valuable are phenacetin in the dose of 5 grains four or five times a day, if 
need be. Acetanilid may be given in similar dose, and antipyrin in slightly 
larger dose. In other cases better results accrue if to these products of 
the coal-tar group are added small doses of codeine or morphine. If the 
pain does not yield to these remedies, hypodermic injections of morphine 
may be necessary for a short time, but their continued use is dangerous, as 
the patient only too readily develops the morphine habit. If the neuritis 
affects the arm or some portion of the body which does not by its disability 
force the patient to lie in bed, it is essential that the part involved shall be 
placed at rest. Thus, if the arm is affected it should be carried in a sling, 
and it may be necessary to protect it by a splint. 

For the restoration of function no therapeutic measure should be insti- 
tuted beyond those already named until the acute stage of the inflammatory 
process has ceased. When it is evident that the acute process is no longer 
present, strychnine or nux vomica may be given internally in full doses. 
These may also be combined with phosphorus and small quantities of quinine. 
The area of the skin which is supplied by the affected nerve should also be 
stimulated by the application of faradic electricity, care being taken that 
the current employed is not so strong as to damage the part. It is a good 
rule never to use a current so strong as to produce suffering. This method 
of treatment not only tends to rapidly restore sensation in the paralyzed 
part, but also to bring back faradic contractility in the muscle, and so ulti- 
mately restore motor power. If, however, the parts fail to respond, then 
galvanic electricity must be used, and the current interrupted so as to pro- 
duce a stimulant effect. In some instances the muscle seems to respond 
better to the negative than to the positive pole, much depending of course 
upon the stage of degeneration which is present. Care should be taken that 
the applications of electricity are not prolonged for more than a few minutes 
at a time, and that they are not made oftener than once a day. Additional 
measures for improving the nutrition of the part are massage and manipula- 
tion. None of these measures should, however, be employed if there is 
tenderness in the nerve trunk or if they produce exhaustion in the parts 
affected. Indeed, it is possible in some instances to produce injuries of 
the nerve by too active manipulation. It must be remembered that the 
electricity, the massage, and the Swedish movements only do good by 
increasing the circulation and modifying the nutritional processes in the 
parts affected. If anaesthesia of an extremity exposes it to injury, by reason 
of the patient being unconscious of the presence of heat or cold, or of objects 
which are capable of doing damage, the part should be carefully protected 
by a splint or soft dressing. 



1006 DISEASES OF THE NERVOUS SYSTEM 



Special Forms of Neuritis. 

Cervicobrachial Neuritis. — Cervicobrachial neuritis follows injuries to 
the neck and shoulder, and is usually produced by falls or severe blows. 
Symptoms may also arise as the result of disease of the vertebrae or from an 
aneurysm. In other cases the acute infectious diseases or gouty or rheu- 
matic conditions, associated with exposure to cold, seem to be responsible 
for the condition. The symptoms depend to a large extent upon the portion 
of the cervicobrachial plexus which is affected. If the four upper cervical 
nerves are involved, severe pain in the neighborhood of the occiput is felt, 
and the head is held in a fixed position because movement increases the 
suffering. When the fifth or sixth cervical nerves are involved, the pain is 
in the neck and the upper portion of the shoulder and axilla, and it may be 
felt down the back of the arm. Whereas, when the lower cervical nerves 
are affected, including the branches of the first dorsal, the pain is clavicular 
and axillary in the area of its distribution and extends down the front of the 
arm and forearm into the fingers. There is also loss of power in all the mus- 
cles which are supplied by the nerves making up the cervicobrachial plexus 
when their fibres are involved. Because of the fact that the cervical sympa- 
thetic nerve receives fibres from this part of the spinal cord it sometimes 
happens that ocular symptoms accompany manifestations of the neuritis 
in the lower portions of the cervicobrachial plexus, with the result that there 
may be retraction of the eyeball and narrowing of the palpebral fissure, with 
a mild degree of myosis and some pallor of the side of the face affected. 
The skin on this side is dry and does not become flushed on exercise. Cases 
of neuritis of the cervicobrachial plexus show marked evidences of pain when 
pressure is made over the plexus or when the arm is moved away from the 
body. 

In some instances of cervicobrachial neuritis of very sudden onset actual 
hemorrhage may occur into the sheath of the nerves, the so-called "apo- 
plectic neuritis." The same numbness and tingling as has been described 
under neuritis in general, followed by loss of sensation and of motor power, 
occurs in cervicobrachial neuritis. Trophic changes in the skin and muscles 
take place, and the reactions of degeneration develop. 

A form of cervicobrachial neuritis which affects children is sometimes 
called obstetrical paralysis, or birth palsy, and is due to damage of the 
cervicobrachial plexus in parturition. 

Prognosis.— The prognosis in cases of cervicobrachial neuritis, like that 
of neuritis in general, is good provided the injury has not been so severe as 
to sever the nerve fibres, and provided the condition has not lasted too long. 

Treatment. — The treatment consists in absolute rest, the employment of 
hot compresses if the condition is seen early in its course, and later on the 
constant use of counterirritation. Rubbing the parts with some stimulating 
liniment like that of chloroform or ammonia is of value. Electricity, 
massage, and Swedish movements are to be resorted to after all evidence 
of acute inflammation is passed. The rest of the treatment is identical with 
that given for neuritis. 



NEURITIS 1007 

Obstetrical or Birth Palsy. — A paralysis of brachial nerves is a frequent 
occurrence in difficult and protracted labors, especially in cases of breech 
presentation. Pressure with the finger or tenaculum introduced into the 
axilla in order to facilitate delivery will injure the nerves and produce 
paralysis. In birth palsy the following muscles are affected: deltoid, biceps, 
supinator longus, and infraspinatus. This leads to inward rotation of the 
arm, extension of the forearm, and pronation of the hand. The paralysis 
is soon followed by atrophy of the muscles. The prognosis of birth palsy 
is, generally speaking, favorable, except when reaction of degeneration 
exists. As to treatment, massage and electricity are the only means, and 
should commence as early as possible. 

Multiple Neuritis. Definition and Etiology. — Multiple neuritis, sometimes 
called " polyneuritis" or " peripheral neuritis," is a condition in which a large 
number of the peripheral nerves of the body suffer from subacute or chronic 
inflammation as a result of the action of some toxic agent. These toxic 
agents may be derived from external or internal sources. The external 
agents are alcohol, lead, arsenic, copper, mercury, anilin, carbon monoxide, 
and carbon bisulphide. The internal agents are the poisons developed in the 
various acute infectious fevers, as typhoid fever, smallpox, scarlet fever, 
influenza, erysipelas, pneumonia, diphtheria, dysentery, and other infectious 
maladies. Occasionally, too, a multiple neuritis develops as a complication 
of septic infection, either that following a wound or occurring during the 
puerperal period. Cases have also been recorded in which the toxic sub- 
stance apparently has arisen from decomposition changes in the intestines. 
In some instances syphilis, tuberculosis, diabetes mellitus, and malarial fever 
have seemed to be provoking agents, but in all probability these affections 
act indirectly by rendering the nerve trunks susceptible to the action of the 
poison. A special form of multiple neuritis is that which is known as beri- 
beri or " kakke." (See Beriberi.) In several instances small epidemics of 
multiple neuritis have been described. Multiple neuritis occurs most fre- 
quently between the twentieth and the fiftieth year of age, and is very rare in 
children, unless it is due to diphtheria. Whatever may be the cause of an 
attack of multiple neuritis, the pathological changes which are found in 
the affected nerves do not differ greatly from those already described as 
occurring in ordinary neuritis of a more limited extent. 

Symptoms. — The symptoms of multiple neuritis, be the cause what it may, 
are fairly constant, although slight variations in the character of the symp- 
toms occur according to the peculiar influence exercised by the poison. As 
alcoholic neuritis is the type most frequently met with, a description of this dis- 
ease may be used for all forms of multiple neuritis. At the beginning of the 
malady there may be some slight elevation of temperature, but in many cases 
this does not occur. The patient first complains of tingling or numbness in 
the feet and fingers. In other cases dull pain may be experienced. Rarely 
this pain may be severe. These disturbances of sensation are usually 
increased by moving the affected limb and by deep or superficial pressure 
over the nerve trunks, and especially by deep pressure upon the muscle bellies 
of the forearms and of the calves. 

Following these symptoms weakness develops, and it may become so 



1008 DISEASES OF THE NERVOUS SYSTEM 

severe that the patient is unable to move his hands or feet, and foot-drop or 
wrist-drop may develop. After the paralysis has lasted for some little time, 
some wasting of the muscles of the affected parts takes place. The reflexes 
are diminished or altogether arrested. 

A peculiarity of the paralysis of peripheral neuritis is that very often it does 
not involve all the nerves of a limb. Thus, it not infrequently happens that 
the peroneal nerves suffer chiefly. In other instances the tibialis posticus is 
chiefly affected; and it is only when the condition is unusually severe that a 
complete paraplegia is present. In the arms the musculospiral nerve is most 
commonly affected. It is a noteworthy fact that the paralysis is usually 
symmetrical. In some instances the symptoms are more sensory than motor, 
but this is rarely the case. Sensory symptoms are, however, very con- 
stant in alcoholic neuritis, and in most of the other forms. They may, how- 
ever, be absent or be very slight, as in neuritis due to lead, and in such forms 
of infectious disease as diphtheria and influenza. These forms of neuritis 
are often spoken of as "motor neuritis " to indicate that the sensory functions 
escape. 

In addition to the numbness and tingling already mentioned, patches 
of anaesthesia and hyperesthesia are often found existing near one another 
or even coinciding, So, too, there may be a hypersensitiveness to pain and 
a loss of the sense of touch, or vice versa. 

Not infrequently the affection develops a train of symptoms which are so 
exactly like those met with in locomotor ataxia that even the most skilful 
neurologist may have difficulty in differentiating the two diseases. In other 
words, a so-called "pseudotabes" due to multiple neuritis is present. This 
resemblance depends upon the fact that the fibres of " muscle sense " which 
are affected in their spinal course (posterior columns) in tabes are implicated 
in such cases of multiple neuritis at their origins in the joints and muscle 
fasciae. The presence of the Argyll-Robertson pupil in true ataxia, how- 
ever, usually determines that the case is not one of peripheral neuritis. 
As an illustration of how closely multiple neuritis may resemble locomotor 
ataxia, cases have been reported in which perforating ulcer of the foot 
occurred. 

Aside from the trophic changes already spoken of as occurring in the mus- 
cles, local disorders of blood supply and secretion are often present. There 
may be areas of skin which suffer from excessive sweating. In other cases 
localized patches of oedema are found, and rarely the joints become swollen, 
so that the case resembles acute articular rheumatism. Actual breaking 
down of the skin as the result of trophic changes, however, rarely occurs. 
The bladder and rectum are usually unaffected, and this aids materially 
in separating the paraplegia of severe neuritis from that due to myelitis. 
Occasionally, however, this valuable aid to differentiation fails us, and 
retention or incontinence of urine or feces is present. 

Associated with these evidences of impairment in function in the 
peripheral nerves it is not infrequent for disturbances to occur in connec- 
tion with intellection. Confusion of thought and impairment of memory 
are frequently present, occasionally in a peculiar form characterized 
by fabrication or "pseudoreminiscence," the patient relating imaginary 



NEURITIS 1009 

recent experiences. This mental condition, combined with multiple 
neuritis, is sometimes called "Korsakoff's disease." 

The cranial nerves also share in the malady. Indeed, in some instances 
they suffer most. Nystagmus, or squint, may be present, but the optic 
nerve is not often affected, although occasionally it may suffer very slight 
atrophy. The paralysis of the cranial nerves may be symmetrical. Thus, 
Oppenheim has reported cases of double facial palsy due to this cause. 

Tachycardia and interference with the function of the diaphragm may be 
manifested from the infection involving the pneumogastric and phrenic 
nerves. Mannaberg asserts that the multiple neuritis may be confined 
entirely to the cranial nerves. 

When tbe multiple neuritis is due to lead, it is a noteworthy fact that the 
inflammatory process is not, as a rule, very widely distributed, and that the 
sensory nerve fibres usually escape. In association with the symptoms of 
neuritis, already described, there may be a history of lead colic, which will aid 
in determining the cause of the paralysis. The presence of a blue line on the 
gums is also pathognomonic. Ansemia is often marked. Aside from the 
fact that sensation is usually not involved, the multiple neuritis caused by 
lead is noteworthy, in that it chiefly, and it may be exclusively, affects the 
extensor muscles of the hand and fingers. Indeed, the paralysis may be so 
localized in mild cases that only the extensor communis digitorum may be 
involved, so that the ring and little finger cannot be extended. When the 
paralysis is very marked, double drop-wrist is present. Another peculiarity 
of lead palsy is that the supinators, especially the supinator longus, and the 
triceps, escape. The deltoid, however, may be partially paralyzed, and the 
abductor pollicis longus and the interossei may be palsied. Occasionally, 
however, the supinators are affected, as is also the biceps. Muscular atrophy 
is nearly always marked in lead paralysis, and the reaction of degeneration 
usually speedily develops. Muscular tremor may also be present. The 
noteworthy fact that sensation is not disturbed in most cases may be well 
reiterated. Drop-foot is rarely seen in cases of lead paralysis. Paralysis 
of the cranial nerves due to lead is exceedingly uncommon. (See Lead 
Poisoning.) 

When the paralysis is due to arsenic, it is not infrequently associated with 
gastrointestinal disturbances, and, unlike that due to lead, it is usually asso- 
ciated with marked disturbances of sensation in the affected parts. Wasting 
of the muscles supplied by the affected nerves usually develops quite early. 
Not only are the extensors affected, as they are in lead poisoning, but the 
flexors are also involved. Another point of difference between arsenical 
paralysis and that due to lead lies in the fact that the lower extremities are 
quite as frequently affected as the upper extremities, so that quadriplegia, 
that is, a paralysis of all four extremities, is present. Reactions of degenera- 
tion speedily develop. The pulse is apt to be rapid. Disturbances of the 
psychic functions are said to occur, which is rare in lead poisoning, unless 
encephalopathia saturnina is present. Symptoms of ataxia are usually 
marked. The reflexes are lost, and these two factors may make the case 
more closely resemble true locomotor ataxia than any other form of multiple 
neuritis. Nutritional changes in the skin are quite frequent in arsenical 
64 



1010 DISEASES OF THE NERVOUS SYSTEM 

neuritis. In some instances herpetic eruptions develop. In others the skin 
becomes glossy, and there may be falling out of the hair. It is exceedingly 
rare for the cranial nerves to be involved. 

Of all the forms of multiple neuritis due to toxic substances having their 
origin in the body, that due to the poison of diphtheria is most frequently 
met with. As diphtheria is essentially a disease of childhood, it is evident 
that diphtheritic multiple neuritis must be more commonly met with in 
young persons. The peculiarity of this form of neuritis is that it most fre- 
quently affects the muscles of the soft palate, changing the character of the 
speech and rendering swallowing difficult. This paralysis is both motor and 
sensory, and is often accompanied by wasting. Sometimes the external 
ocular muscles are paralyzed. In other instances the internal ocular 
muscles suffer chiefly, and accommodation may be paralyzed as the result 
of oculomotor involvement. The pupillary reflex is, however, usually pre- 
served. In other instances the paralysis produced by diphtheria is almost 
universal. I have seen more than one instance in which the child was not 
only paralyzed in all its extremities, but was unable to exercise any control 
over the movements of its head, and could only swallow when put in such a 
position that the liquids could readily pass down the gullet. Such cases are 
usually characterized not only by loss of motor power, but by loss of sensa- 
tion as well. The bladder and rectum usually escape the general paralysis, 
but they may be involved. It is a noteworthy fact that diphtheritic paralysis 
is not a concomitant symptom, but a sequel to an attack of diphtheria, and the 
full severity of the symptoms may not be present for several weeks after the 
diphtheria has ceased. In some instances the diaphragm is paralyzed, and 
if the nerve supply of the heart becomes affected sudden death may occur. 
(See Diphtheria.) 

Diagnosis. — The presence of numbness and tingling followed by more or 
less impairment of motion and sensation in certain nerve trunks, with com- 
plete or partial escape of other nerve trunks, of course, points to multiple 
neuritis as the cause of the malady, particularly if the history of the patient 
reveals the fact that he or she has been exposed to one of the provoking causes 
already named, In some instances more than one of these causes has been 
effective, and, therefore, the precise factor in determining the neuritis cannot 
be relied upon. Thus, I have known more than one instance in which the 
administration of very large quantities of alcohol as a stimulant during 
typhoid fever has produced a multiple neuritis, which was attributed to a 
typhoid toxin, when in reality the alcohol was the active agent. In those 
cases in which the paralysis comes on very rapidly and is severe, the differ- 
entiation must be made between this condition and Landry's paralysis (which 
see) , and this is the more important because Eichhorst has described a neu- 
ritis acutissima progressiva. A so-called apoplectiform type has been 
described by other observers. The presence of the Argyll-Robertson pupil, 
optic nerve atrophy, and the history of exposure to a poison may be the only 
means by which we can differentiate between true locomotor ataxia and 
multiple neuritis. 

Prognosis. — The prognosis is favorable in nearly every case, unless the 
patient has been exposed to the evil influences of lead or arsenic or alcohol 



NEURITIS 1011 

for so long a time that the nerves cannot undergo regenerative change. In 
cases of profound alcoholic intoxication sudden death may take place 
when the pneumogastric nerve becomes involved. In nearly all instances 
recovery is exceedingly slow The first symptom of improvement is a 
diminution in the pain and a decrease in tenderness of the nerves on pal- 
pation. In other instances the power of motion returns before the sensory 
functions are restored to their normal condition, and inability to get about 
may be caused by the intense hypersensitiveness of the feet. Even if the 
patient does not recover for eighteen months or two years, the condition is 
by no means hopeless. Care should be taken, however, that complete 
recovery should not be promised in cases which have been exposed to the 
poisons for very long periods of time. Not infrequently great disappoint- 
ment is caused by periods in which no improvement takes place, or, indeed, 
in which a relapse seems to be threatened. 

The prognosis in multiple neuritis due to lead is good so far as the preserva- 
tion of life is concerned. It is bad in direct proportion to the duration of the 
condition and of the exposure to the poison. The same facts hold true in 
regard to the peripheral neuritis due to arsenic. 

Occasionally secondary contractures occur as the result of the contraction 
of non-paralyzed muscles, whereby deformities are produced. 

After diphtheria, even in those cases in which the paralysis is most severe, 
the prognosis is not necessarily very grave. The immediate danger is that 
some nervous mechanism connected with a vital function may be involved. 
If this does not occur, partial or complete recovery of motion or sensa- 
tion nearly always takes place, although twelve months may pass before 
recovery occurs. Usually, however, two or three months is sufficient. 

Treatment. — The treatment of multiple neuritis gives better results than 
that devoted to the relief of any other form of paralysis. If the cause of the 
malady is one of the metallic poisons already named, the patient must be 
removed from further exposure to the poison. Thus, workers in lead and 
arsenic must cease following such occupations. For the purpose of aiding in 
the elimination of any of the poisons which may remain in the body, moderate 
doses, 20 to 30 grains, of iodide of potassium may be given twice or thrice a 
day. If the patient uses alcohol to excess, this agent must, of course, be 
withdrawn. While the nerves are hypersensitive to pressure and while pain 
is present, strychnine and faradic electricity should not be applied to them, 
since they tend to increase irritation; but when there is anaesthesia and loss 
of power, full doses of strychnine and phosphorus are often useful, and the 
rapidly interrupted faradic current may be used to stimulate the affected 
nerve fibres. Muscles which are suffering from loss of power may be exer- 
cised by the use of the slowly interrupted faradic current. Massage may also 
be employed, but it is of vital importance that no form of exercise shall be 
used to the point of exhaustion of the affected parts, In other words, only 
healthy exercise designed to improve the nutrition of the parts affected should 
be resorted to. 

If it is thought that the neuritis is due to toxic materials arising inside 
the body, these should be removed, if possible. The administration of laxa- 
tives or purges is usually needful. If ansemia is present, particularly if it 



1012 DISEASES OF THE NERVOUS SYSTEM 

is associated with septic conditions, such as are met with in sepsis and puer- 
peral fever, iron and arsenic are useful. If the patient is rheumatic or of gouty 
tendency, hot baths, or a visit to any of the well-known hot springs may be 
resorted to, and the various salicylates or iodides should be administered 
in sufficiently full doses to produce mild physiological effects. For the pur- 
pose of aiding in the elimination of toxic materials, pure water should be 
drunk freely to flush the kidneys, and Turkish baths may be taken to produce 
sweating. Pain is to be relieved by the use of such remedies as phenacetin or 
acetanilid, and by hot applications to those areas which suffer most. Some- 
times the application of splints to provide perfect rest for the painful part is 
useful. 

In those forms of multiple neuritis which depend upon infection, such as 
diphtheria, smallpox, or typhoid fever, the heart should be carefully exam- 
ined, and if any evidences of tachycardia, bradycardia, or arhythmia are 
present, the patient should be warned against sitting up in bed, and should 
be protected from all causes which may throw an increased strain upon the 
circulation. This is particularly important in diphtheritic multiple neuritis. 
Contractures should be prevented by massage and Swedish movements and 
remedied, if they occur, by tenotomy. 



DISEASES OF THE CRANIAL NERVES. 

The Olfactory Nerve. — Disease of the olfactory nerve, of course, inter- 
feres with the special sense of smell, and if this sense is entirely lost the 
condition is called anosmia. Partial or complete loss of this sense results 
from lesions of the peripheral ending of the nerve in the nasal mucous 
membrane and from pathological states of the tissues beneath it, such as 
morbid growths or disease of the ethmoid bones. Similar loss of function 
results from meningitis, from injury of the bones forming the base of the 
skull, or morbid growths affecting these bones. Tumors of the brain may 
destroy the olfactory nerves or the olfactory bulbs. When complete loss of 
the sense of smell occurs and no local lesion in the nasal bones or mucous 
membranes is present, it is usually an evidence of a tumor or abscess in the 
anterior cranial fossa. 

The Optic Nerve. — The optic tract of either side arises by two roots from 
structures in the midbrain called the primary optic centres. These struc- 
tures are the external geniculate body, the posterior part (pulvinar) of the 
optic thalamus, and the anterior quadrigeminal body. 

It is important to remember that the fibres from the optic tract undergo 
partial decussation in the chiasm. The outer fibres do not decussate and they 
connect the outer half of the retina with the primary optic centres of the same 
side. The inner fibres, on the other hand, all cross to the opposite side, and 
they connect the inner half of the retina with the nuclei on the opposite side. 
It is evident, therefore, that the right optic tract contains fibres which carry 
impulses from the right halves of both retinae to the right side of the brain, 
and that the left optic tract contains fibres which convey impulses from the 
left halves of both retinae to the left side of the brain. It is essential to remem- 



DISEASES OF THE CRANIAL NERVES 1013 

ber these facts in order to understand the condition known as hemianopsia, 
which will be described shortly. 

Optic neuritis, sometimes called papillitis, is an inflammatory condition 
which is manifest in the intraocular end of the nerve, and it may be due 
to several causes. In the great majority of cases it is due to brain tumor. 
Choked disk is an cedematous state. The degree of neuritis has no direct 
relationship to the size of the tumor, nor to the area of the brain which it 
affects, although a tumor of the corpora quadrigemina seems to cause the 
condition more commonly than do growths elsewhere. Tumor of the parieto- 
occipital' region and of the cerebellum also produces papillitis in a large 
proportion of cases in which these growths occur, while a tumor of the 
frontal lobes of the cerebrum very rarely causes it. The condition is not 
materially affected as to frequency or severity by the character of the growth. 
Meningitis in any of its forms may cause papillitis, but tuberculous meningitis 
does so more commonly than any other form. Rarer causes are cerebral 
softening, inflammation, and atrophy, or any cause, such as aneurysm or 
hydrocephalus, which produces an increase in intracranial pressure. Very 
rarely disseminated sclerosis, general paresis, or myelitis may cause papil- 
litis, as may the various acute infectious diseases, or the excessive use of 
alcohol, or lead poisoning. 

Symptoms. — There are often no symptoms whatever which point to optic 
neuritis, at least in so far as the patient complains of impairment of vision. 
The diagnosis rests solely upon the use of the ophthalmoscope and upon a 
study of the fields of vision. The ophthalmoscope reveals an indefinite out- 
line of the head of the nerve, with redness, followed by swelling of the papilla, 
which becomes grayish in hue. Finally, the disk protrudes, its outlines 
become lost and whitish patches may be seen upon its surface. The retinal 
arteries are contracted and the veins congested and tortuous. At the point of 
exit and entrance of the vessels this part may seem devoid of vessels, because 
they are hidden in the infiltrated mass. Small, narrow, flame-like hemor- 
rhages may be seen along the vessel walls. The field of vision is concentrically 
contracted, and the perception of red and green is lost before the other color 
senses are destroyed. Hemianopsia is present if the lesion is so situated as 
to cause this symptom. 

Another form of optic neuritis, called retrobulbar neuritis, exists in which 
the inflammatory process develops in the optic nerve in the orbit. In the 
acute form the symptoms consist in dimness of vision which always occurs 
in the centre of the field, and which may end in complete blindness in from 
one to eight days. With the ophthalmoscope, when the disease is well 
developed, the edges of the disk are seen to be indistinct, its surface hyper- 
semic, and its main bloodvessels shrunken. The cause of the acute form is 
usually some one of the acute infections, such as influenza, scarlet fever, 
or one of the diathetic diseases, such as rheumatism, gout, and sometimes 
syphilis. 

The treatment of retrobulbar neuritis consists in the production of profuse 
sweating by pilocarpine, the use of large doses of the salicylates if gout or 
rheumatism is present, or the employment of mercury and the iodides if 
syphilis is suspected. Counterirritation on the temple is also advisable. 



1014 DISEASES OF THE NERVOUS SYSTEM 

The chronic form of retrobulbar neuritis is usually a toxic condition pro- 
duced, in the majority of instances, by tobacco, alcohol, arsenic, lead, or 
poisons made by infectious diseases. Its symptoms consist in diminution 
of vision and in color scotomata. The prognosis when the cause is tobacco 
and alcohol is good, if the patient will give up these drugs and if he does so 
in the early stages of the disease; otherwise the prognosis is bad. 

The treatment consists in the elimination of the causes as far as possible, 
in the use of massive doses of strychnine, and the employment of the iodides 
and free sweating. 

Treatment. — This depends upon the cause. If it is due to brain tumor or 
abscess, operative treatment is required, unless a gummatous growth is 
present, when mercury and the iodides are needful. Trephining of the 
skull to relieve pressure may be resorted to as a palliative measure in cases 
where a growth cannot be removed. 

Optic Atrophy. — Atrophy of the optic nerve, as its name implies, is a 
condition in which a degenerative process affects its fibres. It is divided 
into five forms: the primary, secondary, consecutive, retinitic, and choroi- 
ditic atrophy. The last two forms are really of the consecutive class. 

Etiology. — Primary atrophy of the optic nerve has been thought to be 
due to impaired nutrition, sexual excesses, and to such diseases as chronic 
malarial infection, diabetes, syphilis, and to the overaction of certain drugs. 
The most important causes of primary optic atrophy are diseases of the 
spinal cord, notably locomotor ataxia. It is also seen in cases of general 
paresis and disseminated sclerosis. In many instances the optic atrophy 
may be one of the early symptoms of ataxia. It has also been met with in 
cases of lateral sclerosis, chronic myelitis, and bulbar palsy. 

Secondary atrophy arises from causes which produce pressure upon the 
optic tract and the optic fibres, as, for example, the growth of a tumor or an 
aneurysm, or meningitis. So, too, injuries to the head sometimes produce 
atrophy. Consecutive atrophy follows the various forms of optic neuritis. 

Pathology. — The axones lose their medullary sheaths and are converted 
into fine fibrils, between which are interspersed numerous fatty granules. 
When the condition is far advanced, the nerve elements entirely disappear 
and there is a marked increase in connective-tissue formation. 

Symptoms. — The subjective symptom complained of by the patient is 
diminution in the acuity of vision. The other symptoms are developed by 
the use of the ophthalmoscope. When this instrument is used it is found 
that the optic disk is gray or greenish-gray, or actually white in color, although 
there may be patches of red throughout it. The centre of the disk is depressed 
in direct proportion to the degree of atrophy which has taken place. The 
margin of the disk is distinct, and in some cases, when the condition of the 
optic nerve is due to disease of the spinal cord, there is broadening of 
the normal scleral ring. The bloodvessels are narrowed, but in some cases 
only the arteries seem to be affected, the veins escaping. An examination 
of the central vision shows that it is markedly impaired, or absolute blindness 
may be present. The field of vision is greatly narrowed and there may be a 
central scotoma or hemianopsia. The color fields are markedly diminished, 
the green being most affected; after it the red, and then the blue and yellow. 



DISEASES OF THE CRANIAL NERVES ]()15 

Sometimes the field for red is first affected. The pupil usually manifests 
some degree of paralytic dilatation, and when the nerve is completely atro- 
phied the pupil is dilated and the iris motionless. In secondary atrophy 
the disk is apt to be whiter than in the primary forms, when it is usually gray. 
In that form of optic nerve atrophy called retinitic and choroiditic atrophy, 
the disk is often slightly yellowish in hue, but its borders are not distinct. 

Diagnosis, — The mere discovery that the optic disk is grayer than normal 
and that its margins are sharply defined, does not justify the diagnosis of 
optic atrophy. If, however, any of the diseases so far named are also present, 
such a diagnosis is usually correct. 

Prognosis. — The prognosis as to complete recovery is bad. On the other 
hand, it must be remembered that the atrophic process is often a slow one 
which may last for years. Indeed, the prognosis in secondary cases depends 
largely upon the rapidity with which the underlying disease is advancing. 

Treatment. — The treatment consists in the administration of full doses of 
mercury and the iodides if there is any suspicion that a recent or ancient 
syphilitic infection has been present. Strychnine in large doses combined 
with nitroglycerin is also useful. 

Of the functional disorders of the optic nerve the most important are 
blindness due to uraemia, that due to diabetes, malaria, profound anaemia, 
and the abuse of drugs. When ursemia is the cause the presence of the 
symptoms of that condition, in association with dimness of vision or blind- 
ness, make the diagnosis clear. The so-called albuminuric retinitis may be 
present, but the ophthalmoscope may, however, reveal no morbid changes. 
If the patient survives, vision usually returns. 

When the dimness of vision is due to diabetes, the prognosis is unfavorable 
because the disease is incurable. That form which is due to malarial infec- 
tion has associated with it other symptoms of this disease. Recovery 
usually takes place if proper treatment is administered. So, too, in cases 
of dimness of vision, due to hemorrhage and profound anaemia, the prog- 
nosis is good, unless the anaemia is one of the so-called essential anaemias 
which always go from bad to worse. The treatment in such a case consists, 
of course, in the use of drugs designed to combat anaemia. 

Hemianopsia. — Hemianopsia, or blindness of one-half of the visual field, 
occurs in three forms: that known as bitemporal hemianopsia, binasal hem- 
ianopsia, and homonymous hemianopsia, each variety being named not 
from that part of the retina which is blind, but from the visual field which is 
affected. In the first there is loss of vision in both temporal fields, in the 
second in the nasal half of each eye, and in the third form the same side of 
each eye is lacking in function — that is, for example, the outer half of the 
left eye and the inner half of the right eye. When the left half of each retina 
is inactive, the condition is called right homonymous bilateral hemianopsia, 
and when the right half is functionless it is designated left homonymous 
bilateral hemianopsia. Homonymous hemianopsia is the most common. 
Binasal hemianopsia is very rare. Bitemporal hemianopsia is produced by 
a lesion, such as a tumor or an aneurysm, which presses upon the middle of 
the chiasm. Homonymous lateral hemianopsia is produced by a lesion of 
one optic path at any point back of the chiasm, either in the neighborhood 



1016 



DISEASES OF THE NERVOUS SYSTEM 



of the calcarine fissure (occipital lobe), in the optic radiations, including the 
point where they pass just back of the internal capsule, in the primary optic 



Fig. 128 




'**«**<£ 



The visual tract. The result of a lesion anywhere between the chiasm and the cuneus is to produce 
homonymous hemianopsia. H. Lesion at chiasm causing bilateral temporal hemianopsia. N. Lesion at 
chiasm causing unilateral nasal hemianopsia. T. Lesion at chiasm causing unilateral temporal hemi- 
anopsia. SN. Substantia nigra of crus. L. Lemniscus in crus. RN. Red nucleus. III. Third nerves. 
P, Q, R, S, U. Lesions in the occipital lobe and in front of it, producing left homonymous lateral 
hemianopsia. 

centres, or in the optic tract. (See Fig. 128.) It is important to remember 
that the lesion in cases of hemianopsia is on the opposite side to that of the 



DISEASES OF THE CRANIAL NERVES 



1017 



dark field. 1 (See Fig. 129.) De Schweinitz has condensed the following 
rules as to the significance of various forms of hemianopsia from a series 
prepared by Dr. Seguin: 

(a) The lesion in hemianopsia is on the opposite side of the dark 
fields. 

(b) If the preserved fields are accompanied by concentric contraction, 
the smaller half-field will be in the eye opposite to the lesion; contraction of 
the preserved half-field is most common with lesions of the cortex, but also 
may occur in lesions of the tractus. 

Fig. 129 

IEFT VISUAL FIELD. RIGHT VISUAL FIELD, 

FixationPowt. Fixation Poi/it. 




Diagram illustrating why it is that the lesion is on the opposite side to the dark field. (Oliver.) 

(c) If the hemianopsia is relative, the lesion is probably in the cortex; 
but cortical lesions are not excluded by absolute hemianopsia. 

(d) A lesion confined to the cuneus, or to it and the gray matter immedi- 
ately surrounding it, on the mesial surface of the occipital lobe, produces 
homonymous lateral hemianopsia without motor or sensory symptoms, at 
least without these as a direct consequence of the lesion, although they may 
appear as indirect or, as they are sometimes called, distant symptoms. 
Slight motor symptoms such as deviation of one eye inward may, however, 
be added to the visual symptoms of a lesion in the occipital lobe (Mills). 

(e) A lesion producing typical hemiplegia, aphasia, if the right side is 



1 For a more complete study of the significance of this difficult subject see the author's Practical 
Diagnosis, fifth edition. 



1018 



DISEASES OF THE NERVOUS SYSTEM 



\ 






w 



paralyzed, little or no anaesthesia, and lateral hemianopsia, is probably 
due to disease in the area supplied by the middle cerebral artery. 

(/) A lesion causing hemiplegia, hemianesthesia, and lateral hemianopsia 
is probably situated in the posterior portion of the internal capsule. 

(g) A lesion causing hemianesthesia, ataxic movements of one-half of the 
body, no distinct hemiplegia, and lateral hemianopsia, could be situated in 
the posterior lateral part of the optic thalamus. 

(h) A lesion causing the symptoms of disease of the base of the brain, 
associated at the same time with changes in the pupil, changes in the nerve 

head, and lateral hemianopsia, 
FlG - 130 could be situated in one optic tract 

or in the primary optic centres on 
one side. 

(i) Incomplete hemianopsia, as- 
suming usually a quadrant-shaped 
defect, may be present on account of 
a lesion confined to the lower half of 
the cuneus. It may also occur with 
less definite limitations in lesions 
of the subcortical substance of the 
occipital lobe, and then may be 
associated with other symptoms, 
as hemiplegia and hemianesthesia. 
Finally, it may occur from a lesion 
of the tract, but then will be accom- 
panied by other symptoms indicating 
basal disease, or from a lesion of 
the external geniculate body. 

(j) A hemianopsia in which there 
is preservation of the light sense, but 
loss of either the color sense or the 
form sense, indicates that the lesion 
is in the visual centre of the cortex. 
The Third or Oculomotor Nerve. 
— The third nerve has its origin 
from groups of cells in the floor of 
the aqueduct of Sylvius. It then 
passes through the tegmentum of the 
crus cerebri, and makes its exit in a 
bundle on the inner side of the crus. 
(Fig. 130; see also Plate IX.) It 
then passes from the crus to the 
sphenoidal fissure and so into the 
orbit, where its fibres divide and go 
to supply the ciliary muscle, the sphincter of the iris, the superior rectus, 
internal rectus, inferior rectus and inferior oblique muscle. (See Plate VIII.) 
It also sends fibres to the levator palpebrse muscle. As it is a motor nerve, 
paralysis follows its injury. The causes of disturbance in its function are 




Showing the nearness of origin of the oculomotor 
(3), pathetic (4), and abducens (6). Tne roots of 
these nerves are shown by an incision which has 
divided the pons. III. The third nerve, arising from 
several roots. IV. The fourth nerve. VI. The sixth 
nerve, arising from three roots. (Modified from 
Arnold.) 



PLATE VIII. 







Showing the Distribution of the Troehlearis, Oculomotor, and 
Trifacial Nerves. (Modified from Rudinger.) 



1. The troehlearis nerve. 

2, 3, 4, 5, 6, 7. The oculomotor nerve fibres. 
8, 9, 10, 11. The trifacial fibres. 



PLATE IX. 




Base of Brain, showing the Superficial Origin of the Cranial 

Nerves. 



The Roman numerals refer to the twelve cranial nerves. 



DISEASES OF THE CRANIAL NERVES 1019 

numerous. They may exist at the base of the brain, where the nerve leaves 
the cms, in the sphenoidal fissure, in the orbit, and even in its peripheral 
filaments in the eye itself, although change in its functional activity in the 
latter area* is usually due to the effect of drugs. Of the causes which pro- 
duce disturbance of its function at its origin in the crus, we find tuberculous 
meningitis or that due to some acute infectious disease, abscess of the brain, 
and hemorrhage. For this reason meningitis of either form in infancy very 
frequently involves this nerve, and so produces symptoms which call the 
attention of the physician to the existence of the disease at the base 
of the brain. In adults, aside from tuberculous meningitis, there may be 
syphilitic exudation, or the nerve itself may be inflamed, owing to the 
presence of this same disease. Tumors or abscess at the base of the 
brain may press upon it. When the nerve is injured in its passage through 
the sphenoidal fissure, the cause is usually some traumatism which results 
in fracture of the bone, or very rarely a severe blow which damages the 
nerve by pressure against the bone. In a case which came to the writer's 
attention, a severe blow with the hilt of a sword upon the forehead caused 
paralysis of this nerve, probably in this manner. 

In the orbit a tumor may press upon the nerve fibres. Occasionally the 
nerve loses power through the action of the poison produced by diphtheria 
or typhoid fever. 

Symptoms. — The dominant symptoms of paralysis of the oculomotor 
nerve are ptosis, mydriasis, and consequent loss of pupillary reaction to light 
and accommodation. As it supplies the internal rectus, external squint may 
be present. The paralysis of the ocular muscles also results in diplopia. 
If the patient is directed to look upward, downward, or inward he is unable 
to do so. The inability of the pupil to contract when light is thrown into the 
eye may be due to a lesion of the nerve before it enters the orbit, or, as 
already stated, to the action of a drug upon its peripheral filaments. It will 
be remembered that pupillary contraction, when produced by the entrance 
of light into the eye, is due to a reflex impulse which passes along the optic 
nerve to the neighborhood of the corpora quadrigemina, thence to the third 
nucleus and along the fibres of the third nerve to the ciliary ganglion, from 
which, by way of the ciliary nerves, it goes to the iris and causes contraction 
of its circular muscular fibres. A lesion in any portion of this reflex arc 
interferes with pupillary reaction. In addition to those injuries of the oculo- 
motor nerve already mentioned which cause paralysis, a loss of pupillary 
reaction may occur in locomotor ataxia, in multiple sclerosis, in general 
paresis, in bulbar palsy, and in myelitis when that disease involves the fibres 
of the arc. When these diseases are responsible for the loss of pupillary 
reaction, the lesion is supposed to exist, in the majority of instances, in 
fibres which connect the optic tracts in front of the corpora quadrigemina 
with the oculomotor nuclei. When drugs produce paralytic mydriasis, 
their action is usually exercised upon the peripheral ends of the nerve. 

Diagnosis. — The diagnosis of paralysis of the oculomotor nerve is readily 
made if the symptoms just described are kept in mind. 

Prognosis. — The prognosis depends upon the underlying cause of the 
paralysis. In diphtheria and typhoid fever recovery usually takes place, 



1020 DISEASES OF THE NERVOUS SYSTEM 

and unless the damage produced by an injury is very great, the outlook is 
favorable. On the other hand, if the cause is tuberculous meningitis, tumor, 
or abscess, or any one of the progressive nerve diseases just named, recovery 
is, of course impossible. 

The Fourth or Trochlearis Nerve. This nerve supplies the superior 
oblique muscle of the eye (1 , Plate VIII. ). Interference with the action of this 
nerve is not uncommon and is rarely recognized by the general practitioner. 
The symptoms are not developed until the eye is tested bymeansof placingacol- 
ored glass over one eye, when it will be found that the object which is placed 
before the patient stands in its normal position as seen by the normal eye, but is 
displayed outward and obliquely when seen by the eye supplied by the im- 
paired pathetic nerve. As the nerve arises from an area almost identical with 
that of the third nerve, the centric causes of trochlearis paralysis are practically 
identical with the causes of oculomotor paralysis. It is important to remem- 
ber that, should paralysis of the fourth nerve be present without involvement 
of the third or sixth nerve, it probably indicates a growth in the cerebel- 
lum or an inflammatory exudate upon the under surface of its middle 
lobe 

The Fifth or Trifacial Nerve.— The trifacial nerve contains motor and 
sensory fibres, the sensory fibres being by far the more numerous. The 
motor fibres have their origin in the pons, a little above its middle, receiving 
also the root descending from the midbrain ; they pass out in a bundle sepa- 
rate from the sensory fibres until, outside the cranial cavity, they take part 
in forming the inferior maxillary division of the nerve, through which they 
supply the muscles of mastication. 

The sensory fibres of the fifth nerve arise from a nucleus at about the 
middle of the pons, and, in addition, by the spinal root, from a chain of cells 
descending through the medulla as far as the first cervical segment of the 
cord; they emerge from the pons in a heavy trunk, which passes to the 
Gasserian ganglion (8, Plate VIII.) and then, beyond the ganglion, divides 
into three branches: ophthalmic (9), superior (10), and inferior maxillary 
(11). In addition to providing sensation to the greater portion of the 
face, it also supplies the anterior two-thirds of the tongue. 

Symptoms. — When the fifth or trifacial nerve is paralyzed in its motor 
fibres, the patient is unable to contract his masseter muscles and there is 
dropping of the lower jaw. Unless the paralysis is bilateral, however, it may 
not be easily discovered, since the muscles on the unaffected side may hold 
the jaw in position. And, moreover, if the lesion be in the brain the function 
of mastication is maintained from the other side by bilateral innervation. 
In some instances of paralysis of the fifth nerve, deafness arises as the result 
of interference with the function of the tensor tympani muscle, for a small 
branch from the motor fibres of the fifth nerve passes through the otic 
ganglion and supplies this muscle. When this muscle is paralyzed, the 
tympanic membrane is relaxed and this interferes with its function. Motor 
paralysis of the fifth nerve is rarely met with. Certain poisons like gelsemium 
may cause dropping of the jaw by paralyzing the muscles of both sides. 
When the sensory portion of the nerve is affected there is anaesthesia of the 
skin of the face in the areas supplied by the particular branches affected. 



DISEASES OF THE CRANIAL NERVES 1021 

If the area be that of the forehead, the upper eyelid, the conjunctiva, and 
the nostril, the ophthalmic branch of the fifth nerve is at fault, and the 
lesion is probably at the sphenoidal fissure or within the orbit, reflex wink- 
ing of the eye no longer takes place because the conjunctiva is anaesthetic, 
and for the same reason a flow of tears does not occur upon irritating the 
conjunctiva, because the lachrymal reflex is abolished. 

If the skin of the upper part of the face is anaesthetic, the superior maxil- 
lary branch is involved; and if the skin of the temporal region and that of 
the jaw and the under lip are anaesthetic, the inferior maxillary branch is 
diseased. When both of these branches are paralyzed there is probably a 
tumor of the superior maxillary bone; and if the entire area of the three 
branches is anaesthetic, the Gasserian ganglion may be the part affected, 
and this will be accompanied by trophic changes in the anaesthetic parts. 
The most common cause of anaesthesia of the trifacial is, however, neuritis. 

Romberg makes the following differential statement: 

(a) The more the anaesthesia is confined to single filaments of the tri- 
geminus, the more peripheral the seat of the cause will be found to be. 

(6) If the loss of sensation affects a portion of the facial surface, together 
with the corresponding faucial membrane, the disease may be assumed to 
involve the sensory fibres of the fifth pair before they separate to be dis- 
tributed to their respective destinations; in other words, a main division 
must be affected before or after its passage through the cranium. 

(c) When the entire sensory tract of the fifth nerve has lest its power, and 
there are at the same time derangements of the nutritive functions in the 
affected parts, the Gasserian ganglion, or the nerve in its immediate vicinity, 
is the seat of the disease. 

(d) If the anaesthesia of the fifth nerve is complicated with disturbed func- 
tions of adjacent cerebral nerves, it may be assumed that the cause is seated 
at the base of the brain. 

When the fifth nerve is paralyzed the mucous membrane of the nose 
and mouth are also anaesthetic and usually dry. The sense of taste is lost 
and trophic lesions may develop, although it is questionable as to whether 
these depend upon affection of the sensory fibres. These lesions consist in 
ulceration of the cornea, loosening of the teeth, atrophy of the gums, and the 
development of herpes zoster. As the sensation in the anterior two-thirds of 
the tongue is impaired, this organ is often damaged by the teeth. The 
dryness of the mucous membrane of the nose also interferes with the 
sense of smell, and irritating substances may be inhaled through the nostrils 
without pain, because of the lack of sensation in the nasal mucous mem- 
brane. Paralysis of this nerve is, however, very rarely met with. 

In the great majority of instances in which a physician is called on to 
treat a lesion of the trifacial nerve, the patient complains of severe neuralgic 
pain, which in most cases arises from the Gasserian ganglion (8, Plate 
VIII.). When trophic changes are very w T ell marked, they result in hemi- 
atrophy of the face. In those cases in which the motor fibres of the fifth 
nerve are irritated, there may be lockjaw as in true tetanus, and so-called 
masseter spasm may have a reflex origin because of the presence of dental 
irritation. 



1022 DISEASES OF THE NERVOUS SYSTEM 

Paralysis of the Sixth Abducens Nerve.— The sixth nerve has its origin 
from cells in the floor of the fourth ventricle, passes through the pons, and 
makes its exit in the groove between the pons and the medulla (Plate 
IX.), whence it passes through the sphenoidal fissure. It is subject to 
the same lesions at the base of the brain as is the oculomotor nerve, such 
as tuberculous meningitis and syphilitic exudation, tumor and fracture of 
the base of the skull. Injury may occur to it in the sphenoidal fissure. 
The sixth nerve supplies the external rectus and its paralysis thus causes 
internal squint, the patient being unable to rotate the eye outward. 

The exact lesion which produces paralysis of the sixth nerve can only 
be determined by a study of the associated symptoms. In those cases 
in which there is facial palsy on the same side as the squint, and paralysis 
of the arm and leg upon the opposite side, in other words, "crossed hemi- 
plegia," the lesion is in the pons or at the base of the brain in such a position 
that it produces pressure on the pons on one side and above its lower 
third. 

Disturbances of Motility in the Ocular Muscles Depending on the 
Third, Fourth, and Sixth Nerves.— The movements of the eyeballs depend, 
of course, upon the associated action of different muscles supplied by different 
nerves. When the axes of the eyeballs converge, they do so by the action 
of the internal recti muscles supplied by the third nerve, and when they 
diverge they move in these directions by the external recti supplied by the 
sixth nerve. If, however, there is conjugate deviation, then a much more 
complicated nervous mechanism is brought into play, for if the axis of each 
eyeball is turned to the right, for example, this motion is made by contraction 
of the external rectus of the right eye and the internal rectus of the left 
eye, each being supplied by different nerves, the right sixth and the left 
third, and yet it is essential that they shall act in accord. This is accom- 
plished by the presence of association fibres which, by joining together the 
nuclei of the nerves, enable them to act in unison. If by disease these asso- 
ciation fibres are destroyed (in the posterior longitudinal bundle), conjugate 
deviation of the eyes becomes impossible. When the eyeballs are deviated 
by reflex action, the pathway of the nervous impulse is through the optic 
nerve by connecting fibres to the motor nuclei of those nerves governing 
the ocular movements, which not only join the nuclei of the different nerves 
of one side, but connect them with the nuclei of the opposite side as well. 
When they are moved by voluntary action, the impulse leaves the motor 
centres in the anterior part of the motor area of the cortex, and thence passes 
down through the anterior part of the knee of the internal capsule, thence 
through the crus cerebri, and finally crosses in the raphe, passing to the 
nuclei of the oculomotor nerves and of the fourth and sixth nerves. When 
the impulse for conjugate deviation arises in the motor cortex, it passes first 
to the nucleus of the opposite sixth nerve, and thence is sent along the associa- 
tion fibres through the posterior longitudinal bundle to the nucleus of the 
third nerve on the opposite side, just as it is in reflex deviation. When a 
nervous explosion takes place in the motor cortex, as in cases of epilepsy, 
it often happens that there is conjugate deviation of the eyes away from 
the side on which the lesion exists, and, conversely, if the ocular centres in 



PLATE X. 




Showing Exit of Facial Nerve ( 1 ) from Stylomastoid Foramen and 
its Distribution to the Muscles of the Face. (Rudinger. ) 



DISEASES OF THE CRANIAL NERVES 



1023 



the cortex are destroyed, there is conjugate deviation of the eyes toward the 
oide on which the lesion exists. This has given rise to the statement that 
in the coma of ordinary apoplexy the patient "looks toward his lesion" at 
least in those instances in which an apoplexy destroys these centres. (See 
Apoplexy.) 

There are two states which give rise to an erroneous diagnosis in connec- 
tion with these symptoms, namely, ' rheumatic palsy" of the ocular muscles, 
which disappears under the free use of the iodides and salicylates, and so- 
called "recurrent oculomotor paralysis," which is probably the result of 
congestion and oedema, and which is accompanied by sick stomach, diplopia 
and fever. 

Ophthalmoplegia or Paralysis of the Internal and External 
Muscles of the Eyeball). — This condition depends not upon disorder 
of function of any single cranial nerve, but upon interference with the action 
of the third, fourth, and sixth nerves. As already stated, the third nerve 
supplies the ciliary muscle, the circular fibres of the iris, the superior rectus, 
internal rectus, inferior rectus, inferior oblique, and the levator palpebral. 
The fourth nerve supplies the superior oblique, and the sixth the external 
rectus. When morbid changes take place in the nuclei of these nerves the 
normal co-ordinated movements of the eye are impaired or lost, that is 
to say, ophthalmoplegia is developed. 

Ophthalmoplegia is of two forms: ophthalmoplegia externa, when the 
paralysis affects the external muscles of the eyeball and the levator palpebral; 
and ophthalmoplegia interna, when 

only the pupillary and ciliary muscles FlG m 

are involved. Ophthalmoplegia in- 
terna is quite rare, although a modi- 
fied form of it occurs in that state 
called the Argyll-Robertson pupil, a 
condition in which the pupil reacts to 
accommodation, but not to light. 
In this condition the lesion exists not 
in the nuclei of the nerves, for if it 
did there would be no reaction to ac- 
commodation, but in the association 
fibres, whereby the reflex pathway 
is destroyed. Ophthalmoplegia ex- 
terna, on the other hand, is by no 
means uncommon. It is a condition 
depending upon a centric lesion, and 
occurs in an acute and chronic form 
(see below). Because of the fact 
that the lesion is centric it is usu- 
ally bilateral, and if all the muscles 
are paralyzed it is said to be com- 
plete external ophthalmoplegia, 

while, on the other hand, if they are simply impaired in function, or if one 
nerve escapes while the others are involved, it is spoken of as partial (Fig. 131). 




Patient suffering from chronic ophthalmoplegia 
externa. The wrinkling of the forehead in the 
effort to open the eyes is noticeable. The external 
strabismus can be seen. (Starr.) 



1024 DISEASES OF THE NERVOUS SYSTEM 

Etiology and Pathology. — Ophthalmoplegia is due to a large number of 
causes, such as tumors, areas of degeneration, or inflammatory exudations, 
where the nerves take their exit at the base of the brain. (See Plate IX.) 
The additional causes are small hemorrhagic extravasations, arteritis, throm- 
bosis, or embolism of the small vessels which supply the nuclei of these 
nerves. In some cases the lesions resemble those of acute poliomyelitis, and 
belong to the affection called by Wernicke "polioencephalitis superior/' 

Symptoms. — The symptoms of ophthalmoplegia externa vary, of course, 
with the nerves which are affected and with the severity of the lesions. 
When the morbid process is severe, there is not only loss of p6Ver in the 
ocular muscles, but in other parts as well, so that the symptom-complex of 
bulbar paralysis may be present; or if the tracts to and from the higher areas 
of the brain are involved, such symptoms as hemiansesthesia, hemiplegia, or 
hemiataxia may be present. The pathological processes just described 
are varied not only as to cause and situation, but as to acuteness as well. 
The acute form is ushered in by a train of symptoms which necessarily 
arise when areas of the nervous system so important to life are affected. 
Thus, the patient suffers from vertigo, headache, vomiting, and even coma. 
Unconsciousness may last for several days and end in death, or, after a 
period of a week or ten days, consciousness gradually returns and the symp- 
toms connected with the eyes alone remain. These consist in double ptosis 
and various palsies of the ocular muscles, or total ophthalmoplegia. The 
chronic form arises when the nervous lesions are gradual in onset, although 
it may result from the acute type just discussed. Here again the degree of 
the paralysis depends upon the severity of the lesions. In one case a total 
palsy may be present, in another a partial palsy, and in still a third the palsy 
may be progressive, one muscle after another failing. Sometimes one mus- 
cle improves as another fails. Ptosis and other forms of ocular palsy may 
be a part of the transient and recurrent paralysis in myasthenia gravis. The 
prognosis depends upon the cause. If syphilis is a factor the outlook is 
favorable as compared to that type which is due to disseminated sclerosis 
or bulbar palsy. In no case is the outlook anything but grave as to recovery, 
although about one-half of the mild cases recover. 

The treatment also varies with the cause, and yet it may be said that, be 
the cause what it may, the only drugs which offer any promise of relief in 
the chronic form are mercury and the iodides. Hot baths may be useful. 

In the acute form freedom from any cause of excitement, the application 
of cold to the head, and the use of aconite to quiet the circulation, if it is 
excited, may be of some value. 

The Seventh or Facial Nerve. — The nucleus of the facial nerve is found 
in the lower part of the pons. From this nucleus its fibres pass upward and 
backward to the floor of the fourth ventricle, where they make a sharp turn 
inward and forward about the nucleus of the sixth nerve, and finally 
make their exit between the pons and the medulla (Plate IX.) near the 
eighth nerve. After leaving the pons, the seventh nerve passes into the 
internal auditory foramen of the petrous portion of the temporal bone, and 
after passing through the aqueduct of Fallopius emerges from the stylo- 
mastoid foramen upon the surface near the lobe of the ear, (See Plate X.) 



DISEASES OF THE CRANIAL NERVES 1025 

At this point it is divided into many branches which supply the muscles 
of the face with motor impulses. (See Plate X.) Upon the fibres of the 
facial nerve just as it enters the auditory foramen a ganglion occurs, com- 
monly called the geniculate ganglion. This ganglion consists of an aggre- 
gation of cell bodies connected with sensory fibres from the chorda tympani 
nerve, which is a nerve of sensation and is concerned with the special sense 
of taste. The fibres of this nerve do not, however, remain in contact with 
those of the facial, but leave it at once, and by way of the Vidian, or superficial 
pe + "osal, nerve pass to the superior maxillary branch of the trifacial. In 
addition to these sensory fibres of the chorda tympani, the facial nerve also 
has associated with it the nerve of Wrisberg, which is probably sensory in 
function, and which lies by the side of the facial nerve as its fibres pass from 
the pons to the auditory foramen, where the ganglion of the chorda tympani 
just named exists. The fibres of the nerve of Wrisberg then pass to the 
nucleus of the glossopharyngeal nerve. 

Etiology. — Interference with the function of the facial nerve arises from 
many causes, of w T hich the chief and most frequent are injuries in its course 
after it leaves the pons. These may be called peripheral lesions, and when 
the paralysis is peripheral it is called Bell's palsy. Thus, it not infre- 
quently happens that a child is born with facial palsy, which is usually due 
to injury to the nerve during labor as by the pressure of forceps. So, too, 
facial paralysis is sometimes seen in children and in adults as a result of a 
severe blow at the lower part of the ear, or of an attack of mumps in which 
the inflammation and swelling has been severe. Tumors of the neck and 
inflammation in the middle ear also may cause facial palsy in this manner. 

In adults facial palsy is often due to an inflammation in the stylomastoid 
foramen as the result of exposure. * It is thought by some that this takes place 
in certain individuals by reason of the fact that this foramen is so small that 
very slight swelling causes pressure on the nerve and ablation of its function. 
It is this type of paralysis following exposure to cold which has given rise 
to the belief among certain ignorant persons that it is possible to be 
"moon-struck/' because a person has slept out-of-doors in the moonlight 
and has developed facial palsy afterward. The real cause is, of course, the 
exposure to cold, and not the influence of the moon. That cold cannot 
always be the cause of this particular form of facial palsy is, however, 
evident from the fact that the condition is no more frequent in winter than 
in summer. Perhaps the condition is really one of rheumatic neuritis. 

More serious causes of facial palsy are disease processes inside the skull 
which press upon the nerve before it passes through the aqueduct of Fallo- 
pius. These conditions are tumor, inflammatory processes at the base of 
the brain, most commonly arising from injury, syphilis, or tuberculosis, and 
occasionally one of the acute infectious diseases. So, too, a fracture of the 
base of the skull may produce facial paralysis. Facial palsy due to a lesion 
in the pons is exceedingly rare as a single symptom, as is also facial palsy 
due to a lesion in the cortex. On the other hand, facial paralysis is usually 
present in cases of hemiplegia, but in hemiplegia the upper part of the face 
escapes the paralysis, being innervated from both hemispheres of the brain. 

The pathological changes which take place in the facial nerve in cases of 
65 



1026 DISEASES OF THE NERVOUS SYSTEM 

facial paralysis depend, of course, upon the situation of the lesion. If the 
lesion occurs in the nucleus of the nerve, or involves its fibres in such a way 
that it fails to receive its normal trophic impulses, degenerative changes at 
once ensue, the neuritis being of the so-called parenchymatous type. 

Symptoms. — The symptoms of facial paralysis are very characteristic. The 
paralysis is nearly always unilateral and often total, in the sense that all the 
muscles upon one side of the face are impaired in function. It sometimes 
happens, however, that the muscles of the forehead partly escape. Because 
of the paralysis of the muscles of one side of the face the patient is unable to 
wrinkle the brow upon one side, and is not able to close the lids, either as a 
reflex act, as in winking, or by volition. The corner of the mouth on the 
paralyzed side is drooped, and if the patient attempts to smile only one- 
half of his visage is wrinkled. The nasolabial fold is obliterated on the 
paralyzed side and is usually accentuated on the normal side as a result of 
the contraction of the muscles which are no longer counterbalanced by 
opposing muscles. The condition is not painful. If recovery does not 
promptly ensue the reactions of degeneration speedily develop in the 
paralyzed muscles, and there may be contractures in them. 

Diagnosis. — The manifest paralysis of the muscles of one side of the face, 
which is particularly noticeable when the patient attempts to smile or frown, 
renders the diagnosis of facial palsy easy and the symptoms which the patient 
presents can, moreover, be used very successfully in many cases in determin- 
ing the site of the lesion. Thus, in some cases of facial paralysis the sense 
of taste is modified or lost upon the anterior two-thirds of the tongue on the 
side affected. If this symptom is present, it indicates that the lesion is one 
which involves the facial nerve between the geniculate ganglion and the 
point a quarter of an inch above the stylomastoid orifice, where the chorda 
tympani fibres leave it; or, to put the proposition reversely, if loss of taste 
does not accompany a facial palsy the lesion is either in the stylomastoid 
foramen within a quarter of an inch of the orifice or it may involve the nerve 
before it enters the bone. So, too, if there is unusual sharpness of hearing 
with some buzzing in the ear, this also is an indication of a lesion near the 
pons or in the Fallopian canal, since it is due to paralysis of the stapedius 
muscle which is supplied by the stapedius nerve. If deafness and vertigo 
are present it is probable that the condition is due to middle-ear disease or 
to some lesion which also involves the auditory nerve at the base of the 
brain. A study of the electrical reaction of the paralyzed muscles is also 
of great value for the purpose of localizing the lesions. Thus, if the lesion 
exists in the stylomastoid foramen, the muscles of the face are cut off from 
the trophic impulses which they normally receive from their nuclei in 
the pons, and as a result the reaction of degeneration speedily develops 
and may become complete; whereas, on the other hand, if the lesion which 
causes paralysis is situated in the motor tract above the nucleus of the facial 
nerve, or, in other words, if it involves the fibres which descend from the 
motor area of the cortex, the reaction of degeneration does not develop 
because the muscles still receive trophic impulses. Further than this, in 
these cases the paralysis is never so complete as in the peripheral type, the 
patient usually being able to wink and to wrinkle the forehead, the muscles 



DISEASES OF THE CRANIAL NERVES 1027 

of the forehead frequently escaping. Centric facial paralysis is, however, 
exceedingly rare unless associated with other symptoms, as already stated. 
In those rare instances in which the facial paralysis arises from damage to the 
nucleus of the facial nerve in the pons, there are other symptoms of a pontile 
lesion producing, in some instances, a crossed hemiplegia, as already 
described, an associated paralysis of the sixth nerve, or the symptoms of 
ordinary bulbar paralysis. In these cases, too, reactions of degeneration 
speedily develop. 

Prognosis — The prognosis in cases of facial paralysis varies, of course, 
with the situation of the lesion and with its severity. The majority of 
instances get well because they have their origin in an inflammatory process 
in the stylomastoid foramen. The outlook when the lesions are back of 
the stylomastoid foramen are not so favorable, and when the nucleus of 
the nerve or the motor area of the cortex is diseased, the prognosis is, of 
course, very doubtful as to recovery of power in the muscles of the face. 

Treatment. — The treatment of paralysis of the seventh nerve depends 
somewhat upon the lesion which produces it. For the relief of that form 
which is due to inflammation in the stylomastoid foramen, it is customary to 
administer mild alteratives, such as small doses of the iodide of potassium 
or sodium, in order to hurry the absorption of the inflammatory exudate. 
It is also advisable to apply a small blister, about the size of a postage 
stamp, immediately in front of the ear for its counterirritant effect. In 
those cases in which there is a gouty or rheumatic diathesis, the best 
results are often obtained by the use of the salicylates in moderately large 
doses, 10 to 15 grains three or four times a day, or 10 drops of the wine of 
colchicum root and 10 grains of iodide of strontium m.ay be administered 
three times a day. The use of electricity for the purpose of maintaining 
the nutrition of the facial muscles in any case of peripheral facial palsy 
is not only futile, but may be harmful, for the cause of the muscular wasting 
is lack of trophic impulse, and as these impulses cannot reach the mus- 
cle, it is speedily exhausted if stimulated by the electrical current, when 
deprived of its ordinary means of recuperation. If middle-ear disease is 
present, it must, of course, be treated by those measures which are com- 
monly employed by aurists. In cases where the lesion is centric, counter- 
irritation is useless. The only hope is that nature aided by alterative drugs, 
such as the iodides, may cause an absorption of the results of the local inflam- 
matory process. Where the lesion is severe enough to have destroyed the 
nerve cells, treatment is also useless. 

Facial Spasm. — Facial spasm due to irritation of the facial nerve is a 
frequent affection. It may be general or localized in one or two muscles. 
When the orbicularis palpebrarum is affected, the condition is called " ble- 
pharospasm." As a rule, the muscles about the mouth are also affected. 
When this is the case, the condition is called one of " blepharofacial 
spasm." To this condition the French term "tic convulsif " is sometimes 
applied. The cause of facial spasm is unknown. It sometimes develops 
in nervous individuals as a result of a severe nervous shock. In some 
instances it seems to partake of the nature of a habit spasm, and in these 
cases not infrequently a lightning-like contraction of the muscles of the face 



1028 DISEASES OF THE NERVOUS SYSTEM 

takes place. Sometimes in addition to facial spasm there is also torticollis. 
Very rarely facial spasm is due to an irritating focus in the motor area for the 
face in the cortex, and sometimes it is the early or first symptom of an oncom- 
ing epileptic seizure. In ordinary facial spasm the muscles are not persist- 
ently contracted, but suffer from twitchings which come on in paroxysms, 
or which occur singly at varying intervals. 

The prognosis in a case of this kind is not very favorable, although, as a 
rule, there is no organic lesion to maintain it. 

The treatment of facial spasm consists in a careful investigation to deter- 
mine if there is any localized focus which gives rise to reflex irritation, as, 
for example, disease of the middle ear. If such an area is found, it should 
of course be removed. In some instances a hypersesthetic spot in the nasal 
mucous membrane may be discovered. If no such local area of irritation 
can be found, there is little left for the physician to do except to administer 
nervous sedatives, such as the bromides, chloral, and cannabis indica, but 
these in turn rarely do good in this annoying, harmless, but persistent con- 
dition. In young persons who have a tendency to facial spasm as a result 
of habit, a powerful mental impression may aid in breaking up the habit, 
particularly if there is a tendency to hysterical manifestations. 

The Eighth or Auditory Nerve. — Disease of the auditory nerve may 
result in deafness, tinnitus, vertigo, and loss of equilibrium. 

When deafness is due to disease of this nerve it commonly arises from 
some degenerative change, which in turn may be due to the effect of an 
infectious disease. In other instances the deafness is due to a congenital 
defect, but in still others it occurs as a part of the course of locomotor ataxia, 
disseminated sclerosis, or general paralysis of the insane. More rarely it 
arises from a tumor of the brain or from cerebral syphilis. In deafness due 
to these causes the so-called cochlear fibres of the auditory nerve are in- 
volved. The condition may be differentiated from that form of deafness 
which is due to disease of the middle ear, the peripheral fibres of the 
auditory nerve not being affected, and by the fact that the latter class of 
patients possess the power of perceiving sound transmitted through the 
bones of the head. Thus, if a tuning fork is placed against the head, or 
the teeth, the patient can perceive the sounds which it generates if the deaf- 
ness is due to a peripheral cause, which produces interference with aerial 
sound conduction in the external or middle ear, but he cannot perceive its 
sound if the deafness is due to a centric cause, such as a lesion of the 
cochlea of the internal ear, or of the auditory nerve trunk, or of the auditory 
pathway to the cortex. Again, in those cases of disease of the auditory 
nerve of a centric character, the patient does not find it easy to hear in the 
presence of loud noises, as he often does in cases of deafness due to a 
peripheral lesion. 

The prognosis in deafness due to centric disease of the auditory nerve 
is very bad. 

When tinnitus is present, it arises as the result of irritation of the cochlear 
portion of the auditory nerve which supplies the organ of Corti in the internal 
ear, or of those fibres which pass from this organ in the nerve trunk itself. 
The sound may vary from a slight buzzing to a roaring, ringing, or explo- 



DISEASES OF THE CRANIAL NERVES 1029 

sive noise which may be so severe as to be insufferable. Suicide is some- 
times threatened by persons who are not only persecuted by these noises 
during the day, but are unable to sleep by night from the same cause. Little 
can be done for many of these cases. In those instances in which tinnitus 
arises from middle-ear disease or from anaemia or from the use of drugs, 
such as quinine and salicylic acid, the condition can often be relieved, as it 
depends upon an irritation and not upon an actual lesion, as a rule. 

The treatment depends upon the cause of the tinnitus. If it is due to an 
actual lesion of the internal ear the prognosis is bad and treatment is futile. 
If it is due to gout, anaemia, or similar causes, the prognosis is fairly good. 

Vertigo is a condition in which the patient loses the sense of his normal 
relation to surrounding objects. In some instances he seems to be whirled 
about in space. In other instances he seems to remain stationary, while 
other objects are whirled about him. As the patient's conception of his 
relation to surrounding objects is disturbed, he frequently falls, since this 
conception has much to do with the motor impulses by which he controls 
his muscles in connection with the function of muscle sense. The cause of 
vertigo may be a functional disorder of the branches of the auditory nerve 
which supply the vestibular portion of the internal ear, as when it occurs in 
the course of indigestion (autotoxaemia) or under the influence of a drug 
such as quinine, or it may be due to actual lesions in connection with these 
nerve fibres such as hemorrhages into the internal ear, or other damage to 
the semi-circular canals. Sometimes also it seems to be due to reflex irrita- 
tion produced by disease in the middle ear or in the external meatus. In 
other instances the presence of a foreign body in the meatus produces vertigo. 
When vertigo is severe, there may be associated with it great nausea and 
vomiting, palpitation of the heart, profuse sweating, a sense of approaching 
syncope, and even collapse. The respirations may be rapid. These symp- 
toms are in part doubtless due to the mental distress or fright from which 
the patient suffers. There is probably no symptom which causes so much 
fright and which is so rarely followed by death as severe vertigo. Nothing 
but the awful apprehension of true angina pectoris approaches the mental 
distress of the patient who suffers from this condition in its well-developed 
form. 

One form of vertigo arising as the result of disease of the internal ear is 
called Meniere's disease. It is usually severe in its nature. Its onset is 
sometimes sudden, the patient being seized with prostration, pallor, vomit- 
ing, roaring in the ears, and deafness immediately after hearing a loud 
report which has not, of course, arisen from any extraneous source. This 
form of vertigo is supposed to be due to a hemorrhage in the semi-circular 
canals, and resembles in its onset an apoplectic stroke, but it is not charac- 
terized by paralysis. In some instances it seems to depend upon arterio- 
capillary fibrosis. It may or may not be associated with absolute deafness. 
In the majority of cases the patient suffers from recurrent attacks, but as 
the disease progresses the attacks last longer and longer, and finally he not 
uncommonly has constant vertigo. 

The prognosis in cases of vertigo depends entirely upon the cause of the 
disorder. If it is due to an organic disease, unless that disease exists in the 



1030 DISEASES OF THE NERVOUS SYSTEM 

middle or external ear and is removable, the outlook is serious. Indeed, the 
condition may be considered incurable if an actual organic and centric lesion 
is its cause. 

In Meniere's disease the treatment consists in rest in bed, the use of an 
ice-bag on the head, or blister behind the ear, and the employment of large 
doses of nervous sedatives, such as the bromides and chloral. Certain 
practitioners claim to have obtained good results from the administration 
of large doses of quinine, but it is difficult to see how this drug can do good 
under these circumstances. Indeed, one would expect it to make the con- 
dition much worse. 

Vertigo which is due to autointoxication arising from an abnormal state 
of the bowels or kidneys should be treated by the administration of diuretics, 
cholagogues, purgatives, and free sweatings. 

The Ninth or Glossopharyngeal Nerve.— The ninth nerve is the nerve 
of sensation of the pharynx, the palate, and the middle ear. It is also prob- 
ably connected with the special sense of taste in the posterior third of the 
tongue, although it is considered by some physiologists that those fibres 
which are connected with this function join the glossopharyngeal fibres 
from the fifth nerve. Some of its sensory fibres enter the medulla oblongata 
near the olivary body and terminate in the gray matter on the floor of the 
fourth ventricle, while another set of fibres ends in the substantia gelatinosa. 
From the latter point some of its fibres ascend into the brain. In addition 
to its sensory function it also contains motor fibres which spring from cells 
known as the nucleus ambiguus. These fibres make their exit from the side 
of the medulla back of the olivary body, and escape from the skull through 
the jugular foramen. The motor fibres supply the muscles of the larynx, 
the oesophagus, and pharynx, and are also connected with the function of 
respiration, deglutition, and phonation. 

Paralysis of the glossopharyngeal nerve is exceedingly rare, and therefore 
we possess but little information, either clinical or pathological, concerning 
its condition in disease. Should the nerve itself be damaged, the symptoms 
consist in loss of sensation in the upper half of the pharynx, loss of the sense 
of taste on the posterior half of the tongue, and difficulty in swallowing 
because of paralysis of the pharyngeal muscles and because of the loss of 
reflex irritability of the mucous membrane of the pharynx. Such a con- 
dition sometimes develops during postdiphtheritic paralysis. When lesions 
of the nuclei of this nerve take place, the symptoms are practically those 
of bulbar paralysis (which see). 

The Tenth or Vagus Nerve.— This nerve, sometimes called the pneumo- 
gastric nerve, is composed of both sensory and motor fibres. The sensory 
fibres pass upward from the various portions of the body which they supply 
and enter two ganglia, one of which, the upper, is large and oval, and the 
other is long and irregular in outline. After leaving these ganglia the fibres 
pass to the medulla, some of them terminating in the gray matter which 
exists in the floor of the fourth ventricle, thereby forming the sensory centres 
connected with respiration and the heart. Other of these fibres join the 
ninth nerve and end in the substantia gelatinosa and from this point new 
fibres ascend to the brain. Those fibres of the pneumogastric which are 



PLATE XL 




The Vagus and Sympathetic Fibres of the Right Side and Their 
Anastomoses. (Modified from Rudinger.) 

1, origin of vagus; 2, anastomosis with sympathetic; 3, superior laryngeal and pharyngeal plexus; 
4, the pulmonary plexus; 5, the inferior cardiac fibres, with sympathetic fibres; 6, the oesophageal plexus. 
The course of the optic nerve (7), the oculomotor (8), the trochlearis (9), the abducens (10), and the facial 
(11) are also shown. 



DISEASES OF THE CRANIAL NERVES 1031 

motor in function take their origin from the cells of the nucleus ambiguus 
and escape from the side of the medulla, forming the main trunk of the nerve. 
The distribution of the afferent and efferent fibres of this nerve is well shown 
in Plate XL 

The tenth nerve has a far larger distribution than any other cranial nerve, 
supplying the pharynx, the larynx, the heart, the lungs, oesophagus, stomach, 
and intestines, and even the external ear through an auricular branch. 
According to some physiologists it is the chief motor supply of the palate. 
It joins the glossopharyngeal, or ninth nerve, and certain sympathetic 
nerve fibres, in the formation of the pharyngeal plexus which supplies the 
pharyngeal muscles. 

The superior laryngeal branch supplies the cricothyroid muscle, the 
thyroepiglottic and aryepiglottic muscles, and the inferior laryngeal branch, 
sometimes called the recurrent laryngeal, supplies the other laryngeal mus- 
cles. By means of the sensory fibres which exist in the superior laryngeal 
nerve, the mucous membrane of the epiglottis possesses sensation, and by 
means of those sensory fibres which exist in the recurrent laryngeal the 
mucous membrane below the vocal cords is supplied with sensory filaments. 
If the sensory fibres in the superior laryngeal nerve are stimulated, the respi- 
rations become slower and deeper, or they may be arrested as the result of a 
reflex impulse which passes to the centre in the medulla. Closure of the 
glottis may also be produced in this manner. 

The pulmonary branches of the vagus contain motor fibres which supply 
the unstriated muscles of the bronchi, and sensory fibres for the mucous mem- 
brane of the bronchi. They apparently also contain fibres centripetal in 
character, which when stimulated diminish the inhibitory action of the pneu- 
mogastric nerve upon the heart, thereby producing tachycardia. Those 
branches of the vagus which supply the oesophagus innervate its muscles, 
on the one hand, and supply its mucous membrane with sensory filaments 
on the other; while those which pass to the stomach contain not only fibres 
which govern its muscles, but also other fibres which control its secretion 
and its blood supply. The same facts hold true of those fibres which pass 
to the intestines. Last, but by no means least, the pneumogastric sends fibres 
to the heart, and through these pathways an inhibitory action is exercised 
which if stimulated may temporarily arrest the heart in diastole. 

Not only is the pneumogastric nerve of very great importance because 
of the multiple functions which it possesses, but it is also of great importance 
to the clinician because it not infrequently suffers from disease. Though 
it is rarely the victim of primary neuritis, cases of rheumatic neuritis of both 
recurrent laryngeal nerves have been reported, and instances in which this 
nerve has been involved in cases of multiple neuritis due to poison, such as 
alcohol, for example, are by no means rare. So, too, it sometimes suffers 
in diphtheritic paralysis, and from neuritis arising from the poisons of 
various infectious diseases such as typhoid fever, pneumonia, scarlet fever, 
malaria, and influenza, from tumors and inflammation in the mediastinum, 
disease of the jugular vein, tuberculosis of the mediastinal glands, and from 
pressure upon the nerve exercised by reason of dilatation of the left auricle 
in cases of mitral stenosis. In those instances in which the centres of the 



1032 DISEASES OF THE NERVOUS SYSTEM 

pneumogastric nerve are affected by disease, we find that tumors, hemorrhagic 
extravasations, the lesions of locomotor ataxia, and disseminated sclerosis 
are the causes. In still other instances the disorder of the function of this 
nerve develops as the result of bulbar paralysis. Cases are also on record 
in which the fibres of the nerve outside of the medulla have been pressed 
upon by tumors, by the exudations due to meningitis, hemorrhages, and by 
bone disease. 

The symptoms of disorder of the function of the vagus nerve are, of 
course, very varied. If the lesion exists at the base of the brain it nearly 
always happens that there is paralysis of the other cranial nerves, particu- 
larly of the ninth, eleventh, and twelfth. In such a case if the fibres on one 
side alone are affected, there is unilateral paralysis of the fauces, the palate, 
and the larynx. The speech is nasal, and the act of swallowing may be 
impaired. There is also interference with the action of the vocal cords. If 
the recurrent laryngeal branch is affected, there is laryngeal paralysis. The 
vocal cord on that side remains midway between adduction and abduction, 
and fails to move during phonation. If both of the recurrent laryngeal nerves 
are paralyzed, the patient suffers from aphonia, inspiratory stridor, and 
dyspnwa. When the pulmonary fibres are affected, particularly if the lesions 
are bilateral, the respirations may become rapid and irregular. 

Irritation of the pulmonary fibres, directly or indirectly, may cause spasm 
of the bronchial muscles, and hyperemia and congestion of the bronchial 
mucous membrane (asthma). 

If the gastric fibres are involved, there may be vomiting, pain in the 
stomach, and loss of the sense of hunger and thirst. When the cardiac fibres 
are severely affected, the pulse rate may be markedly accelerated. If they are 
irritated, an exceedingly slow pulse may be present. 

The treatment of disorders of the vagus nerve depends largely upon the 
cause which underlies the disturbance. If there is reason to believe that 
there is a syphilitic exudate at the base of the brain, or a syphilitic arteritis, 
the iodides and mercury are, of course, indicated. So, too, in that form of dis- 
order of the vagus which results from lead poisoning, the iodides, hot baths, 
and purgatives are required. If it is believed that a gummatous growth 
exists in the thorax which irritates the vagus by pressure, antisyphilitic 
treatment is necessary. If there is a distinct rheumatic history leading one 
to believe that the recurrent laryngeal nerves are suffering from rheumatic 
paralysis, already mentioned, the iodides and the salicylates are advisable. 
Digitalis may also be useful for the purpose of stimulating the pneumogas- 
tric nerve in those cases in which tachycardia is present, and atropine may be 
used with the object of diminishing irritation in this nerve by depressing 
its peripheral fibres when the pulse is unduly slow. 

Eleventh or Spinal Accessory Nerve. — The eleventh or spinal accessory 
nerve is composed of two parts, an accessory portion, which goes to the 
pneumogastric, and a spinal portion. The accessory branch is formed 
by several fasciculi which spring from the medulla in series with the 
roots of the vagus. These fasciculi form a trunk, and to this trunk are 
joined the fibres from the spinal portion. The nerve leaves the cranium 
with the pneumogastric. In its passage through the jugular foramen it 



DISEASES OF THE CRANIAL NERVES 1033 

sends fibres to the root ganglion of the vagus, while others pass over 
the surface of this ganglion into the pharyngeal, superior laryngeal, and 
recurrent laryngeal nerves. Most of the motor fibres of the pneumogastric 
are derived from this accessory branch. The spinal portion of the nerve 
arises by a series of roots which spring from the lateral portion of the spinal 
cord, even as low as the sixth or seventh cervical nerve roots. They spring 
from the lateral column near the origin of the posterior nerve roots and 
form an ascending trunk, which enters the skull and unites with the acces- 
sory portion, as already described. Before entering the jugular foramen, 
however, certain of its fibres leave the accessory portion, make a sharp 
turn backward near the internal jugular vein, and enter the deep surface 
of the sternomastoid muscle, which muscle it supplies. Passing through 
this muscle, it enters under the trapezius, a short distance above the clavicle. 
Here it anastomoses with fibres from the third and fourth cervical nerves, 
forming a plexus, which supplies the trapezius muscle. 

Symptoms. — Disturbances in the function of the accessory nerve, so far 
as its spinal part is concerned, result in torticollis, which occurs as congenital 
wryneck, as- wryneck due to injury, and true spasmodic wryneck. The 
congenital form is due to some defect in development or to injury of the 
sternomastoid muscle at the time of delivery. The right side is affected in 
the majority of cases. The sternomastoid muscle is not in the spasm, but 
the head is drawn to one side and rotated to the opposite side as the result 
of shortening of the muscle upon the side to which the head is drawn. Not 
rarely there is associated with this atrophy some wasting of the muscles of 
the face upon this side. Spasmodic wryneck, on the other hand, is due to a 
true spasm of the muscles supplied by the spinal accessory. It is not met 
with in children, and very rarely in advanced life, but occurs most frequently 
in middle-aged persons. In a certain proportion of cases the patients are 
distinctly hysterical, and the spasm follows some nervous shock. In other 
cases no hysterical stigmata are present, and it is thought that the condition 
is due to that somewhat indefinite state called " rheumatism." This form 
of wryneck differs from the congenital variety in that it is usually accom- 
panied by pain. The spasm may not be constant but intermittent. The 
chin is often protruded and raised. At times the spasm extends to the 
muscles of the face, and facial twitching may occur. Often the condition 
becomes one of tonic spasm after having begun as clonic spasm, and if the 
condition persists for any length of time the affected muscles may undergo 
hypertrophy, and those on the opposite side may atrophy from disuse. 

Those forms of wryneck in adults which are characterized by intermittent 
or clonic spasms are rarely due to rheumatism, so called, but depend upon 
some neurosis; whereas, the tonic spasm may be due simply to muscular 
fixation through pain. In the latter class of cases the prognosis is exceed- 
ingly good, the condition usually disappearing under the use of hot appli- 
cations or counterirritant liniments, and the internal administration of the 
salicylates and the iodides. Certain persons have advised the intramuscular 
injection of atropine, in the dose of ■£$■ of a grain, directly into the belly of 
the afflicted muscle in order that it may depress the peripheral motor nerve 
endings. While this is efficacious in some cases, it is prone to produce 



1034 DISEASES OF THE NERVOUS SYSTEM 

moderate systemic symptoms, and is not to be resorted to unless the 
condition fails to yield to the plan of treatment already suggested. 

The type depending upon a neurosis is much more difficult to treat. It 
often remains unchanged for many months, and indeed may become a 
permanent condition. Sometimes a nervous shock, or some accident, may 
suddenly end the spasm. 

Under the unfortunate name of " spurious wryneck," a condition of wry- 
neck develops as a result of caries of the spine, the spasm of the muscle 
being due to the lesions in the vertebrae, or the distortion is due to the fact 
that these bones do not properly support the head. 

Under the name of " spasmus Nutans," or " nodding spasm," a condition 
is met with in which the muscles upon both sides of the neck are affected in 
such a way that there is a nodding movement. It occurs in poorly nourished, 
neurotic individuals, and closely resembles habit chorea. The symptoms 
become most marked when attention is called to them, and are usually 
absent during sleep. 

Paralysis of the spinal accessory may be due to injury, disease of the 
vertebrae, muscular atrophy, or any form of disease of the spinal cord in the 
cervical region. As the result of the paralysis there may be loss of power 
to rotate the head upon the vertebral axis. The sternomastoid muscle does 
not stand out prominently as it does when affected by spasm, and there is 
difficulty in raising the arm at a right angle to the body. In those com- 
paratively rare cases in which the paralysis is bilateral, the head may appear 
to be fixed, as if the fixation were due to spasm. 

Twelfth or Hypoglossal Nerve.— The twelfth or hypoglossal nerve arises 
from a group of cells in the floor of the fourth ventricle, at its lowest point. 
Its fibres emerge from the medulla, and escape from the skull through the 
anterior condyloid foramen of the atlas, and so pass to the muscles of the 
tongue. Injury and disease of this nerve rarely take place in its peripheral 
filaments. Nearly always when it is affected, the lesion is in the bulb or in 
the brain. Thus, out of 79 cases collected by Ascoli, in only one-third were 
the peripheral fibres affected. The causes of centric disease of the hypo- 
glossal nerve are an inflammatory process or growth at the base of the brain, 
or in the medulla oblongata. When the lesion is in the medulla, there is 
usually bilateral paralysis with wasting of the tongue, but as the nuclei of 
all the cranial nerves have their origin nearby, it nearly always happens 
that there are evidences of paralysis of the other cranial nerves present. 
Inside the bony casement the causes of hypoglossal paralysis are inflamma- 
tory exudates, hemorrhages, and disease of the bone. Very rarely the 
peripheral filaments of the nerve, after they take their exit from the atlas, 
suffer from neuritis. 

In some cases of locomotor ataxia, syringomyelia, and multiple sclerosis, 
there is hemiatrophy of the tongue with paralysis. The same symptom 
also occurs when damage is done to the peripheral fibres of the nerve. 
The tongue lies on the floor of the mouth, and it is impossible for the 
patient to move the tongue upon the paralyzed side. If the tongue is pro- 
truded, it deviates to the paralyzed side, but sometimes while the main 
body of the tongue may be deviated in this manner, the tip points toward 



MUSCULAR DYSTROPHIES 1035 

the sound side. Remak points out that while the tongue lies on the 
floor of the mouth apparently paralyzed, it can be easily pushed about 
by the finger if the paralysis is organic; whereas, in hysteria, all attempts 
to move the tongue by the finger-tip cause efforts to resist these move- 
ments. The paralysis of the tongue impairs the speech, and also inter- 
feres with deglutition and mastication when the paralysis is bilateral. 

The prognosis varies with the cause of the lesion. In syphilitic cases 
recovery sometimes occurs under active mercurial treatment. In the so- 
called rheumatic cases, it may take place under the influence of the iodides 
or salicylates. If an actual lesion at the point of origin exists, the prog- 
nosis is bad. 

DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE 
IN THE MUSCLES. 



MUSCULAR DYSTROPHIES. 

Definition. — Under this term are described several related maladies, 
characterized by alterations in the trophic state of the muscles, which are 
met with almost always in early life and which are not due to disease of the 
nervous system — that is to say, they are primarily muscular in origin. 
The alterations in the muscles cause loss of power and the paralysis may 
be thought to be due to a spinal lesion, but this is not the case. 

Muscular dystrophy has been divided by Erb into three forms, namely, 
pseudomuscular hypertrophy, Erb's juvenile dystrophy, and the Landouzy- 
Dejerine type of dystrophy. Several other types have been described by 
other writers. (See below.) 

Etiology. — The etiology of these dystrophies is not known, but they are 
all believed to be dependent upon faulty development of the muscles affected. 
In other words, it would seem as if the vitality of certain muscles is of such 
a character that they undergo senile changes early in life. When injuries 
and the acute infectious diseases seem to be causative factors it is probable 
that they act only indirectly in that they hasten the degenerative changes 
in the feeble parts. 

Pathology and Morbid Anatomy. — The changes in the muscles in cases 
in which atrophy takes place consist in a wasting and thinning of the muscle 
fibrils within the sarcolemma. They become shortened and pigmented. 
In other cases a true degenerative process goes on, the fibrils become swollen, 
suffer from fatty or albuminoid changes, and show fatty and granular masses 
within the sarcolemma, until finally the sarcolemma may contain nothing 
but fatty globules. In a third form of dystrophy there is, in addition to fatty 
degeneration in the fibrils, a deposit of fat between the sheaths covering the 
fibrils. With these changes there is also an overgrowth of connective tissue, 
and as a consequence a muscle which is so large as to appear strong and 
powerful is in reality feeble or powerless. 

Pseudomuscular Hypertrophy. — This form of muscular dystrophy is 
essentially a disease of early childhood beginning between the second and 



1036 DISEASES OF THE NERVOUS SYSTEM 

seventh year. It is characterized by enlargement of the muscles of the 
calves of the legs, which soon are seen to be proportionately too large for 
the rest of the child. It is then noticed that these muscles lack power and 
this weakness causes the patient to walk awkwardly, to stumble over trifling 
obstacles, to tire easily, and to have difficulty in rising from the prone 
to the erect posture, so that the patient gets on his feet very much as a dog 
does, largely by the aid of the forelimbs. But while inspection of the mus- 
cles of the calves and of the anterior portion of the thighs reveals that they 
are enlarged, it will also show that the gluteal muscles are atrophied and 
that the muscles of the back are weakened, with the result that there is 
developed anterior curvature of the spine and a protruding belly. 

When the disease is still further advanced alterations in the nutrition of the 
muscles about the shoulder-blades is usually present. The deltoid and the 
supraspinatus, the biceps, and the triceps undergo atrophy and do not 
appear to be increased in size because they seldom have the deposit of fat 
which makes the muscles in the legs seem unusually large. Occasionally, 
however, such a fictitious hypertrophy may be present in these muscles, 
because of loss of power in the rhomboidei, in the levatores anguli scapulae, 
and in the serrati. The shoulder-blades occupy a peculiarly prominent 
position, and because of the wasting of the muscles already named there 
may be great feebleness in the movements of the upper arm. The muscles 
of the forearm and hand, however, usually escape. 

Contractures appear, which, like contractures in other forms of mus- 
cular atrophy, result in deformities such as club-foot or flexion of the legs 
upon the thighs and the thighs upon the pelvis. Contractures may also 
take place in the arms. It is a fact worthy of note that, unlike other forms 
of muscular atrophy, this disease does not show fibrillary contractions in 
the muscles, nor are the reactions of degeneration present, even when the 
muscles are considerably atrophied. Sensation is intact, and the reflexes 
are preserved, unless the muscles are so completely wasted that they are 
unable to contract. 

Prognosis. — The prognosis in these cases is invariably unfavorable. 
Periods of arrest in the advancement of the disease may occur, but ulti- 
mately the patient is absolutely helpless. Death never occurs from pseudo- 
muscular hypertrophy directly, being caused in most cases by intercurrent 
diseases which attack the enfeebled body. 

Erb's Juvenile Muscular Dystrophy or Scapulohumeral Type.— 
This form of dystrophy begins at about the time of puberty, usually be- 
tween twelve and sixteen ; rarely as late as the twentieth year. The pectoral 
muscles, the trapezii, the latissimus dorsi, the rhomboidei, and the del- 
toids undergo apparent hypertrophy with progressive weakening. This 
results in the falling forward of the shoulders, so that very much the same 
attitude is maintained as if there was a fracture of the clavicles. The 
scapula? are prominent. In some cases the disease ceases to develop; but 
if it does not, the loss of power extends to the muscles of the back, and 
various forms of spinal curvature develop. After this, the gluteal muscles 
and those of the thigh become enfeebled. They may atrophy or may undergo 
seeming hypertrophy. When the muscles of the leg are enfeebled club-foot 



MUSCULAR ATROPHY OF THE PERONEAL TYPE 1037 

may be present. The chief difference, therefore, between pseudomuscular 
hypertrophy and Erb's juvenile type of muscular dystrophy is the fact that 
the latter disease develops later in life, that it affects the upper extremities 
before it affects the lower extremities, and that atrophy is more marked 
than hypertrophy. 

Landouzy-Dejerine Type of Muscular Dystrophy or Facioscapulo- 
humeral Type. — This type of muscular dystrophy may appear in early 
childhood or in adult life. It is characterized by the peculiar fact that the 
atrophy develops in the muscles of the face, particularly the orbicularis oris, 
and extends to the muscles of the cheeks and those of the forehead, with 
the result that the lips lose power; the mouth cannot be closed, but has a 
peculiar pouting expression, and speech, at least so far as labial and lingual 
sounds are concerned, becomes very defective. So, too, the face loses its 
power of expression from a similar cause, and there is dribbling of saliva 
because the lower lip sags. Both sides of the face are usually affected. The 
orbicularis palpebrarum usually escapes, as do also the masseter muscles. 
Later, the muscles of the shoulders become affected, and finally those of the 
trunk and legs become involved until the case closely resembles either one 
of the forms of muscular dystrophy just described, save that the facial symp- 
toms are prominent. 

In some cases the symptoms of these three forms of dystrophy overlap one 
another to such an extent that it is difficult to determine to which type an 
individual patient belongs. 

Treatment. — Xo form of special treatment can produce advantageous 
results. The best that can be done is to order for the patient an out-door 
life, if possible in the country, and in a climate where he can remain for many 
hours in sunshine and in a place where he can receive excellent food. Gentle 
massage and Swedish movements may be employed, but care must be taken 
not to tire the wasting muscles. The most that can be expected from this 
plan of treatment, however, is the temporary arrest of the malady. No real 
improvement usually occurs. Efforts to correct deformities produced by 
contractures are generally useless, since the relief is but temporary. 



MUSCULAR ATROPHY OF THE PERONEAL TYPE. 

Definition. — This is a form of progressive muscular atrophy which begins 
in the muscles innervated by the peroneal nerves, and which does not extend 
higher than the knee. After the symptoms in the legs have developed, a 
somewhat similar condition may affect the muscles of the hand and fore- 
arms. It is sometimes given the name of the "Charcot-Marie-Tooth" form 
of progressive muscular atrophy, or is called the " progressive neural muscu- 
lar atrophy of Hoffman," or primary neuritic or neurotic atrophy. It is 
an uncommon disease, but not so rare as was formerly believed. 

Etiology. — There seems to be a distinct hereditary predisposition, since 
it frequently affects several members of a family, and can be traced through 
several generations. It usually develops during the first two decades of 
life. 



1038 DISEASES OF THE NERVOUS SYSTEM 

Pathology and Morbid Anatomy. — The condition depends upon degen- 
erative changes in the muscles, in the nerves, and sometimes in the pos- 
terior columns of the spinal cord. There is also sometimes a circumscribed 
atrophy in the anterior horns of the gray matter, and perhaps degeneration of 
the lateral columns of the cord. Whether the disease arises in the peroneal 
nerves primarily, or whether the lesion begins in the posterior horns of the 
gray matter in the spinal cord, is unknown. 

Symptoms. — The symptoms of this form of muscular atrophy consist in 
weakness of the muscles of the foot and of the peroneal muscles of the leg, 
followed by atrophy in the anterior and posterior tibial muscles, with the 
production of drop-foot, which makes it impossible for the patient to walk. 
Unlike the two forms of muscular dystrophy just described, fibrillary con- 
tractions are present in the affected muscles, and there is a loss of reflex 
activity and of electric excitability, so that the last stage of the reaction 
of degeneration may finally be present. The various forms of club-foot may 
come on as secondary conditions. When the upper extremities are affected, 
fibrillary contractions can be seen in the muscles of the hand, and after loss 
of power has been present for some time, deformities of the hand may arise 
from contractures. In some cases the progress of the disease is exceedingly 
rapid, but in others it is equally slow. In still others the wasting extends 
so that all the muscles of the extremities and trunk, and even those of the 
face, may undergo atrophy. 

Prognosis. — The prognosis as to recovery is hopeless, but patients may 
live for many years unless destroyed by some intercurrent disease. 

Treatment. — Aside from hygienic measures, no method of treatment can 
arrest the progress of the malady. 



FUNCTIONAL NERVOUS DISEASES AND DISEASES OF 
DISPUTED PATHOLOGY. 

MYOTONIA CONGENITA. 

Definition. — Myotonia congenita, commonly called Thomsen's disease, 
is an exceedingly rare affection not dependent upon disease of the ner- 
vous system, and characterized by hypertrophy of the muscular fibres 
with the proliferation of their nuclei. These changes result in loss of 
power. 

Symptoms. — The chief symptom of Thomsen's disease is a rigidity of the 
muscles, which develops after they have been quiescent. This spasm of the 
muscles comes on when the patient attempts to move, and may be so severe 
as to make walking practically impossible. Because of the inability of the 
patient to balance opposing muscles in different portions of his body, he 
may fall. After a time, if the patient persists in his endeavor to walk or to 
make other movements, the spasm passes off, and the muscles respond as in 
the normal individual so that ordinary movements can be carried on with 
ease; but if the muscles are irritated by percussion or are allowed to rest and 



PARAMYOCLONUS MULTIPLEX 1039 

another attempt is made to move, they instantly pass into spasm. The 
affected muscles develop electrical reactions of a peculiar type, namely, 
a tonic contraction under the galvanic current, which comes on sluggishly 
and lasts longer than in health. If the electrical application is continued 
contraction waves pass over the muscles, but there is no marked atrophy 
or great loss of power except in so far as the spasm interferes with ordinary 
muscular movement. The disease is so exceedingly rare that less than 40 
cases have been reported. A physician named Thomsen, himself a sufferer 
from the disease, first described it. 



PARAMYOCLONUS MULTIPLEX. 

Definition. — Paramyoclonus multiplex is a condition of the motor nervous 
system in which sudden contractions of the muscles take place, the con- 
tractions resembling those produced by the use of a slowly interrupted 
faradic current. It is sometimes called myoclonus, multiple myoclonus, 
myoclonus epilepticus, spinal epilepsy, and Friedreich's disease, but it is 
not to be confused in the mind of the student with Friedreich's ataxia, a 
very different malady. It is a rare affection. 

Etiology. — The cause is unknown. In a very few instances it has been 
thought to be hereditary, but in all probability this is the case only in the 
sense that the parents or grandparents have suffered from neurotic states. 
It is not rarely associated with epilepsy, and it may develop when a nervous 
system naturally unstable is sapped by excessive mental overwork or other 
stress. 

The contractions may simultaneously affect similar muscles in both 
limbs, or may occur in series involving first one side and then the other, or 
pass from muscle to muscle. Very rarely only one side is affected. In most 
instances the face and trunk muscles escape as in Friedreich's original case. 
The ocular muscles are never affected. The arms are more commonly 
affected than the legs and the muscles about the arm and shoulder and 
those of the thigh are more frequently and severely affected than those of 
the forearm or leg. The muscles of the hands and those of the feet escape. 
The severity of the contractions varies greatly. In some instances they are so 
moderate as to be noticeable only when the patient is stripped of his clothing. 
In others they are severe enough to throw him off his feet. The motions 
or attitudes of the patient vary, of course, with the muscles affected and the 
degree of their contractions. The effect of voluntary movements upon the 
contractions is also varied. In some instances, as in Friedreich's first case, 
a voluntary movement inhibits or diminishes the contractions, but in other 
cases voluntary movement seems to exaggerate it. Mental excitement 
increases them. They cease during sleep and are usually less severe when 
the patient is standing than when he is sitting or lying down. If the affected 
muscles are irritated by tapping them a spasm is induced. The deep reflexes 
may be increased or diminished, but electrical irritability is not altered nor 
do any trophic changes occur. Some superficial vasomotor palsy may be 
present in the extremities. 



1040 DISEASES OF THE NERVOUS SYSTEM 

Diagnosis. — Paramyoclonus multiplex is separated from chorea by the 
fact that the movements of chorea resemble those of the will in that cer- 
tain groups of muscles act together and do not contract suddenly as from 
an electrical shock. Voluntary movements are prone to decrease those of 
myoclonus and to increase those of chorea. Chorea is usually a unilateral 
affection, while myoclonus is usually bilateral. The facial muscles, which 
are so commonly affected in chorea, are rarely affected in the malady 
under discussion. Electrical chorea, or Dubini's disease, is separated from 
paramyoclonus multiplex by the fact that it is accompanied by pyrexia, 
progressive muscular atrophy, and paralysis, and by loss of response on the 
part of the muscles to faradic electricity. From hysterical spasm para- 
myoclonus is separated by the presence in hysterical cases of the stigmata 
of that state, such as disorder of the color fields and areas of hyperesthesia 
or anaesthesia. In those cases of hysteria in which these stigmata are absent 
the differential diagnosis may be impossible. 

Paramyoclonus multiplex may be separated from the "maladie des tics 
convulsifs" described by French neurologists, by the fact that in that affec- 
tion the movements are more like gestures and not infrequently echolalia 
is present. 

Prognosis. — The prognosis as to complete and permanent recovery is not 
good. Rarely death ensuesin a few months. More commonly the condition 
persists in varying severity for years. 

Treatment. — The treatment consists in measures devoted to the improve- 
ment of the general health by out-door life, good food, and avoidance of all 
causes of nervous irritation and exhaustion. Remedies like arsenic, phos- 
phorus, iron, and similar roborants are useful to this end, but are not cura- 
tive. Occasionally a carefully regulated course of hydrotherapy at some 
well-equipped and well-managed sanatorium is servicable. 



PARALYSIS AGITANS. 

Definition. — Paralysis agitans, sometimes called "shaking palsy," or 
"Parkinson's disease," is a condition in which different parts of the body, 
especially the forearms and hands, are affected by a continuous tremor. 
When the disease is well advanced, the patient leans forward, assuming a 
peculiar attitude, and may suffer from festination. 

Etiology. — The precise cause of paralysis agitans is not known. It has 
been thought to follow severe nervous shock and injuries to the central ner- 
vous system. In other instances it has followed excessive nervous strain. 
Thus, in one case under the writer's care, the treasurer of a very large 
corporation, after many years of hard work, developed a well-marked degree 
of paralysis agitans. He was quite certain that the tremor first began in 
those muscles which were employed in the signing of several hundred papers 
a day. 

Paralysis agitans develops most frequently between the ages of fifty and 
fifty-five. Gowers analyzed 80 cases and found the average age incidence 
to be fifty-two years, and Wollenberg found that 10 out of 20 cases occurred 



PARALYSIS AGITANS 1041 

at ages varying from fifty to fifty-five. The disease also not infrequently 
develops during the fifth and seventh decades of life. A few cases occur- 
ring in early adult life and in childhood have been reported. Hadden, 
Gowers, Berger, and others have seen the disease in individuals whose ages 
ranged from twenty to thirty, and Weil and Rouvillois have reported a case 
occurring in a child of ten. Lannois also mentions a case occurring in a 
child aged twelve. 

Men are more frequently affected than women. Thus, of 67 cases col- 
lected from the reports of St. Thomas' and St. Bartholomew's Hospitals, 
London, 47 occurred in men and 20 in women. In 78 American cases Dana 
found the proportion of men to women to be as 5 to 3. 

The neuropathic constitution may be considered as a predisposing cause, 
but direct inheritance of the disease is rare. A few instances of apparent 
direct transmission from parent to offspring have been reported, and Berger 
cites one in which the disease appeared in three successive generations. 
Borgherini reported 7 cases occurring in a family of 9 brothers and sisters. 
Three children of these individuals developed paralysis agitans between their 
fortieth and fiftieth years. 

Pathology — Nothing is known of the pathology of this affection which 
throws any light on the cause of the symptoms. 

Symptoms. — The symptoms of paralysis agitans are tremor, muscular 
rigidity, a retardation of ordinary voluntary movements, and a change in the 
gait. The tremors are rhythmical in character, amount to four or five per 
second, and move the part in various directions. Thus, when the hand is 
affected, the fingers may be flexed and extended, abducted and adducted. 
The most common movement is a rubbing of the thumb against the index 
finger, in much the same way that a pill might be made by such a rolling 
movement. In some instances, particularly if the patient becomes excited, 
the amplitude of the movements becomes greatly increased, so that the hand 
or the head shakes as it does in a severe rigor. Unlike the intention tremors 
of certain forms of organic nervous disease, the tremor of paralysis agitans 
is passive. Be the position of the body and arms what it may, the trembling 
continues, and while certain attitudes may diminish the amplitude of the 
tremor, it is always present except when some definite and active movement 
is attempted, when the tremor diminishes or even ceases. Thus, if the fist 
is clenched, or the patient shakes hands with a friend, the movement may 
stop momentarily. On the other hand, nicely adjusted muscular move- 
ments such as are involved in writing do not stop the tremor, and for this 
reason handwriting is usually impossible when the disease is well developed. 
The tremor not only involves the head and arms but extends to the legs 
as well, and it may affect the muscles of the thigh. Rarely the muscles of 
the jaw are affected. The tremor continues only during the waking hours, 
and usually ceases in sleep. Not rarely paralysis agitans is associated with 
insomnia because the twitching movements keep the patient awake, or the 
aching in the affected muscles makes the patient so uncomfortable that 
sleep is postponed until the patient is exhausted. As the patient stands in 
front of the physician, the chin is usually pushed forward and the body bent 
forward. The arms and the elbows are slightly flexed. 
66 



1042 DISEASES OF THE NERVOUS SYSTEM 

After the disease is well developed, chronic muscular rigidity becomes a 
symptom which is even more constant than tremor. It not only involves the 
parts that we have spoken of, but also the muscles of the neck and back, and 
even those of the face. As the patient walks, his gait usually increases in speed 
and the attitude is that of a person who is attempting to progress rapidly. 
It is unfortunate that the term "paralysis agitans" is applied to the early 
stages of this disease, for paralysis, in the sense of great loss of power, only 
occurs in its very last stages, and not infrequently the patient will suffer 
from the malady for years without developing paralytic symptoms. The 
skin covering the parts affected is not infrequently unduly moist by reason 
of profuse perspiration. There are no disturbances of sensation, and the 
mind is unaffected save by the mental depression which is produced by the 
annoyance of the disease. 

Diagnosis. — Paralysis agitans is to be separated from multiple sclerosis 
by its onset late in life, by the fineness of the tremor, by the fact that it 
is present when no voluntary movement is made, and by the presence of 
rigidity. An examination of the eyes fails to reveal the nystagmus or the 
changes in the optic nerve which are characteristic of multiple sclerosis. In 
paretic dementia the tremor is not rhythmical, occurs when the patient 
makes a movement and not when at rest, and there is associated with the 
tremor the mental disturbance, the scanning speech, and evidences of 
paralysis. 

Sometimes in old persons a senile tremor develops. This chiefly affects 
the head, and is increased rather than decreased by active movements; but 
in some instances senile tremor bears a close resemblance to paralysis 
agitans. Indeed, it has been suggested that the latter disease is essentially 
a premature nervous senility. 

Prognosis. — Paralysis agitans does not materially shorten life. It fre- 
quently lasts for twenty years. Recovery practically never occurs. Tem- 
porary remissions in the severity of the symptoms may take place. 

Treatment. — As in many diseases which apparently depend upon func- 
tional derangement, treatment is not followed by very satisfactory results. 
The patient should be forbidden to subject himself to nervous stress and 
worry, which materially increase the severity of the malady. Everything 
should be done to reinstate his nervous balance by a healthy out-door life 
and freedom from care. Massage and electricity, as a rule, do little good. 
In some cases they do harm by increasing the exhaustion of the affected 
muscles. 

A very large number of drugs have been employed with asserted good 
results, but none have the confidence of those members of the profession 
who have had large experience. Of all the remedies which have been 
recommended, hyoscine seems to have received the greatest amount of 
praise. It should be given in the dose of yfo °f a g ram once, twice, or 
thrice a day; the size of the dose and the frequency of its administration 
being governed by the severity of the tremor and by the susceptibility of 
the patient to drugs of this character. Duboisine may also be given in 
similar doses. Where there is much aching of the affected muscles, hot 
compresses give relief, and if the patient is in a condition of nervous irri- 



CHOREA MINOR 1043 

tation, the bromides and chloral are advantageous. The employment of 
such powerful nervous and vascular sedatives as veratrum viride and gel- 
semium must be resorted to with great caution. In doses large enough to 
quiet the tremor they are prone to produce too much circulatory depression. 



CHOREA MINOR. 

Definition. — Chorea minor, or acute chorea, sometimes called "Syden- 
ham's chorea," or "St. Vitus' dance," is a nervous disease characterized 
by irregular, purposeless movements, sometimes limited to certain muscles, 
but at others involving all the muscles of the limbs, face, and trunk. It 
affects, in the great majority of instances, children between the fifth and 
fifteenth years of life. 

Etiology. — That sex acts as a predisposing cause of chorea is shown by 
the fact that girls are affected three times as often as boys, and in the period 
of life from the fifteenth to the twenty-fifth year males escape almost entirely. 
The age which predisposes to its development, or is most susceptible, 
is from the fifth to the fifteenth year. After the fifteenth year it steadily 
decreases in frequency until the twenty-fifth year is reached, after which 
it is very rarely met with. The disease may, however, occur at all ages. 
Nervous, high-strung children suffer from it more frequently than those 
of a more phlegmatic temperament, particularly if, in addition, they are 
anaemic, and have a family history indicating that they are prone to attacks 
of acute rheumatism. 

Of the exciting causes may be named sudden shock or acute mental 
excitement, but in all such cases these causes are indirect, that is, they 
serve to disturb the nervous equilibrium, already unstable from other 
causes. In some cases the disease seems to be acquired by association with 
a choreic child, and in this way a large number of children in homes and 
asylums may become affected. Whether many of these cases are true chorea 
or merely imitations of it, or due to hysteria, is difficult to determine. 

That there is a very close relationship between acute articular rheu- 
matism and true chorea is certain. Even those physicians who deny 
that the rheumatism produces chorea are forced to admit that the occur- 
rence of chorea after attacks of acute rheumatic infection is remarkably 
frequent. Not rarely chorea complicates the development and progress of 
the acute endocarditis produced by this infection. Whether the poison of 
rheumatism affects the nerve cells of the brain, or whether the disease is 
due to changes in the finer capillaries supplying the brain, or to minute 
emboli, is unknown. Certain clinicians have endeavored to show that 
chorea is due to a specific infection, and Pianese isolated a diplococcus 
which was capable of producing an experimental chorea. There is no 
proof, however, that such a specific agent exists. 

Under the name of chorea gravidarum, & form of the disease is met with 
in pregnant women, usually only in primiparse. In these cases the gravid 
state seems to develop a condition of lack of nervous equilibrium, for the 
condition ceases, as a rule, with the termination of pregnancy. Occasionally 



1044 DISEASES OF THE NERVOUS SYSTEM 

in old age a senile chorea develops, but it is a distinct entity from the 
chorea of childhood. 

Frequency. — Chorea is much more frequently met with in England than 
in the United States. Morris Lewis has shown that its period of greatest 
frequency is March. 

Pathology and Morbid Anatomy. — Cases of chorea come to autopsy infre- 
quently, and therefore we have not as much information in regard to post- 
mortem findings in this disease as is desirable. In most of those instances 
in which death occurs during an attack of chorea, the autopsy reveals acute 
endocarditis, or chronic endocarditis with an acute exacerbation, and not 
rarely some degeneration of the myocardium. In the great majority of 
instances the results of examining the brain have been negative, and if the 
positive results which have been obtained are compared, they are found to 
be most variable. In some instances an intense hyperemia has been 
present; in others minute hemorrhages; in still others there have been 
small areas of inflammation and softening; while other cases have shown 
signs of meningitis, or thrombosis of the smaller bloodvessels supplying 
the brain. So, too, the changes which have been found in the spinal cord 
have been too varied to lead one to believe that they are in any way closely 
connected with the disease. Some observers have considered that they were 
the result rather than the cause of the condition. Choreiform movements 
sometimes develop in persons who have suffered from an organic brain 
lesion, but there is no reason to believe that this form of chorea and chorea 
minor have any close anatomical relationship. 

Symptoms. — The onset of chorea may be either sudden or gradual. In 
those cases in which it is gradual, it is first noted that the child is restless, 
and seems unable to keep still. Not rarely it is awkward in its movements, 
and falls over, or bumps into articles of furniture. When the disease is 
developed the child is continually restless, the arm or arms being moved 
in every possible direction. Sometimes the muscles of the shoulders are 
worked as if the child was uncomfortable by reason of ill-fitting clothes. 
The body is rotated from one side to the other, and the chin drawn first to 
one shoulder then to the other, then elevated, then depressed. When the 
movements are marked, walking is interfered with and it may be difficult 
for the patient to stand. Unlike most involuntary movements, the move- 
ments of chorea are not confined to one group of muscles, but usually 
attack different groups alternately. Neither is the movement in the nature 
of a tremor. It is like a voluntary movement, but is purposeless and incom- 
plete. Not infrequently the child laughs and cries without adequate cause. 
The movements affect the upper extremities more than the lower extremi- 
ties. The tongue is sometimes involved, and for this reason the speech may 
be disturbed. The child also frequently gives vent to curious guttural or 
smacking sounds, due to the action of the muscles of the mouth, pharynx, 
and tongue. These sounds may also be increased by spasm of the diaphragm. 
Occasionally, chorea may be limited to one limb, when it is called mono- 
chorea, or when it is confined to one side of the body it is called hemichorea. 
These motions distinctly interfere with ordinary voluntary movement, 
and it becomes almost impossible for the child to perform an ordinary act 



CHOREA MINOR 1045 

slowly; if it is to be successfully carried out, it must be done with great 
rapidity. Any cause which produces mental excitement in the patient 
greatly increases the severity of the jerking. Some clinicians have 
recorded an exceedingly severe form of chorea in which the patient has such 
violent muscular movements that he bites his tongue, can not eat, and is 
thrown about from side to side as if he were in a violent convulsion. The 
twitchings of chorea may or may not stop with sleep. In those cases in 
which the movements continue at night, the disease is usually severe, and 
it is in this type of cases that death sometimes occurs from exhaustion. 

The mental state of the patient is one of irritability and peevishness. In 
adults there may be hallucinations, and even a violent delirium. Some 
have thought that those cases in which insanity develops, and to which 
the name chorea insaniens is applied, do not belong to ordinary chorea 
minor. These mental disturbances not rarely complicate the chorea of 
pregnancy. 

Except for the exhaustion of the general system which is produced by 
the movements, there is no impairment of strength, nor is the electric 
reaction of the muscles altered. In some cases of a severe type, leading to a 
fatal issue, hyperpyrexia has been noted, which is probably due to endo- 
carditis. Many years ago I reported a case of monochorea in which the 
temperature of the affected part was raised. In some instances weakness 
or even marked paralysis occurs in one or more of the affected limbs, and to 
this type of cases is applied the term " paralytic chorea." 

Complications. — As already stated, chorea is a disease which is associated 
with a lack of nervous stability. It is manifest, therefore, that it may often 
be complicated by symptoms of hysteria. Indeed, it may be difficult to 
determine whether the patient is hysterical or choreic. That endocarditis 
frequently precedes, or accompanies, or complicates chorea, has also been 
stated, but every case of chorea that presents a cardiac murmur is not neces- 
sarily suffering from endocarditis, since the murmur is not infrequently 
due to ansemia, or to relaxation of the fibres surrounding the mitral orifice. 

Diagnosis. — Ordinary cases of chorea in childhood are easily diagnosed, 
particularly if the history of the patient is borne in mind. Between the ages 
of fifteen or twenty-five care must be taken that it is not confused with 
hysteria. Sometimes, too, choreiform movements develop in those parts 
which are affected by infantile cerebral palsy, but in such cases paralysis 
is present and muscular rigidity is noticeable, while the movements are 
really different (athetosis). 

Duration and Prognosis. — Chorea minor usually lasts from two to three 
months, and sometimes extends over a year. Mild cases may continue 
for only a few weeks. The prognosis as to recovery is good, the mortality 
being about 3 per cent., if all cases are included, death being due to com- 
plications rather than to the disease itself. Relapses are not infrequent in 
chorea. Unfavorable symptoms are rapid loss of flesh, fever, and delirium. 
The prognosis is worse as to duration in adults than in children. In the 
chorea of pregnancy the prognosis is very much more grave than any other 
form of the disease, the mortality varying from 20 to 25 per cent. Senile 
chorea is often a permanent affection and is rarely fatal. 



1046 DISEASES OF THE NERVOUS SYSTEM 

Treatment. — From what has been said in regard to the general condition 
of the patient who suffers from chorea, it is evident that mental and nervous 
quiet are absolutely essential. The child should not be exposed to the 
excitement or mental stress of school-work, neither should it be subjected 
to punishment or to criticism because of its movements. On the contrary, 
the fact that it is suffering from choreic movements should be ignored unless 
the physician is convinced that the case is one of hysteria and not of chorea. 
Iron and arsenic are to be given if anaemia is present, and the salicylates are 
useful if there is a rheumatic history. If the movements are severe enough 
to exhaust the child, it should be kept in bed and sleep should be obtained 
by the use of hypnotics. These drugs, however, must be used cautiously 
lest they produce general depression, and it should always be remembered 
that a hot pack will often put a choreic child to sleep and temporarily or 
permanently arrest the choreic movements. I have seen life saved in at 
least two instances by the hot pack. 

Although there is no specific remedy for chorea, arsenic nearly approaches 
the position of a specific. How it acts is not known. The best way to 
administer it is in the form of Fowler's solution, starting with 2 drops three 
times a day for a child of ten, and increasing it a drop a day until some 
puffiness about the eyes and nose or gastrointestinal irritation indicates that 
the full physiological effect of the drug is present, when it should be stopped 
or cut down to one-half the quantity. If this is not done an arsenical 
neuritis may develop. 

Next to arsenic in value is cimicifuga, given in the dose of \ drachm of 
the fluid extract twice or thrice a day. Antipyrin and acetanilid have also 
been employed with success. Bromides should be tried after the other 
drugs have failed. 

If the chorea of pregnancy becomes severe it may be necessary to induce 
labor. 

Other Forms of Chorea. 

Huntington's Disease. — Under the name of " hereditary chorea/' or 
Huntington's disease, an affection is met with which must be clearly differen- 
tiated from chorea minor. It is a rare condition which, as its name indicates, 
is hereditary, although it does not always affect consecutive generations, 
sometimes passing from the grandparent to the child, although in such cases 
the parent is usually excessively neurotic. Both sexes suffer from it equally. 
The disease begins between the thirtieth and fortieth year of life in most 
instances, and no exciting cause can usually be discovered. 

Its early symptoms consist in twitchings of the muscles of the face and 
upper extremities, which gradually increase in severity and in the area 
which they involve, until the entire muscular system may be affected. The 
patient, under these circumstances, carries on a series of grimaces and ges- 
ticulations, but it is a noteworthy fact that he, or she, can inhibit these 
movements at least for a period long enough to permit the voluntary 
movement which it is desired to make. When the muscles of the trunk 
and legs are involved the body is tossed hither and thither with rapid 



HYSTERIA 1047 

movements. Sensation is not involved. Paralysis of a hemiplegic type 
develops very rarely. The mind gradually fails, the mental failure being 
preceded by depression and irritability. 

Huntington's chorea is an incurable disease. It usually ends in the 
patient becoming bedridden and dying from some intercurrent malady. 
It may, however, last for many years. Cases are on record in which the 
patient has lived thirty years after the disease began to manifest itself. The 
progressive character of the malady, the period of life at which it develops, 
the progressive dementia, and the history of heredity all aid in separating 
it from chorea minor. 

The morbid anatomy is not understood. In some cases the lesions of 
the brain have resembled those of paretic dementia. 

The treatment consists in a healthy out-door life, and the use of nervous 
sedatives, and tonics, with the object of maintaining the patient's general 
health. Cases apparently identical with Huntington's chorea, but occur- 
ring singly, are spoken of as chronic chorea. 

Dubini's Disease. — Under the name of " electrical chorea," or "Dubini's 
disease," a form of chorea characterized by severe muscular contractions 
resembling those produced by electricity has been described by Dubini as 
affecting peasants in Northern Italy. Occasionally, the movements may be 
epileptiform in character. Paralysis soon develops; pain is suffered in the 
head, neck, and back, and death results, as a rule, from exhaustion. A few 
cases have been reported as having recovered. 

Another form of electrical chorea seen in children has been described by 
Bergeron. Such cases usually recover. I showed such a case before the 
Neurological Society of Philadelphia many years ago. The patient, a boy, 
a little past puberty, suffered from violent contractions which were electrical 
in character. 



HYSTERIA. 

Definition. — Hysteria is a chronic functional disturbance of the nervous 
system in which the motor nervous system may manifest its disorder by 
convulsions, palsies, or contractures, the psychical nervous apparatus by 
emotional disturbances, and the sensory apparatus by lost, diminished, or 
increased sensibility. It is manifest, therefore, that the disease involves 
both the central and peripheral portions of the nervous system, but there can 
be no doubt that the dominating condition is a psychosis. Hysteria 
undoubtedly depends upon a condition of disturbed nervous equilibrium. 

Etiology. — There can be no doubt that this affection is, to some extent, 
hereditary; that is, a parent or parents who possess an unstable nervous 
system naturally transmit a similar condition to their offspring, and in a very 
large proportion of cases it will be found that the patient is a child of parents 
who have at various times manifested neurotic or hysterical disorders. 
Age has a distinct influence upon the disease. Its most frequent period of 
occurrence is from fifteen to twenty-five years of age in women, although 
in males it usually appears at from twenty to thirty. Occasionally, how- 



1048 DISEASES OF THE NERVOUS SYSTEM 

ever, children suffer from it, particularly before puberty, and sometimes 
much earlier than this. The condition is met with far more frequently in 
females than in males, but statistics vary from 40 to 1 to 4 to 1 or even 2 
to 1, according to different writers. It is much more common in the very poor 
and in the rich than in the middle classes, and in the Latin races than in the 
Anglo-Saxon race. In America it is most frequently met with in the poorer 
class of Jews, who are often underfed, poorly housed, much confined, and 
under great nervous excitation and stress. It is much more common in 
France and Italy than in Germany and England. 

If it be true that the underlying cause of hysteria is a lack of nervous 
control or balance, it is evident that a number of conditions may be con- 
sidered as direct causes of the malady. In other words, any condition which 
upsets the nervous balance may provoke the disease. It is, therefore, fre- 
quently found that some great grief or intense joy has been productive 
of the first manifestation of the disease, or, again, that some injury or 
fright has acted in a similar manner. Great worry in business, or over a 
love affair, may produce a similar result. None of these causes would pro- 
foundly affect a healthy nervous system. All of them are sufficient to 
disturb the balance of a nervous organization already abnormal. 

Pathology. — -As already stated, hysteria is a purely functional disease, 
and the central and peripheral nervous systems show no alterations which 
can be considred as responsible for the malady. 

Symptoms. — Hysterical individuals usually present evidences of nervous 
irritability which may manifest itself in great excitement, in violent anger, 
in undue anxiety, or in great mental depression. All of these manifesta- 
tions may follow one another with extraordinary rapidity. The patient also 
manifests distinct lack of self-control, both in regard to her emotions and 
her impulses. At times she may seem utterly incapable of accomplishing 
anything which ought to be done. At another time she can develop an 
amount of energy and persistence which is surprising, provided that she 
conceives it to be her duty or her wish to accomplish such an end. The 
power of thought is in no way impaired, but judgment is warped and uncer- 
tain. Not infrequently the patient has perverse ideas which may seem to 
amount to delusions, but which do not remain constant as in cases of insanity. 

In some instances the first symptoms of the malady are manifested by a 
hypersensitiveness, so that the girl cries easily, and perhaps laughs more 
readily and for a longer time than is necessary in the appreciation of a 
remark which is amusing. Restless sleeping also may be present. As the 
condition develops, attacks of headache and vomiting may come on, and she 
may suffer from somnambulism. 

When the condition becomes still more severe, so that it amounts to 
that state which is sometimes called "hysteria major," the disturbances of 
sensation and motion become intense. In addition to attacks of crying 
and laughter, the patient may pass into a trance or into a condition of 
catalepsy. Or, again, the patient may suddenly fall and be seized by a 
convulsion which is distinctly epileptiform in character. Often, however, 
the convulsion is more largely tonic than clonic, the hands and fingers 
being flexed and the forearm flexed on the arm, while the legs and feet are 



HYSTERIA 1049 

extended and the eyes closed. If the eyelids are lifted, the eyeballs are often 
found to be fixed in convergence or undergo irregular movements. The pupils 
are dilated. The surface of the body is more or less anaesthetic. As a rule, 
the patient does not froth at the mouth as much as in true epilepsy, nor does 
she bite her tongue as is done in epilepsy. So, too, she rarely hurts herself 
when in the convulsive seizure. The attack may last from a few minutes 
to several hours, or even longer than this, and may vary in its intensity 
from semi-consciousness with slight twitchings of the muscles to apparent 
total unconsciousness and severe convulsive seizure. The expression of 
the face is often quite characteristic. In some instances it is remark- 
ably peaceful after the convulsion passes by. In others it is ecstatic or 
terror-stricken. In very young patients curious guttural and other sounds 
may be made, and the patient may bark like a dog or mew like a 
cat. 

It is noteworthy that many of these patients are conscious of what is going 
on around them during the attack, although at the time they may manifest no 
evidence of this. Not rarely a sharply spoken word of command may bring 
the attack to a close, or the threat of applying some instrument which is capa- 
ble of causing pain may do likewise. When the patient returns to conscious- 
ness, it may be found that there is loss of power in an arm or leg, or upon one 
side of the body, with or without loss of sensation. Frequently the so-called 
hysterogenic zones may be discovered, pressure upon which causes pain and 
may provoke an hysterical attack, or if pressure on these parts is used during 
the attack it may arrest it. 

The sensory symptoms of hysteria, in distinction from those just described 
in connection with a critical period, consist in ancesthesia in all its forms, par- 
ticularly analgesia of the cutaneous and mucous surfaces and disturbances 
in the special senses. The most common form of cutaneous ancesthesia is 
hemiancesthesia involving exactly one-half the body. After this, the most 
common type is segmental anaesthesia, in which an arm, or leg, or part of the 
face is anaesthetic, the margin of the anaesthetic area being sharply defined, 
while the disturbance of sensation does not correspond to the distribution 
of any one nerve trunk. Much more rarely patches of anaesthesia occur 
in different portions of the body. In these anaesthetic areas the senses of 
touch and of heat and cold are usually preserved to some slight extent. 
Occasionally, the affected part has a subnormal temperature. When the 
anaesthesia is limited to one side it affects the left far more frequently than 
the right half of the body. If the anaesthesia is of the hemianaesthetic, or 
segmental, type there is usually more or less complete loss of motor power 
in the same limb. 

The disturbances of special sense consist in an anaesthetic condition of 
the retina whereby the visual field is greatly narrowed, particularly for cer- 
tain colors and often for those colors which normally have the widest field, 
and the color sense is disturbed or reversed. These disturbances may or 
may not complicate those just named. When hemianaesthesia is present, 
the eye upon the affected side is sometimes partly or even totally blind, not as 
in organic hemianopic hemianaesthesia. So, too, the acuity of the auditory 
nerve may be diminished, particularly upon that side of the body which is 



1050 DISEASES OF THE NERVOUS SYSTEM 

most affected. The sense of taste may also be perverted and the sense of 
smell may be lost. 

Neuralgic pains are not common in hysteria except when there is present 
grave ansemia and other common causes of neuralgia. In certain portions 
of the body, however, hyperesthesia of the skin may be present as in the 
hysterogenic zones described. These zones are most frequently found in 
females in the groin, whence the name "ovarian" tenderness, and under 
the mammary glands, and in males on the scrotum, also along the spine, 
but they may be found in any part. Paralysis of the extraocular muscles 
is sometimes met with. Usually the internal rectus is affected, and some- 
times the external rectus. Speech may be impaired by paralysis of the 
adductors of the vocal cords. The development of this condition is called 
" hysterical aphonia/' the patient being speechless, or able to converse only 
in a whisper. The onset of this condition is usually sudden. 

The paralysis of motion already referred to often persists for a long period 
of time, and in association with this paralysis it not rarely happens that 
other muscles, often those which are antagonistic to the ones which are 
paralyzed, suffer from contractures. At first these muscles may be simply 
abnormally irritable and the contractures may be fleeting, or they may last 
as long as the paralysis of motion and sensation, and in this way resemble 
the contractures which are sometimes met with in cerebral diplegia. Tremors 
may also affect the muscles of an arm, of the face, or of a leg, and these 
tremors may resemble those of paralysis agitans or other diseases charac- 
terized by tremor, particularly if the patient has been associated with such 
a case. The amount of atrophy or wasting which occurs in a paralyzed 
part is usually very slight, and depends almost entirely upon lack of use. 

Of the internal viscera it may be said that the functions are not gravely 
impaired in most instances, unless perchance these viscera suffer from the 
chief manifestations of the disease. A very common symptom of hysteria, 
present in the majority of cases is the sensation as if a ball or small orange 
rose into the pharynx. This is called "globus." In other instances violent 
attacks of vomiting develop. In still others, the "rifting" of large quantities 
of gas, or of air which has been swallowed, takes place, accompanied by 
much rumbling in the abdomen. In still other instances rumination, or, as 
it is sometimes called, "merycismus," occurs; that is, the patient regur- 
gitates food, which has been swallowed, into the mouth for a second chewing. 
At other times intestinal disorders are present. I have seen a large phantom 
tumor of the intestine, in a patient who had constantly refused food until she 
was emaciated to the last degree, give rise to the belief that a malignant 
growth was present. At times these patients have a perverse appetite, eat- 
ing chalk or other materials not commonly swallowed. The urine is some- 
times very limpid and free. At other times it is scanty and high colored. 
After an acute attack of hysteria it is usually limpid. 

Of the circulatory disorders attacks of tachycardia are by no means 
uncommon. Sometimes the patient will complain of severe pain in the 
neighborhood of the heart. This pseudoangina is characterized by a sensa- 
tion of distention of the heart in distinction from the pain of true angina, 
which is usually described as if the heart were being tightly compressed. 



HYSTERIA 1051 

The peripheral vascular system may also be disturbed. Abnormal flushing 
or blushing or local anaemia and pallor may be present. At times even 
oedema may develop. In other instances the part becomes so pallid or slate- 
like in color that it resembles Raynaud's disease, but true gangrene does not 
develop. Very rarely, indeed, a sharp febrile movement may take place. 
Sometimes hysterical patients suffer from attacks of hiccough or of sneezing, 
or of rapid breathing, cough, or difficulty in swallowing. 

Under the name of " hysteroepilepsy," a form of hysteria characterized 
by violent convulsions closely resembling those of true epilepsy is described 
by many foreign authors. It is rare in this country. In some instances 
the convulsive seizure is not epileptoid, but cataleptoid or tonic. The 
patient may lie in bed with the arms extended, as in ecstasy, or with the 
hands tightly clinched, as in terror or anger, or the state may resemble 
simple stupor or even coma. At other times a psychical disturbance is mani- 
fested so that the patient develops a delirium. Often several of these processes 
are combined. At first the patient experiences an aura as in epilepsy. This 
is followed by the epileptoid form of convulsion, and this again by the con- 
tortions and emotional attitudes just described. An emotional confusion 
is not rare; hallucinations and delusions may occur and confinement in an 
asylum may be necessary. Finally a stage of delirium may develop. 

Diagnosis. — Under some circumstances there is no more difficult diagnosis 
than the differentiation of hysteria from organic nervous disease, particularly 
if the patient has had an opportunity of studying the symptoms presented 
by patients with organic nervous lesions. The important points in differ- 
entiation are the contraction of the visual fields and the alterations in the 
color fields, the fact that the areas of anaesthesia are not confined to any 
given distribution of sensory nerves, the presence of hysterogenic or hyper- 
aesthetic spots, the fact that wasting does not develop to any degree in the 
paralyzed muscles, the absence of the reaction of degeneration, the 
maintenance or persistence of the deep reflexes, and the peculiar emotional 
state. Again, the anaesthetic area may be moved from the first place affected 
by the mere placing of a coin or a magnet over the affected part. Hysterical 
contractures also usually disappear in sleep or when the patient is under 
the influence of an anaesthetic. In the epileptoid form of attack the tongue 
is never bitten nor the limbs injured. 

Prognosis. — The prognosis as to life is good. The attacks usually diminish 
in frequency and severity with advancing years, but the question of prognosis 
is also governed by the degree of nervous instability in the patient and in 
her parents. When the hereditary influence is bad and the surroundings 
of the patient are unfavorable the malady may last a lifetime. In those 
who are well-to-do and who can afford to take the treatment required by 
such cases, the outlook is better than in those who are continually exposed 
to bad surroundings, with nervous stress and strain. 

Treatment. — The treatment consists in the removal of the patient from 
those causes which tend to produce nervous irritability and stress. If the 
home surroundings of the patient are such as to increase nervous irritation, 
the patient must be removed from those surroundings. Such a patient 
should always be taken from school and given lessons under a private instruc- 



1052 DISEASES OF THE NERVOUS SYSTEM 

tor. If the symptoms are severe the Weir-Mitchell rest cure is essential. 
If they are not severe enough for this, an out-door life with a moderate 
amount of healthy exercise carried to the point of fatigue, but not of exhaus- 
tion, is needful. If anaemia is present it must be overcome by proper tonics. 
Insomnia and peripheral nervous irritation should be treated by hot and 
cold packs and the various forms of hydrotherapy. Sedatives may be needed, 
but it must be remembered that the administration of hypnotics to neurotic 
patients frequently produces a drug habit. Local anaesthesia, in addition 
to being treated by hydrotherapy, will also be benefited by the use of the 
rapidly interrupted faradic current administered by means of the ordinary 
wet sponge, or, if the anaesthesia is marked, through the dry wire brush. 
The physician must exercise a dominant influence over the patient, and she 
must be put under the charge of a trained nurse of strong character, who, on 
the one hand, will not be irritated by peculiarities, but will tactfully dis- 
courage them. This mental side of the treatment is too frequently 
overlooked. 

The treatment of the hysterical attack itself consists in the administration 
of nitrite of amyl. There are few cases of true hysteria that will not be at 
once relaxed if convulsed, and the attack stopped by this drug, which, on 
the one hand, is perfectly safe, and, on the other, produces so powerful a 
mental impression that its use is appreciated by the patient. If nitrite of 
amyl cannot be employed, ether may be used and pushed freely, but chloro- 
form is usually too agreeable to the patient to be advantageous. Not rarely 
the use of the dry electric brush or even of the actual cautery, which may 
be touched at various points on either side of the spine, is advantageous 
through the powerful mental impression it produces. 



EPILEPSY. 

Definition. — Epilepsy is a disease characterized by attacks of unconscious- 
ness, which, in the well-developed form of the malady, are accompanied or 
followed by convulsions. The convulsions at the moment of onset are 
usually tetanic or tonic in type, but almost immediately become clonic. 
Indeed, so typical of epilepsy are clonic convulsions that all convulsions 
of this class are called "epileptiform.' J Epilepsy separates itself from other 
convulsive conditions associated with unconsciousness by the fact that it is 
a chronic malady, whereas epileptiform convulsions arising from other 
causes occur but a few times in the lifetime of the individual, as, for example, 
in puerperal eclampsia or uraemic poisoning. Hysterical convulsions, how- 
ever, closely resemble it. 

Etiology. — The etiology of epilepsy is unknown, although in a certain 
proportion of cases injuries to the brain substance arising from external or 
internal causes undoubtedly predispose to or produce the disease. In some 
instances it has been thought that the condition is hereditary, and this is cer- 
tainly true in the sense that epileptic parents often have epileptic children. 
By far the largest number of cases collected by any one writer, so far as 
the author is aware, are those of Gowers, who analyzed no less than 1450 



EPILEPSY 1053 

cases of epilepsy, finding that an inherited tendency was indicated by the 
presence of insanity or epilepsy in ancestors or collateral relations in rather 
more than one-third of the cases (35 percent.), and rather less frequently in 
males than in females, for there was this history in 33 per cent, of the males 
and 37 per cent, of the females. There was a family history of epilepsy in 
two-thirds of the inherited cases, of insanity in one-third, and of both dis- 
orders in one-tenth of the cases. In the 56 cases recorded by Sieveking 
heredity was the cause in 11. Reynolds, in his collection of cases, found 
the proportion to be 31 per cent. Hasse has collected 1000 cases, and has 
found heredity the cause in no less numbers than the others. If we take 
the average result of the conclusions reached by the clinicians just named, 
who give exact figures, we find that we have to deal with 4300 cases of 
epilepsy, of which a little over 26 per cent, were due to heredity. Whether 
epilepsy can be induced in a child by hereditary influences arising from 
chronic alcoholism or chronic lead poisoning is open to debate. Certain 
neurologists are firmly convinced that these factors are active. 

In other instances, apparently healthy children develop epilepsy after 
suffering from some of the infectious diseases such as scarlet fever. In these 
cases the infection has either produced some definite lesion in the brain 
or has so impaired the normal growth of certain cells in the cerebral cortex 
that their natural balance is destroyed, with the result that periodic explo- 
sions of nervous energy take place. 

Syphilis acts as a cause of epilepsy in two ways. When the parent is 
syphilitic, the child may suffer from hereditary syphilis or from a para- 
syphilitic disease of the nervous system, with imperfect cerebral develop- 
ment. In other cases acquired syphilis produces epilepsy in adults. Indeed, 
more than one writer has expressed the belief that an epilepsy beginning 
after the twenty-fifth year is syphilitic in origin. This is rather an exag- 
gerated statement, but it is nevertheless true that more than three-fourths 
of all cases of epilepsy begin before the twentieth year. About half of 
them begin in the second decade of life. Quite a large proportion begin 
between the seventh and tenth years. 

In some instances the epilepsy dates from the reception of some severe 
injury to the head. Cases that have a traumatic origin, those which are 
due to syphilitic gumma or other form of brain tumor, usually belong to 
that type which is called "Jacksonian" or " localized " epilepsy, although 
they may ultimately develop all the characteristics of the so-called idio- 
pathic form. 

For many years it was considered that a host of conditions tended 
to produce epilepsy by reflex irritation. Such causes as foreign bodies 
in the ear or in the nose, intestinal worms, and uterine disorders have been 
considered as causative factors, but in all such cases it cannot be denied that 
these agents act indirectly in the sense that they provoke an irritation which 
reflexly unsets the nerve balance or equilibrium of an unstable motor area 
of the brain. In other words, in any case of epilepsy it is to be understood 
that the underlying factor is a lack of stability or nervous balance. 

The influence of sex is not very great, but males are affected somewhat 
more frequently than females. Althaus has examined an enormous 



1054 DISEASES OF THE NERVOUS SYSTEM 

amount of statistics to obtain results bearing on this point. He found that 
in 54,442 cases there were 28,960 males and 25,482 females. 

Posthemiplegic epilepsy due to cerebral injury may occur at any age, but 
there can be no doubt that it far more commonly occurs in infants than in 
adults. In at least two-thirds of the cases the onset is before the fifth year 
of age, and in nearly one-half it is during the first two years of life. It is not 
uncommon for the paralysis to occur in infancy and the epilepsy to begin 
at puberty. This prolonged interval is rare in adults, in whom the epileptic 
seizures usually begin in less than one year. 

The frequency with which epilepsy comes on after the hemiplegia of 
childhood has been very exhaustively studied. Thus, in Osier's cases, 
20 children out of 97 suffered from it. In the 80 cases collected by 
Gaudard 11 children had hemiepilepsy, and 66 children out of 160 cases 
collected by Wallenburg were epileptic after hemiplegia. In another series 
of cases collected by Osier 15 children out of 23 were thus affected. 

Pathology. — The pathology of epilepsy is not known. It is true that at 
autopsy many cases of epilepsy show atrophic or degenerative changes in the 
cerebrum, but this holds true of only a certain proportion, and not of those 
instances of so-called idiopathic epilepsy in which there is no history of 
syphilis, or of injury, or of damage to the brain through disease of its blood- 
vessels. In this idiopathic form the most careful macroscopic and micro- 
scopic examinations of hundreds of cases have failed to reveal any alteration 
which can be considered as responsible for the malady. Some of the micro- 
scopic lesions which have been described by certain investigators are with- 
out doubt present, but in these cases the question arises whether they are 
not the result rather than the cause of the affection. 

That epilepsy is a result of an explosive discharge of nervous energy from 
the motor areas of the cortex is proved by the fact that similar convulsions 
can be produced in man and in the lower animals by irritating these areas, 
and that growths and injuries which irritate them produce similar symptoms. 
The somewhat ancient theory that the convulsive disturbance is the result 
of lesions in the medulla and the pons is no longer accepted. 

Symptoms. — One of the first and most marked symptoms of an oncoming 
attack of epilepsy is a peculiar sensation felt in some portions of the body, 
generally below the head, which gradually rises up over the patient, either 
rapidly or slowly, like an oncoming cloud, until, the head having been reached, 
the patient is immediately convulsed and unconscious, and almost instantly 
is seen to be in the very acme of the nervous storm. Simultaneously with the 
arrival of this aura in the cervical region the person utters a peculiar cry or 
scream, so characteristic that it has been called the "epileptic cry," being 
probably due not so much to a voluntary impulse as to a sudden expulsion 
of the air from the thorax by the convulsive contraction of the abdominal 
muscles, as well as those of the thorax, and its rapid passage through the 
glottis narrowed by rigid spasm of the muscles governing this opening. 
Synchronously with this cry the muscles of the whole body, in a widespread 
attack, become strongly contracted until they are in a tonic spasm, and then, 
having momentarily relaxed, pass into alternating relaxations and contrac- 
tions, which throw the patient now to this side, now to that. 



EPILEPSY 1055 

During the tonic spasm the muscles of the face often produce marked 
distortions of the features, in some cases bringing about the so-called risus 
sardonicus; the head may be drawn to one side, and under these circum- 
stances the eyes are generally turned in the same direction; the jaws are 
locked one against the other, and the lower jaw may also be drawn away 
from the median line of the face in the same direction as the eyeballs. Some- 
times the whole body is rotated. In 970 cases analyzed by the writer, com- 
plete rotation to the right is mentioned as being present in 49 persons, and 
to the left in 52 cases. There is, therefore, no difference worthy of note 
in these numbers. 

The arms are strongly flexed at the elbows, while the hand is still 
more strongly flexed at the wrist; the fingers are also so bent into the 
palm of the hand that not unfrequently the skin in this region is found 
indented by the nails. The arms, legs, and body are drawn and jerked in 
the direction of the most powerful muscles, and, as a consequence of this, 
opisthotonos, during the tonic stage, is by no means uncommon. Excep- 
tions to this rule do, however, frequently occur, and when present show that 
the paroxysm is exerting its chief influence on the weaker muscles, while the 
stronger ones are affected at least to a less degree. As a general rule, too, 
the muscles of one side suffer more than those of the other. Unfortunately, 
in the cases collected by me, in only 158 instances were any remarks 
on this point made. In these 158 the right side was most affected in 77 cases, 
and the left side in 81 cases. It is evident, therefore, that both sides suffer 
about equally. The legs may be firmly flexed on the abdomen, while the 
fingers are rigidly extended. 

The change in the color of the face is very marked and almost typical of 
the disease, being at first pale, then flushed, the flushing deepening often into 
a livid purple, owing to the asphyxia produced by the convulsive contraction 
of the thorax. In some cases the eyelids are widely drawn apart so that the 
eyes, owing to their fixation, have a staring appearance ; in others they are so 
tightly closed that the fingers of the onlooker can scarcely force the lids 
apart. The staring, but blank, expression of the eyes is also increased by 
the slow dilatation of the pupils which always accompanies the asphyxia. 

The duration of the tonic contractions rarely exceeds two minutes, and in 
most cases is limited to but a few seconds. It is followed by the clonic spasms, 
already described, which are ushered in by more or less violent tossings, but 
whose onset is forewarned by peculiar vibratory thrills, which run through 
all the affected muscles. The eyelids tremble, the body changes its position 
never so slightly, and then, as if the vibrations gained greater and greater 
power with each moment, the fibrillary tremors give way to muscular con- 
tractions. The expression of the face, which in the preceding stage was set 
and firm, is now constantly changed by the movements of the facial muscles; 
the jaws, no longer locked together, are gnashed and crunched one upon 
the other; the tongue is alternately protruded and drawn back, and, as a 
consequence, is often caught between the teeth and bitten and lacerated. 
The excessive movements of the muscles of mastication force the increased 
quantities of liquid secreted by the salivary glands from the mouth in the 
form of froth, which is often stained with blood by reason of the injuries to 



1056 DISEASES OF THE NERVOUS SYSTEM 

the tongue. The constancy of the convulsive movements now becomes less 
and less marked; well-developed remissions occur between each toss of the 
body, until the movements cease entirely; but it should be constantly borne 
in mind that the prolongation of the remissions does not produce any decrease 
in the severity of the intervening spasm, the final spasm often being even 
more violent than the first. 

The intense discoloration of the face begins to pass away as soon as the 
remissions, by their length, permit the blood to be oxygenated, its disap- 
pearance being temporarily arrested by each paroxysm. Finally, the spasms 
having ceased, the patient lies before us relaxed, unconscious, and exhausted, 
and passes into a deep sleep or coma, which lasts a variable length of time, 
and from which he cannot be aroused except very rarely, and then with 
great difficulty. 

One of the most interesting and important of all the symptoms is the 
so-called aura. Difference of opinion has arisen as to the frequency of its 
occurrence, some authors stating it to be very rare, while others see it very 
constantly. There can be little doubt that in many cases it is as constantly 
present as in others it is absent, and it would appear that the nationality of 
the patient has something to do with the occurrence of this signal of the 
attack; at least, if we may judge by the statements of the chief authors of 
each nation. Thus, in America, Wood states that "the aura is wanting in a 
very large proportion of the cases of true epilepsy,'' and Hammond agrees 
with him. In England, Gowers stated it to occur in about one-half of the 
cases, and Bristowe states it to be not uncommon. In France and Belgium 
the aura appears to be present in more than half the cases, in one form or 
another, as it is also in Germany, according to Nothnagel. In 970 cases 
collected by the writer it was found that the aura was recorded as present in 
362 cases and absent in 138 cases. 

The aura, or warning, while possessing general characteristics common 
to all cases, is by no means identical in each individual. By far the largest 
number of cases, where it is present, have it in an extremity, and if it be 
not there, then it is often in the stomach; and it is not uncommon to see 
persons suffering from epilepsy who have as an aura a general, indefinable 
sensation all over the body. In much more rare instances the aurse are 
situated in the organs of special sense, and are evidenced by sudden attacks 
of blindness or deafness. It is worthy of note, however, that whereas the 
aura may differ in every case in origin, seat, and limitation, they are remark- 
ably constant in the same individual, rarely, if ever, changing in kind, although 
they may vary in degree. A careful analysis of an enormous number of 
cases by hundreds of observers shows that the aura most commonly met 
with is that beginning in the hand; next, that beginning in the leg or foot; 
next most common, that arising in some of the viscera, and, after these, those 
which arise in the face and tongue. The rarest form of aura is that which 
arises in the sides of the trunk. 

Not only may the seat of the aura be varied, but its sensations may be 
even more aberrant. Undoubtedly the most common sensation is the inde- 
scribable sensation of a vapor or cloud, already spoken of; but in a large 
number of cases the sensations are described as being quite painful, or 



EPILEPSY 1057 

perhaps as partaking of the feeling that the part is in active movement 
when in reality it is still quiet. Others speak of it as a sensation of cold, 
others of heating and burning, and still others of trembling and indescribable 
distress. In certain cases the sensation is confined to the spot where it is 
first noticed, and fails to travel upward or toward the central nervous system. 

Status epilepticus is a condition in which convulsion follows convulsion 
so rapidly that consciousness is not regained. In some instances the patient 
dies within a few hours as a result of exhaustion or asphyxia. As the case 
goes on the convulsions are replaced entirely by coma, or, in rare cases, 
violent attacks of mania may develop. In this state the body rapidly 
emaciates, bed-sores develop, and death ensues from exhaustion. 

An extraordinary number of fits may occur in a brief space of time 
without causing death, or even very great exhaustion. A very good ex- 
ample of this fact is that of a case reported by Newington, which is as 
follows: On the twentieth day of the month, at 5 a.m., the fits began in 
the woman under his care. By 5 p.m. the same day she had had 274 fits, 
and by 5 a.m. on the 21st she had 384 more, or 622 fits in twenty-four 
hours. This makes a rate of one nearly every minute. By 5 a.m. on the 
22d she had 400 more; by 5 a.m. on the 23d, 525; by 5 a.m. on the 24th, 
355, and from 5 a.m. on this day to 5 a.m. on the 25th she had 214 fits. Alto- 
gether she had 2156 fits in five days, and yet survived, being fed by the 
rectum. 

Motor paralysis may succeed epileptic paroxysms, and this is particularly 
the case in those instances where the convulsive movements are largely 
unilateral in character. 

A very important question, connected not only with the prognosis of 
epilepsy, but also with its relation to medical jurisprudence, lies in the influ- 
ence which the disease may exercise on the mental condition of the sufferer. 
Russell Reynolds has arrived at the following conclusions in regard to the 
effects of the disease on the intellect: 

1. That epilepsy does not necessarily involve any mental change. 

2. That great mental impairment exists in some cases, but this is the 
exception rather than the rule. 

3. That females suffer (in mental vigor) more frequently than males, and 
also more severely. 

4. That the commonest failure is loss of memory, and that this, if regarded 
in all degrees, is more frequent than integrity of that faculty. 

5. That apprehension is more frequently preserved than lost. 

6. That ulterior mental changes are rare. 

7. That depression of spirits is common in males, rare in females, but 
that excitability of temper is found in both sexes. 

Complications. — Naturally enough, a very common variety of complication 
is some traumatism, severe or mild, which is suffered as the result of the fall 
accompanying the fit, whereby the head is struck against some hard or 
sharp object. The severity of the injury may be anything from fracture to 
a slight abrasion or bruise. When such an accident happens it should not 
be forgotten that the coma of the fit may be dangerously deepened by the 
concussion, and also that the coma may mislead the physician so that it is 
67 



1058 DISEASES OF THE NERVOUS SYSTEM 

regarded as the natural sequence of the attack rather than the result of the 
injury. Fractures of the clavicle are very common. In the same manner 
various dislocations may ensue. The presence of a fracture in an epileptic 
is a very much more serious matter than would appear at first glance, for 
even if the fits are not very frequent they are almost sure to cause a fresh 
solution of continuity, or even to convert a simple into a compound fracture 
by the jerkings of the muscles. Splints are, of course, of value, and the 
limb may be wrapped in a pillow. Careful watching with quiet rest in bed 
must always be insisted upon, since under these circumstances a second 
fall is avoided on the advent of a new attack. 

In other cases apoplexy may occur, due to the sudden strain upon the 
cerebral bloodvessels during the fit, and if the coma following an attack 
is prolonged or peculiar, this fact should be called to mind. The inequality 
of the pupils, the stertorous respiration, the fact that the tongue cannot be 
protruded straight from the mouth, all point to a cerebral lesion; but the rise 
of temperature, the coma, and, last of all, the hemiplegia are characteristic 
of both states, and cannot be used for differential diagnosis. 

Diagnosis. — Undoubtedly, the most similar convulsive condition that we 
have is that due to hysteria, and the diagnosis of one from the other is 
as difficult in some cases as it is essential and necessary for treatment and 
cure. The other conditions, with which it might be confused, are uraemia, 
alcoholic epilepsy, tetanus, and syncope. In the accompanying table are 
arranged all these disorders, which briefly and succinctly shows the different 
points between them, although of necessity it is somewhat arbitrary on 
account of the lack of space. 

The very irregularity of true epilepsy makes it extremely difficult to 
give clear and well-defined outlines of it against another disease, par- 
ticularly when we remember that epilepsy and hysteria often go hand in 
hand. 

By far the most important differential point between the two disorders 
just named, when not complicated with still another disease, is the character 
of the movements. As already pointed out, in epilepsy they are typically 
at variance with those of daily life, while in hysteria they are often equally 
typical of ordinary muscular contractions, or, in other words, are more 
purposive in character; and frequently there is prolonged tonic contraction 
of the muscles, giving rise to the assumption of positions which bear more or 
less resemblance to normal attitudes. In hysteria, also, consciousness is 
impaired sometimes, but never so completely as in true epilepsy. Indeed, 
most commonly the individual knows all that goes on around her, for, while 
she may give no sign of consciousness by words or looks during the attack, 
she may afterward be able to narrate all that has occurred. Less commonly, 
however, a condition known as automatic consciousness exists, in which, 
during the paroxysm, the patient understands all that is said, but forgets 
everything on the return to quietness. 

The fact that the patient is a female cannot be regarded as affirmative 
evidence of hysteria in the least, but if the fit occurs in a male it may be 
taken as fairly positive evidence of epilepsy; and yet it should always be 
remembered that males may suffer from hysteroid attacks. 



EPILEPSY 



1059 



Table of Differential Diagnosis of Epilepsy from Hysteria, etc. 



Signs. 


Epilepsy. 


Hysteria. 


Uraemia. 


Petit mal. 


Alcoholic 
epilepsy. 


Tetanus. 


Syncope. 


Apparent 
cause. 


None. 


Emotion. 


None. 


None. 


None. 


None. 


Mental 
shock. 


Aura or 
prodro- 
mata. 


Generally 
present* 
but short. 


Globus 
hystericus, 
palpitation, 
choking. 


Headache, 
vomiting, 
and dys- 
pepsia. 


Faintness 
and dim- 
ness of 
vision. 


Tremors. 


Nervous- 
ness. 


Not so well 
defined as 
in epilepsy. 


Onset. 


Sudden. 


Often grad- 
ual. 


Often grad- 
ual. 


Sudden. 


Sudden or 
gradual. 


Gradual, 
begins in 
jaw. 


Sudden or 
gradual. 


Scream. 


At onset 
and sud- 
den. 


During 
attack. 


Frequently 
none. 


Frequently 
none. 


May or may 
not be 
present. 


None. 


None. 


Convul- 
sion. 


First tonic, 
then clonic. 


Rigidity 
more pro- 
nounced 
with more 
aching. 


Rigidity 
generally 
absent. 


No rigidity. 


Movements 
more clonic 
than tonic. 


Always 
touic. 


None. 


Biting. 


Tongue. 


Tongue, 
lips, and 
hands. 


Tongue. 


None. 


Rarely. 


None. 


None. 


Micturi- 
tion. 


Frequent. 


Never. 


Never. 


Rarely, ex- 
cept when 
bladder is 
affected. 


Rarely. 


Sometimes 


Never. 


Defecation 


Occasion- 
ally. 


Never. 


Never. 


Never. 


Rarely. 


Rarely. 


Never. 


Talking. 


Never. 


Frequent. 


Muttering. 


Never. 


Never. 


Never. 


None. 


Duration. 


A few 
minutes. 


Generally 
many 
minutes. 


From a 
minute to 
hours. 


Momentary. 


May be pro- 
longed. 


Hours. 


Indefinite 
time. 


Conscious- 
ness. 


Lost. 


Generally 
preserved. 


Lost. 


Not lost 
always, but 
clouded. 


Lost. 


Preserved. 


Lost. 


Termina- 
tion. 


Spontane- 
ous. 


May be 
induced 
by shock. 


Spontaneous 


Spontaneous 


Spontaneous 


Spontane- 
ous. 


Gradual, 
with no 
somno- 
lence. 



The movements of the hysterical patient after the tonic condition has 
passed awayare as clonic as those of epilepsy, but still possess some purposive 
characteristics, and are not so bizarre as are those of the true disease. Thus, 
the head, arms, and legs are struck with evident endeavor against the floor 
or surrounding furniture. Another point, which, when it occurs, is very 
distinctive, is the onset, toward the close of a hysterical convulsion of a 
second stage of tonic spasm such as occurred at the beginning. It will be 
remembered that this does not occur in epilepsy; although it must be borne 
in mind that in cases of the ''status epilepticus" the rapid onset of another 
attack may show a second tonic stage. This can be separated, however, 
by the fact that it is followed by clonic movements, whereas the secondary 
tonic stage of hysteria is usually followed by relaxation and temporary 
recovery. 

Finally, too, in hysteria, some peculiar emotional position is often assumed, 



1060 DISEASES OF THE NERVOUS SYSTEM 

as of the crucifix, or of intense grief, or, perhaps, immoderate laughter, with 
corresponding movements of the trunk. If the patient is quiet at this time, 
a smile may float across the face, while the eyes, with a look of pleasure, 
pain, or entreaty, may seem to be gazing at some object very far off. In 
some very well developed cases the expression of pleasure is followed by a 
look of pain, with painful movements, or an appearance of voluptuous 
entreaty, with sensual and venereal desire evidenced by gestures. Very 
commonly areas of anaesthesia and hyperesthesia occur in these patients 
and are of all degrees of intensity and limitation. Search for them gen- 
erally shows their presence after attacks of convulsions, but they may persist 
from one attack to the other, or develop spontaneously. In nearly all cases 
these areas are unilateral, and may extend over one-half of 'the body, the 
line of demarcation of the anesthesia or hyperesthesia, from the sound 
area, being clearly and abruptly defined, generally at the median line of the 
front and back of the trunk. It will be called to mind that such conditions 
are absent in true epilepsy. Hallucinations are far more common after 
the fit in hysteria than in epilepsy, and sometimes they even occur during 
the attacks. 

A very useful differential point, strongly insisted upon by Charcot and 
Bourneville, is that in true epilepsy there is generally a very considerable 
rise of temperature during an attack, while in hysteroepilepsy the tempera- 
ture remains normal or only slightly raised. Not rarely malingerers simulate 
attacks of epilepsy, and very serious injuries are sometimes submitted to 
by these persons to carry out their designs. The points to be looked into 
are: the condition of the pupils, which, in the simulated attack, always react 
normally; nor can the corneal reflexes be held back; the color of the face is 
rarely changed, and the thumbs are rarely flexed as they should be. Marc 
has pointed out that in malingerers the bystander can readily straighten 
out the thumbs, and that they remain so; whereas in epilepsy they instantly 
become flexed again. 

Suggestions as to movements are sometimes followed by malingerers, 
and the movements generally lack the bizarre character so typical of epilepsy. 

If tobacco smoke or ammonia be held to the nose of the fraud, he gener- 
ally is forced to disclose his true condition. The fact that in malingerers 
there is no rise of temperature is a differential point. 

Prognosis. — The physician can always assure the patient and friends that, 
so far as the disease itself in its ordinary form is concerned, there is little 
danger of death, since, as a general rule, unless the attacks are very severe, 
death rarely occurs, unless indirectly by the fall of the body into a stream 
or well, or when iii some position where a steady head is necessary for safety. 
Accidental asphyxia, due to the burying of the face in the pillow at night, 
or to the impaction of food in the larynx, may occur, but even this accident 
is uncommon. 

The question which the friends will always ask is: What is the prospect 
of ultimate recovery, or, at the least, will there be any progress toward an 
improvement ? Unfortunately, the reply ought not in any case to be favor- 
able, even for ultimate improvement, for the experience in the past of every 
practitioner has been that cures rarely occur. 



EPILEPSY 1061 

Jacksonian Epilepsy. — By the term Jacksonian epilepsy we mean an 
affection which separates itself from true or ordinary idiopathic epilepsy 
by several peculiarities. By far the most important of the peculiar signs 
is the character of the onset, which always begins, in the typical Jacksonian 
disease, in some peripheral portion of the body, and most frequently in the 
muscles of the thumb or hand, so that for the moment the movements 
are localized and may remain localized at the point of origin, or imme- 
diately diffuse themselves over muscle after muscle until all the arm, leg, 
or other groups of muscles are involved. It is of the greatest importance, 
however, that the reader should keep the aura of an attack separated in his 
mind from the onset, remembering that the term onset is here used by the 
writer to designate the beginning of the period following the aura, if there 
be one. Jacksonian epilepsy may be of almost any degree of severity, for 
in rare cases but one muscle may suffer throughout an entire attack, or in 
others the entire body may be finally convulsed. There may or may not be 
loss of consciousness, its presence or absence being dependent upon the 
severity of the attack. In those instances in which only a few localized 
muscles are involved, consciousness is more commonly preserved than 
lost. 

Petit Mai or Minor Epilepsy.— Petit mal differs in no way in its essential 
characters from epilepsy of a much more highly developed form, but in its 
minor characteristics it is sufficiently at variance with haut mal, or grand 
mal, to separate it in the minds of clinicians. In its most common form 
petit mal consists of a momentary less of consciousness, accompanied by 
pallor, or, more rarely, flushing of the face. The man who is subject to the 
disease suddenly stops what he is doing for a moment or two, and then takes 
up his work or subject as soon as he recovers, and at the point where he 
ceased, being often unconscious of the break in his conversation or labor. 
Reynolds has divided this minor form of the affection into two divisions. 
In the first he places those who are attacked and have no evident spasm, 
and in the second group are those who have evident spasm. The seizures 
are characteristically fugacious, and if any spasm is present it is nearly, 
always of the tonic variety. Sometimes the disorder of motility lies 
chiefly in an inhibition of an act about to be performed. The fork in 
a man's hand at a dinner-table may be raised half-way to the mouth, then 
held in mid-air for a moment, and then, as the attack passes away, continue 
on its journey to the mouth; or, a woman playing the piano may suddenly 
pause with her fingers raised from the keys, miss the time of three or four 
bars, and then go on exactly where she left off, as if no interruption had 
occurred. 

Treatment. — By far the most valuable drug in use to-day for the relief of 
epilepsy is bromide of strontium. In many cases the remedy undoubtedly 
gives relief when it is pushed in a suitable manner, and, in the majority 
of instances, the seizures are so decreased both in violence and frequency 
that its use may be said to be indicated in nearly every case of the dis- 
ease. In a Y ei y small minority, however, it signally fails. 

A very important point to be borne in mind is that the drug often seems 
to have produced a complete cure, and this results in carelessness in the 



1062 DISEASES OF THE NERVOUS SYSTEM 

regularity of administration. The patient should be impressed by the fact 
that every day passed without a fit is a step forward, and that every fit carries 
him many steps backward. He should also be made to use the drug in 
moderation for at least three years after all fits have ceased, and to watch, 
after that time, for the slightest sign of their return. The quantity taken 
each day should be gradually decreased, not suddenly stopped. 

The iodide of potassium is entirely useless in epilepsy, unless it is due to 
syphilis, when it is of the greatest service. Under this condition the bro- 
mides and all other drugs should be set aside while it is pushed to the 
utmost. As is well known, syphilitics usually bear the drug extremely well, 
and the writer knows of one instance where no less than 800 grains were 
taken every twenty-four hours, with rapid improvement as a result. 

When the convulsions are due to a gumma the iodide of potassium is, 
however, too slow in its action, and should be replaced by mercury in order 
to break down the growth without delay, lest a seizure end the scene by 
asphyxia or some similar accident. 

In every case the physician should make careful inquiry as to the pres- 
ence of an aura, and, if it is present, he should order that the patient be 
provided with pearls of amyl nitrite, one of which is to be broken and its 
contents inhaled the moment the warning of an approaching fit develops. 
By this means attacks can often be abortive. 



ECLAMPSIA. 

The term "eclampsia" is applied to convulsions affecting children and 
pregnant women, or women who have just been delivered. 

Infantile Eclampsia. — In infantile eclampsia the attacks are epileptiform 
in character and seem to depend upon a condition of undue irritability of 
the nervous system, which is still further disturbed by some reflex cause. 
Thus, it is commonly supposed that gastric and intestinal indigestion may 
produce infantile eclampsia, and certainly the presence of foreign bodies 
in the stomach and intestines may act in this manner. Again, many 
physicians believe that the first dentition, by reason of the irritation in the 
gums, may result in such a seizure. A host of other causes of peripheral 
irritation have also been held responsible. Not rarely the underlying cause 
is rickets. It is often stated, in text-books on medicine, that the acute 
infectious fevers are frequently initiated by a convulsive seizure. As a 
matter of fact this rarely occurs in an ordinary child when infected in this 
manner. 

The convulsive attack varies in severity from a mere clinching of the 
fingers and the drawing of the thumb into the palm of the hand to a severe 
clonic or tonic convulsion closely resembling epilepsy or hysteroepilepsy. 
In many instances the child has a single attack and no more. In other cases 
several attacks occur within a few days. In still others the occurrence of 
one or more attacks of convulsions seems to develop a convulsive habit, and 
in these instances the child may become a confirmed epileptic. In such 
cases, however, it is probable that the condition of indigestion, or other 



ECLAMPSIA 1063 

direct cause, simply induces a nervous explosion on the part of a brain, which 
has an impaired stability. 

Diagnosis. — The condition must be separated from the convulsions pro- 
duced by organic cerebral disease (which see). 

Prognosis. — The prognosis in infantile eclampsia is good for single attacks, 
and becomes grave in direct proportion to their severity and repetition. Such 
attacks occurring in feeble, poorly nourished children are more grave than 
in those who are better able to withstand an illness. 

Treatment. — This consists in removing the cause of local irritation, if it 
can be found. If it exists in the stomach or the bowels, it should be removed 
by an emetic or a purge. If the gums are inflamed they should be lanced. 
If rickets is the cause it must be cured if possible. 

The treatment of the attack itself consists in the administration by the 
mouth, if swallowing is possible, of 5 or 10 grains of bromide with from 
2 to 4 grains of chloral, or by the use of 20 grains of sodium bromide with 
5 grains of choral in starch-water, by the rectum. If laryngeal spasm is 
marked, and is a dangerous symptom an inhalation of nitrite of amyl may 
be used, or chloroform may be employed if the heart is not weak. 

Puerperal Eclampsia usually occurs in young primiparse. The convul- 
sions are tonic and clonic. The pathology of the condition is not under- 
stood. Without doubt the condition is toxic. In some instances it is probably 
due to perverted functional activity, or actual disease, of the kidneys. 
In other instances it seems to be dependent upon perverted metabolism. 
Not infrequently, in association with the albuminuria of pregnancy, there 
is albuminuric retinitis, and even blindness with general anasarca. That 
the presence of foetus in utero exercises some influence is shown by the 
fact that not infrequently the convulsions cease as soon as the uterus is 
emptied. 

Puerperal eclampsia is an exceedingly dangerous condition. The mor- 
tality varies from 20 to 30 per cent., or even more than this. In a certain 
proportion of cases it can be prevented, and for this reason the physician 
should repeatedly examine the urine of the pregnant woman for several 
months before the termination of pregnancy to determine that the kidneys 
are carrying out their eliminative function properly. 

Treatment. — The uterus must be emptied, the poisons must be eliminated, 
and the nervous system must be quieted. For the best method of emptying 
the uterus, the reader is referred to books upon obstetrics. If arterial tension 
is high and there is much cyanosis, the patient should be freely bled and 
the intravenous injection of normal saline solution employed, unless there 
is a tendency to pulmonary oedema, when the intravenous injections should 
not be used. Copious irrigation of the large bowel or the injection of an 
ounce of magnesium sulphate dissolved in a half-pint of water and 2 
ounces of glycerin are also useful. If the convulsions are severe in these 
cases many physicians treat the condition by the use of large doses of 20 to 
30 minims of the tincture, or even of the fluid extract, of veratrum viride, 
giving it in some cases hypodermically. This drug lowers arterial tension, 
quiets the spinal cord, and produces sweating. Pilocarpine is never to be 
employed, as it almost invariably causes pulmonary oedema. 



1064 DISEASES OF THE NERVOUS SYSTEM 



TETANY. 

Tetany is a condition in which intermittent unilateral or bilateral tonic 
and painful spasm affects certain muscle groups, usually of the upper limbs, 
although occasionally it involves the legs as well. It is sometimes called 
"tetanilla," or "idiopathic muscular spasm/' The disease is exceedingly 
rare in America, but comparatively common in certain European countries, 
notably Sweden and Austria. It is probable that tetany is merely a symptom 
of several different conditions. One type of it occurs in epidemic form in 
Austria, particularly during the months of March and April, affecting 
chiefly youths between fifteen and twenty-five years of age. These persons 
usually belong to the lower walks of life. Occasionally it develops in women, 
particularly at the time of pregnancy or during nursing. A very few cases 
have been reported in children below puberty and in persons of advanced 
years. 

Etiology. — In the opinion of many persons tetany is due to autointoxica- 
tion or to intoxication due to some infectious agent. Thus, it has been 
frequently reported as occurring in persons who are suffering from chronic 
gastrointestinal disorders, particularly cases of gastric dilatation, and it has 
occurred in such cases after the gastric contents have been removed by 
lavage. It seems to be more frequent in persons who follow certain occu- 
pations than in others. Thus, out of 314 male patients mentioned by Frankl- 
Hochwart no less than 141 were shoemakers and 41 were tailors. This 
has caused certain persons to believe that certain types of tetany were of the 
nature of an occupation neurosis. Tetany sometimes develops in those 
who have suffered partial or total extirpation of the thyroid gland. It is also 
met with in children who are suffering from rickets. In some cases tetany is 
a manifestation of hysteria. 

Pathology and Morbid Anatomy. — As the condition is a functional one, 
and as few of these cases come to autopsy, we know little concerning their 
morbid anatomy. In a few instances autopsy has revealed hyperemia and 
minute hemorrhages in the anterior cornua of the spinal cord, but it is very 
doubtful if these are characteristic of the malady. 

Symptoms. — The prodromal symptoms of tetany are usually those indica- 
tive of a toxaemia. The patient first suffers from some aching or pain in the 
extremities, and may have headache and dizziness, and feel heavy and stupid. 
As already stated, the disorder usually affects one or both arms and involves 
in particular the muscles of the forearms and hand, causing the palm of 
the hand to be flexed upon the wrist while the fingers are extended. Some- 
times the forearm is flexed at the elbow. In other instances the phalanges 
are flexed and the distal phalanges extended. When the lower extremities 
are affected, the feet and toes show somewhat similar contractures. The 
toes may overlap one another and be forcibly flexed, and the foot may be bent 
at the ankle in the position of clubfoot. Occasionally, in very severe cases, 
some of the muscles of the trunk and those of the neck and throat may be 
involved, and even the ocular muscles may contract, so that a form of nys- 
tagmus is present. It is a noteworthy fact, first enunciated by Trousseau, 



TETANY 1065 

that pressure exercised upon the affected limb will generate an attack, pro- 
vided that the nerve trunks or the bloodvessels are affected by the pressure. 
This is known as "Trousseau's symptom." The pressure must be continued 
from thirty seconds to five minutes to produce an effect. While the presence 
of Trousseau's symptom is pathognomonic of tetany, its absence does not 
disprove the presence of the disease. 

Under the name of "Trousseau's sign" tapping of the nerves of the arms, 
or legs, when surrounded by an elastic band, may induce the spasm. 
Spasm may also be induced if the facial nerve is irritated in this manner 
(Chvostek's sign). Under the name of "Erb's sign" lies the fact that the 
motor nerves manifest a marked increase in electrical irritability, particularly 
with the galvanic current. Hoffmann has pointed out that the superficial 
sensory nerves are also exceedingly sensitive, and that moderate pressure upon 
them, which ordinarily would not be felt, may cause a severe pain similar to 
that produced by striking the ulnar nerve at the elbow (" Hoffmann's sign"). 
If the irritation of the motor nerve is repeatedly produced, a marked increase 
in the excitability of the tributary muscles follows. Occasionally, nervous 
lesions appear in the skin such as urticaria or herpes, pigmentation, and loss 
of the hair and nails. An attack of tetany may last from a few minutes to 
several days. It may be so moderate that it can be overcome by the will of 
the patient, or so severe that the limb is entirely beyond control. If an 
attempt is made to reduce the spasm by force it causes great pain, and if the 
contractions of the muscles are marked and cramp-like the pain is also 
severe. The attack passes off gradually and is often followed by impaired 
sensation and loss of power in the affected parts. There is no loss of con- 
sciousness in the great majority of cases. 

Diagnosis. — The development of comparatively localized tonic spasms 
in association with the other symptoms already described renders the diag- 
nosis of tetany quite easy. The disease must be separated from Jacksonian 
epilepsy and hysteria. This can be done by the development of Trousseau's, 
Chvostek's, and the other signs just named, by the absence in tetany of the 
various stigmata, including the reversal of the color fields, found in hysteria. 
It is differentiated from Jacksonian epilepsy by the prolonged character of 
the attack and the fact that it can be produced at the will of the physician. 
Hysterical contractures sometimes assume the form of tetany, and cases of 
apparently true tetany may have hysterical features. 

Prognosis. — The prognosis as to life is good unless the provoking cause 
is in itself serious, as, for example, when the thyroid gland has been removed. 
In other words, in no instance does tetany itself threaten vitality, although 
the underlying cause of the tetany may. Most cases recover. Some 
suffer from only one attack. In others the symptoms disappear after many 
attacks as soon as the cause is removed. 

Treatment. — This deals largely with the removal of the exciting cause. If 
gastric dilatation is present and if its nature is such that it can be benefited 
by lavage or operation, these measures must be instituted. In some instances 
where there is reason to believe that the condition results from autointoxi- 
cation, mild saline purgatives, diuretics, and moderate doses of calomel or 
blue mass are advisable, and, in addition, hot packs may be given to aid in 



1066 DISEASES OF THE NERVOUS SYSTEM 

the elimination of poisons by the skin and to act as nervous sedatives. 
When disease of the thyroid gland is present, the administration of thyroid 
extract is indicated. If there is present a general condition of debility, 
anaemia, iron, arsenic, and similar tonics combined with an out-door life and 
avoidance of nerve irritation are essential. 



LATAH. 

Latah is a state very closely allied to the saltatory spasm described by 
Bamberger, and the patients described by Beard as "jumpers." The chief 
symptom of latah is involuntary and uncontrollable mimicry by the patient 
of everything she sees or hears. There is also frequent coprolalia or the 
spasmodic ejaculation of filthy words. The disease is common among the 
Malay races, and its geographical distribution corresponds with the countries 
inhabited by these people. It occurs commonly enough among the Filipinos 
and is known by the Tagalogs as " mali-mali." It is seen in Ceylon and 
Burmah, and the disease known in Siberia as " myriachit " is probably 
identical with it. Kraepelin allies latah with hysteria. 

The subjects of latah are almost invariably women in early adult life. 
Men rarely, if ever, suffer from the disease. There is a distinct hereditary 
tendency, but the cases show no evidence either of hysteria or epilepsy. It 
is a very common spectacle indeed, in Malay villages, to see one of these 
unfortunate women pursued by a crowd of tormenting boys. They dance 
in front of her, going through all sorts of grotesque and obscene movements, 
and the unfortunate victim, apparently struggling to the utmost to resist 
the impulse, exactly imitates all their actions to her own great rage and 
mortification. Besides such examples of complete echochinesia, or mimicry 
of motion, there frequently is echolalia, or mimicry of speech. When startled 
or frightened these patients utter irrelevant words or incoherent noises 
and make involuntary movements. Consciousness is never lost during 
these attacks. This latter type closely resembles the "jumping Frenchmen " 
of Maine and Canada, who jump violently and suddenly with a loud cry when 
startled or when under strong emotion. Jumpers, and latah patients as well, 
will frequently obey any sharp, sudden command given them. Undoubtedly, 
this represents some form of psychic suggestion acting on a weak and unstable 
will. The Malay is notoriously unstable in his mental makeup, and the 
patients are markedly neurotic. They are pusillanimous and easily startled. 
As a rule, both the superficial and deep reflexes are increased. Many of 
these patients suffer later from serious mental disorders. Among the Philip- 
pine natives " mali-mali" patients are believed to be particularly prone to the 
outbreaks of maniacal furor known as amok. 



AMOK (RUNNING AMOK). 

This term is used, in Malayan countries, to designate cases of maniacal furor 
in which a native rushes out in the streets of his village with kris or barong, 
cutting down every one in his path, until he himself is dispatched or com- 
mits suicide. It is a question whether these outbreaks should be considered as 



ASTASIA-ABASIA 1067 

evidences of a specific disease. Preceding the attack the patient is in a 
stupid, morose, or melancholic condition for several days. During this 
period there frequently is amnesia, and during the attack itself complete 
amnesia is the rule. The exciting causes of the outbreak are usually 
psychical ; grievance over some real or fancied wrong, over financial losses, 
marital difficulties, fear of disgrace or punishment, and the sight or smell 
of blood. The disease almost always attacks young adult males. Vari- 
ous causes have been advanced for this condition. Alcoholism may be 
excluded, as the Malay, although not a total abstainer, is very frugal in the use 
of liquors. So, too, opium smoking cannot be considered the cause of the dis- 
ease. Bevan Lewis believes it to be a psychical epilepsy, and, indeed, transi- 
tory furor very much resembling the attacks of amok are frequently seen in 
epileptics. Earlier travellers and writers ascribed these attacks to religious 
mania. Schuebe discredits this idea on the ground that the Koran does not 
justify the killing of unbelievers, and he quotes Ellis to the effect that amok- 
running occurred among Malays before they were converted to Mohamme- 
danism. The Malayan races chiefly subject to amok are the Bugis, Illanums, 
and the Sulus, or Joloanos, in the Southern Philippines. In many instances 
among this last tribe the motive is undoubtedly religious. During the service 
of the United States army in the Philippines a most melancholy case occurred 
in an officer, corresponding exactly to the typical amok cases. This man, 
an excellent soldier, and a man of exemplary personal habits, after a few 
days of brooding and melancholy, suddenly appeared on the veranda of 
his quarters with a rifle and began to shoot into his company formed up in 
close proximity. He could not be secured, and after wounding a number 
of his men he was shot and killed by one of his own sergeants. With regard 
to the responsibility of these cases no general rule can be laid down. The 
responsibility cannot be affirmed in all cases, nor can it be denied. Most of 
the cases of amok are clearly irresponsible. Mention has been made, under 
Latah, of the occasional outbreaks of furor resembling amok that take place 
in that disease. 

According to Kraepelin, who has studied this condition in Java very 
recently, amok is not an entity, but embraces a variety of conditions in 
which sudden, violent, impulsive acts are committed while consciousness 
is clouded. Some cases belong to the class of the "insanity of adolescence," 
some are epileptics, a few may be instances of "malarial psychosis," but there 
are rare cases of amok that Kraepelin cannot explain. Latah is distin- 
guished from it by the complete preservation of consciousness in that state. 



ASTASIA-ABASIA. 

Definition. — Astasia-abasia is a symptom of hysteria. It occasionally 
follows disturbance of the nervous system produced by injury, and in that 
sense might be considered a traumatic neurosis. Occasionally it has fol- 
lowed the acute infectious diseases. 

Symptoms. — The symptoms consist in a partial or complete inability to use 
the lower limbs in standing or in walking, although if the patient lies upon 



1068 DISEASES OF THE NERVOUS SYSTEM 

her back in bed she can move her legs perfectly. Examination fails to reveal 
any alteration from the normal as to motion, co-ordination, or sensation. 
When the condition simply interferes with walking, it is called "dysbasia." 
Patients who may be quite unable to walk can, nevertheless, swim perfectly. 
The prognosis is as favorable as that of ordinary hysteria, and the 
treatment is the same as that which is employed for patients who are 
suffering from hysteria or neurasthenia. 



NEURASTHENIA. 

Definition. — Neurasthenia is a condition in which the nervous system 
suffers from various functional disorders due to excessive mental and ner- 
vous stress and strain whereby the energies of the patient are exhausted. 
For this reason it is often called nervous exhaustion. 

Etiology. — The most common cause of neurasthenia in men is pro- 
longed mental strain produced by business reverses or the carrying through 
of some important and difficult enterprise. The severity of this strain is 
by no means always in direct proportion to the size of the undertaking. 
The condition is not met with in the lower classes except occasionally, and 
is largely dependent upon the nervous temperament of the individual and 
the condition of his general health and surroundings. In women the condi- 
tion is commonly met with as a result of excessive social duties, as after a 
winter season devoted to late balls and receptions, or it occurs in those who 
have passed through a long period of nervous strain resulting from the 
nursing of a sick husband, child, or some near relative, whereby there is not 
only physical exhaustion but mental anxiety to exhaust reserve energy. It 
is evident, therefore, that many causes may produce this condition pro- 
vided they result in a great expenditure of nervous energy with so little sleep 
that rest cannot be obtained. 

Every individual may be said to possess two funds, or sources, of nervous 
energy. From one of these he takes daily that force which is necessary for 
the performance of his physiological functions and labor. The second fund 
is kept in reserve to meet the demands "of extraordinary occasions and is 
maintained, as is the reserve fund of a bank, to meet conditions which are 
abnormal. The patient who suffers from neurasthenia is one who has not 
only expended his ordinary fund, but drawn so largely upon his reserve fund 
that he is a nervous bankrupt, and he suffers from a large number of more 
or less serious symptoms because the various parts of his body do not 
receive enough nervous energy to cause them to perfectly perform their 
normal functions. If the strain has been very profound and severe, and 
the patient is one whose nervous balance is not very stable, it can be 
readily understood that a very serious state may develop, and that the life 
of the patient may be jeopardized if any intercurrent disease develops. 

Symptoms. — The symptoms of neurasthenia are exceedingly varied, 
depending in many instances upon the organ, or organs, which are chiefly 
affected by the state of nervous exhaustion. In some cases the mental con- 
dition of the patient suffers chiefly and the symptoms may vary from mere 



NEURASTHENIA 1069 

irritability of temper to great mental depression and even to mental aberra- 
tion, in the form of melancholia or even actual insanity. Sometimes per- 
sistent insomnia develops. In other instances the functions of the digestive 
tract suffer chiefly, and in others the heart displays the greatest evidence 
of disturbed nerve supply, so that attacks of palpitation ensue, or instead 
a lack of vasomotor control results in attacks of vertigo or syncope. In 
addition to these definite and specific symptoms the patient often com- 
plains of a host of subjective symptoms which are quite extraordinary in 
character. In spite of the variability of symptoms the following are con- 
stantly met with: sense of chronic fatigue, of exhaustion, and irritability. 
Hysteria is not infrequently associated with neurasthenia. 

Diagnosis. — The physician should never reach a diagnosis of neurasthenia 
until by repeated examinations and study of the patient, and his secretions, 
he is convinced that no grave organic disease exists which may be responsi- 
ble for the symptoms presented. If cardiac and renal disease are excluded, 
and no other organic malady can be found of sufficient gravity to produce 
the illness, and if the history of the patient reveals the existence of some 
cause capable of producing nervous exhaustion, the diagnosis of neuras- 
thenia may be reached. 

Prognosis. — The prognosis of neurasthenia depends upon the ability of 
the physician to remove the patient from exposure to the causes which have 
produced the condition, upon the ability or willingness of the patient to 
follow those methods of life which are conducive to the re-establishment 
of nervous balance and reserve energy, and upon the age and general physical 
state, for if the patient be one who is far advanced in years, or who by reason 
of disease or heredity is possessed of low recuperative power, it is manifest 
that complete recovery may be impossible. Given a case of neurasthenia 
in which all the conditions which are unfavorable may be excluded the 
prognosis is favorable, but the physician must be cautious in stating the 
duration of the period of recovery, for the progress toward health is 
governed not alone by the skill displayed in treatment, but by the recuper- 
ative power of the individual, a power which every physician of experience 
recognizes as a very variable quantity. Not rarely a seemingly frail 
person recovers speedily, whereas another patient of a more powerful 
build and physique makes progress so slowly as to cause great discourage- 
ment. 

Treatment. — From what has been said of the causes of this condition it 
is manifest that the chief aim of the physician must be the re-establishment 
of the normal nervous energy or power. As first pointed out by Weir Mitchell, 
this can only be obtained by the accumulation of energy, and this accumula- 
tion of energy is to be had only by absolute mental and physical rest on the 
one hand and proper feeding on the other, the circulatory and other vital 
functions being maintained by passive exercises and electricity. The patient 
must so arrange his or her affairs that no business worries or family cares 
will be experienced. For this it is essential that the treatment shall be 
carried out in a health resort far removed from the home and office, or in a 
hospital or "rest-cure house," where the patient will be absolutely isolated 
from ordinary surroundings. An attempt to carry out the "cure" at home 



1070 DISEASES OF THE NERVOUS SYSTEM 

nearly always ends in failure, because the needed degree of mental discipline 
is not obtainable and the sounds made by the rest of the family annoy the 
patient or develop curiosity or worry as to their cause. It is also essential 
that a skilled trained nurse shall be in absolute control of the patient without 
any interference by members of the family. The patient is not allowed to 
sit up, but is required to remain in bed at perfect rest. The action of the 
kidneys, bowels, and skin is carefully looked after by suitable remedies, 
and once every day massage is given over the entire body to give the effects 
of passive exercise. In many cases it is well to give massage in the afternoon 
and faradic electricity in the morning, the slowly interrupted current being 
employed to exercise the muscles, and this in turn followed by a general 
application of the rapidly interrupted current from the head to the feet for 
fifteen minutes. These measures combined with a cool sponging in the 
early morning and an alcohol rub at bedtime, with the administration of 
small quantities of food every three hours, will usually cause the patient to 
complain of being "too busy" instead of feeling, as they state they will 
feel at the beginning of the "cure/' that time hangs heavily on their hands. 
The patient must not receive or write letters nor must she read, since 
this requires not only nervous but muscular strain. In some cases the 
nurse is permitted to read aloud to the patient for an hour a day. Under 
such a plan of treatment, in which all the nervous energy which it is possible 
to conserve is secured, and in which every opportunity is offered for the 
addition of units of force by proper feeding, lasting and complete recovery 
is usually obtained. 



TRAUMATIC NEUROSES. 

Definition. — Under the term traumatic neuroses there is described a con- 
dition in which an individual, after exposure to some severe mental shock 
or physical injury, develops a train of symptoms which do not depend 
upon any demonstrable lesion of the nervous system. As the result of 
functional disorder of the nervous system in various parts of the body, fol- 
lowing the accident, the patient presents symptoms which are chiefly sub- 
jective, though they may be somewhat objective, and he may be actually 
and completely incapacitated from performing the ordinary acts of life for 
a long period of time. Rarely the disability may be permanent, but in 
these cases the question always arises as to whether there has not been in 
addition to the functional disturbance an actual organic lesion. It is evident, 
therefore, that cases of this character may, and do, present to the physician 
very difficult problems in differential diagnosis, for not only may functional 
disorders exist side by side with those due to true organic change, but in 
addition the functional disturbances may simulate organic disease so closely 
as to cause great confusion in symptomatology. When to these natural 
difficulties are added the desire of the patient to obtain heavy damages 
from the individual or corporation responsible for the injury, it at once 
becomes evident that malingering or unintentional and subconscious pro- 
duction of symptoms may be commonly met with. 



TRAUMATIC NEUROSES 1071 

Etiology. — The most common cause of traumatic neuroses are railroad 
accidents, trolley-car accidents, falls, and injuries received from falling 
bodies. As a result of exposure to one of these causes, with associated mental 
shock due to terror or horror, the nervous system develops the perversions 
about to be described. 

Symptoms. — It is manifest from what has already been said that the symp- 
toms may be most varied as to severity, distribution, and duration. Prob- 
ably the most common statement of the patient is that he has lost power 
in one or more parts of his body, or he may suffer from disturbances of 
sensation, with or without loss of power. In males it is not infrequently 
claimed that the injury has resulted in a loss of sexual power, particularly 
if the back has received a blow or strain, even if the genital apparatus 
is itself entirely unaffected. In women the most common complaint is of 
pain or weakness in the back, of pelvic pain or displacement of the pelvic 
organs, and of vesical disorders. In other cases the chief claim is that more 
or less violent pain or tingling in the limbs is suffered. When loss of power 
is suffered from it appears usually as a hemiplegia or a brachial monoplegia, 
but if it be a hemiplegia the face nearly always escapes. Paraplegia is very 
rare and the sphincters of the bladder and rectum always escape. 

Those paralyses which are not truly organic can be separated from those 
that are such by the facts that the reactions of degeneration do not develop 
in the paralyzed parts and the deep reflexes are usually preserved. Anaes- 
thesia is practically always present if the paralysis of motion is complete, 
and it is of the type of hysterical paralysis in that it has often a sharp line 
of degeneration which is not coincident with the distribution of the sensory 
nerves of the part. Paraplegic cases do not suffer from anaesthesia of the 
genital organs. Again, it sometimes occurs that the symptoms complained 
of are not constantly in the same part or that positive suggestions may 
cause their development elsewhere. Not rarely an examination of the 
color fields of such a patient will reveal the reversals commonly found in 
hysteria. Disorders of all the special senses may also occur and total dis- 
appearance of these functions may take place — as complete deafness, blind- 
ness, or loss of taste or smell. Occasionally the patient may develop attacks 
which resemble to some degree ordinary epilepsy or catalepsy, but these 
attacks are separated from true epilepsy by the points already named when 
discussing that disease. 

If we carefully exclude from any case of nervous disorder following an 
injury the presence of an actual organic lesion, we may unhesitatingly state 
that the patient is suffering from hysteria or neurasthenia due to injury, 
and we can treat him accordingly. On the other hand, it is not to be for- 
gotten that the patient who suffers from the symptoms he describes is often 
a most miserable and unfortunate individual, as deserving of our pity as if 
we found him the victim of an incurable malady due to destruction of a 
part of his body. His functional disorders are as real to him and cause him 
as much suffering as if they depended upon organic causes, and a nervous 
system functionally perverted may be as useless as one actually grossly 
diseased, just as a watch which needs regulating may be as useless to its 
owner as one in which a spring is broken. While, therefore, it is our duty 



1072 DISEASES OF THE NERVOUS SYSTEM 

to relieve such patients by every means in our power, and to bear in mind 
that their sufferings are often very real, we are forced to recollect that the 
condition may not be permanent, as it would be after a destructive injury, 
and so when the case has become one of medicolegal importance it may 
not be possible to testify that the patient is incurable and permanently 
disabled. Not only is this true, but it is also a fact that the very continuance 
of litigation, and the frequent appearance of the patient before attorneys 
and experts for both sides and before a crowded court-room, may make 
recovery impossible by still further exciting and disturbing nervous balance, 
for aside from this form of excitement the description of the scene of the 
accident impresses its terrors, over and over again, upon a mind already 
horror-stricken by the original occurrence. Perfectly sincere persons often 
suffer all the symptoms they describe up to the period when the trial of the 
case is finished and then speedily improve. 

Treatment. — The treatment varies, of course, with the character of the 
symptoms, but it may be said to be practically identical with that already 
advised in cases of hysteria and neurasthenia. 



OCCUPATION NEUROSES 

An occupation neurosis is a state in which the innervation of a part 
becomes functionally disturbed by the exhaustion of the nervous centres 
supplying it, and in all probability by exhaustion of the nerve endings as 
well. The causes of this exhaustion are exceedingly numerous. Almost 
every pursuit in life which involves the continuous use of muscles of the 
hand and wrist may produce an occupation neurosis of these parts. As a 
result we find spasm, cramp, or palsy developing to such a degree as to 
incapacitate the patient. The most common neurosis, because the pursuit 
is most common, and because small and accurate movements are required, 
is that due to writing, the so-called scriveners' palsy or writers' cramp. 
Another form is telegraphers' cramp, and a third is hammerers , palsy. 
Less common forms are violinists' cramp, pianists' cramp, flute-players' 
cramp, and "sewing spasm." Milkers and cigarmakers sometimes suffer 
from neuroses of this character. In writers' cramp the flexor muscles 
suffer chiefly, while in telegraphers' cramp the extensors are the ones most 
involved. Various disorders of sensation in the hands are also present and 
consist in sensations of tingling, tension, or numbness. Localized sweating 
or excessive dryness of the skin may be present. Occasionally the condition 
depends upon, or is associated with, a true neuritis, which may involve the 
entire brachial plexus and cause pain in the upper arm and even in the 
muscles of the neck and head on the affected side. The history of the case 
in many instances is that the patient first experiences for some days a feeling 
of stiffness and lack of pliability in his fingers, which is generally accom- 
panied by a certain lack of co-ordination in the movements required. This 
inability to move the fingers rapidly and accurately is only present when 
the sufferer attempts to perform the movements which are the cause of the 
trouble, and almost all other motions can be gone through with without 



OCCUPATION NEUROSES 1073 

difficulty. If the patient now insists on keeping on with his duties, the 
stiffness is replaced by violent cramps, more or less painful, which come on 
suddenly and with considerable power. Co-ordination is still further dis- 
ordered, and all attempts at a repetition of the offending act are resented 
by the affected centres and muscles in such a positive manner as to make all 
movements irregular and often jerking in character. Unless absolute rest 
and avoidance of former movements is permitted, the cramps, etc., are 
followed by loss of power, deepening into partial paralysis. Even when 
paralysis exists, however, it is surprising to see how many unoffending 
movements can be performed without discomfort and failure. 

Some discussion has arisen as to whether the several symptoms which 
the disease presents are each in their turn an indication of a more advanced 
stage in the disorder or are merely more prominent in one case than another 
by chance or tendency on the part of the individual to any one of them. 
Thus, some observers have held that the first sign of the disorder was the 
feeling of distress or fatigue in the overworked extremity, and that the tremors 
followed because the warning given by the fatigue was not heeded. Finally, 
the disregard of this second symptom brought about the spasm or cramp, 
or, in other cases, the palsy. Other writers, especially those of the present 
day, have attempted to prove that there is no distinct onward march of the 
symptoms from fatigue to tremor and from tremor to palsy or cramp, but 
rather that the disorder is to be divided into four varieties, each one of which 
may assert itself without the development of another. 

Thus, Lewis tells us that in some cases cramps come on, in others palsy, 
and in others tremors, while still another variety is separated from its fellows 
by the predominance of certain symptoms associated with disturbances of 
sensation. He states, however, that the disorder of sensation is always 
present in all forms of the trouble in some degree, and that it is only in cases 
where the trouble consists in a neuritis that the symptom rises to the impor- 
tance of marking a separate variety. 

Many very prominent writers on scriveners' and hammerers' palsy assert 
that predisposition is one of the prime factors in the causation of these 
maladies. While this is doubtless true to a certain extent, it is nevertheless 
a fact that all persons, be their temperaments nervous or otherwise, are 
affected, and in view of this fact the writer thinks that predisposition should 
not be accorded the leading position in the causation of the malady. It is, 
of course, probable that persons whose temperaments are nervous and 
excitable are naturally susceptible to nervous disorders, whereas the phleg- 
matic temperament is rather opposed to the conditions which are necessary 
for the presence of this disease. 

Rosenthal calls attention to the fact that the loss of power is limited 
entirely to those centres which are the directors of the particular muscles 
involved, and states in substantiation of this assertion that the surrounding 
centres for other groups of muscles always escape, as is proved by the fact 
already mentioned, that other acts can be performed without difficulty. 
While it is true that the surrounding centres are not affected, it is also true 
that the centre governing like movements in the opposite hand is, by sym- 
pathy or other cause, affected with its fellow to a certain extent. This is 
68 



1074 DISEASES OF THE NERVOUS SYSTEM 

proved by the fact that if the operator learns to send messages with this well 
hand, that hand very soon follows the fate of its fellow. 

Experiments performed by the late Dr. N. A. Randolph bear so strongly 
on this subject that they may be quoted at this point. His object was to 
discover if exhaustion of one centre in the brain produced any effect on 
the corresponding centre on the opposite side of the brain; and to this end 
he proceeded as follows: He attached a small lever to a meter, and resting 
the hand of the subject on the table, as when writing, he directed him to 
place the tip of his forefinger on the end of the lever and to depress it as 
often as he could. Each depression was, of course, registered in this way. 
Dr. Randolph found that, normally, the right forefinger possessed power 
for 100 movements, the left forefinger for 75 movements. Having decided 
this primary point he proceeded to search after the main object of his exami- 
nation. He found that if the left forefinger was set to work after the right 
forefinger had performed its 100 depressions, it became exhausted at 50 
movements, and that if the right hand was set to work after the left fore- 
finger had moved 75 times it could only move 75 times. In other words, 
exhaustion of one centre produced exhaustion of the corresponding centre 
on the opposite side of the brain. 

Careful tests prove that in most instances exaggerated reflexes are 
present, denoting a superexcitability of the spinal cord, and in other cases 
evidences of neuritis of the nerve trunks have undoubtedly been observed. 
In .some cases of the disease a species of pseudomuscular hypertrophy comes 
on, due, probably, to some centric nervous lesion, and, perhaps, in part to 
the congested condition which is nearly always present in the affected mus- 
cles. Thus we find the bellies of the muscles hard, firm, and projecting, yet 
devoid of power. 

Treatment. — In the way of treatment rest is the best measure that we 
possess for the cure of the affection; but although absolute rest from the 
exciting cause is one of the essential factors for a complete recovery, the 
affected arm should be used in every other motion which is natural and easy, 
so that it may not become useless from disuse. Next to rest we have as a 
therapeutic agent electricity, which is, however, only indicated in those 
cases where very slight or no inflammatory conditions are present, either in 
the muscle, nerve, or nerve centre; and it should be the invariable rule to 
use that current which causes the most contraction with the least pain. 
Galvanization of the affected muscles should be performed in such a way 
that the disordered nerve centres are not disturbed, and care should be taken 
to gradually increase the exercise, so as not to exhaust or overfatigue the 
muscles which are out of order. Movements which are slowly performed 
with the affected parts are also useful, following the method of muscle train- 
ing proposed by Fraenkel in the treatment of locomotor ataxia. 

Finally, the administration of tonics, such as arsenic, iron, and strychnine, 
is to be resorted to, and these measures combined with massage are the 
best methods we have for effecting a cure. 



ANGIONEUROTIC (EDEMA 1075 



RAYNAUD'S DISEASE. 

Definition. — Raynaud's dsiease is a condition in which one or more of the 
fingers or toes, and rarely the nose and ears, suffer from a disorder of the 
local bloodvessels, with the result that these parts become bloodless and 
pallid or slate colored and mottled in appearance. The affected parts are 
cold and sometimes painful. The malady usually affects persons under 
thirty years of age, and females more commonly than males. The cause 
is unknown save that it seems to be of the nature of a paroxysmal neurosis 
involving the bloodvessels of the parts affected. Various conditions, all of 
them capable of causing a loss of normal nerve tone, have been considered 
as etiological factors, varying from diabetes and neurasthenia to fright and 
exposure to cold air or cold w^ater. 

Etiology. — The onset begins with a sense of tingling, or of heat or cold, 
in the parts which are to suffer from the well-developed state. The skin 
looks shrunken and ashen in hue and numbness is present to a more or less 
well-developed degree, but complete anaesthesia does not occur. The con- 
dition may last for a few hours or for weeks. When it disappears it nearly 
always returns in a short time. 

When the disease occurs in its severe form local gangrene may ensue. 
The part becomes livid and dusky and small blebs develop on the fingers. 
These may dry up and recovery take place, only the skin being destroyed, 
or the process may become so deep that the entire part may be lost. 

This condition is to be separated from senile gangrene by the youth of 
the patient, from frost-bite by the absence of a history of exposure to cold, 
and from chronic ergotism by the absence of any history of eating rye 
bread contaminated by ergot. 

Treatment.— -The treatment consists in the use of tonics and every possible 
measure designed to re-establish good general health. Hydrotherapy is 
often of value. Locally the nutrition of the affected part may be maintained 
to some extent by the use of dry or moist heat. Great care should be taken 
to protect those parts which are usually affected, from extremes of heat and 
cold. 

ANGIONEUROTIC (EDEMA. 

Definition and Symptoms. — Angioneurotic oedema is a condition charac- 
terized by the sudden appearance, in a limited area in one or more parts of 
the body, of well-defined swelling due to some perversion of the normal 
functional activity of the vasomotor nerve supply, so that the bloodvessels 
of the part become dilated, and, in all probability, an extravasation of fluid 
takes place. The condition is to be clearly separated from that character- 
istic of inflammation. The temperature of the part is often lower, but 
sometimes it is higher than normal. The dimensions of the affected part 
vary greatly, but it is rarely more than a few inches in circumference. The 
hue of the area affected may be a deep red, as if suffering from intense 
congestion, or so pallid as to be cadaveric, It may be the seat of a sense of 



1076 DISEASES OF THE NERVOUS SYSTEM 

tingling, or heat, or itching, but actual pain does not occur, and pitting on 
pressure, to the extent that it appears in ordinary oedema, is absent. 

Angioneurotic cedema occurs most commonly on the face or hands. It 
may affect the body and quite rarely the larynx and pharynx, when it may 
produce alarming symptoms by interfering with respiration. Instances of 
death due to this cause have been reported. The attacks last a few hours 
to several days, and are prone to occur at irregular intervals. 

Angioneurotic cedema occurs more frequently during the third- decade 
of life than at any other period, and in the United States affects females 
more frequently than males, although the reverse of this holds true in Europe. 
We do not know what the causative factor is, but it is known that exposure 
to cold and causes which diminish nervous tone bring on an attack in those 
who are susceptible. 

In some cases the condition is induced by digestive disorders, or by the 
ingestion of some food which is toxic, as lobster, fish, or other animal food 
that is not fresh. In nearly all cases the patient is neurotic, and not rarely 
has a neurotic family history, or even a direct inheritance of the disorder 
from the parents. 

Diagnosis. — Angioneurotic cedema must be separated from the local 
vasomotor disturbances of hysteria. This is done by the fact that in hysteria 
there are associated paralysis of motion or anaesthesia and, it may be, hysteri- 
cal contractures. Again, the cedema of hysteria is often persistent, whereas 
this is temporary. From severe attacks of urticaria it is differentiated by the 
fact that "hives" are usually scattered widely over the body, and if they 
appear on the hands are characterized by multiple lesions. In most cases of 
hives, or urticaria, additional lesions can be produced by rubbing a part. 

Prognosis. The prospect of complete cure in the sense of an escape from 
all future attacks is not encouraging. The general health is usually good 
between the attacks, and unless the part affected be the larynx the prospect 
of any serious result is unlikely. 

Treatment. — The treatment can be directed only along those lines which 
will tend to improve the general health, of which the most useful are an 
out-door life, hydrotherapeutics, and the internal use of tonics, such as iron 
and arsenic if there is anaemia, and nux vomica and quinine if the nervous 
system is atonic. Phosphorus may also be useful. When lithsemic or gouty 
conditions are present, the iodides, salicylates, and colchicum may be of 
great value. It is needless to add that all causes known by the experience 
of the patient to be provocative of an attack should be sedulously avoided, 
for there can be little doubt that the occurrence of one attack predisposes to 
another. 

ERYTHROMELALGIA. 

Definition. — This condition was first described by Weir Mitchell in 1872. 
It consists in a hyperemia of the foot and leg, rarely the hand, associated 
with pain which may vary in degree from a sense of weight and heaviness 
to exceedingly severe suffering. The malady first affects the neighborhood 
of the ball of the foot, and thence it spreads to the entire plantar surface. 



MIGRAINE 1077 

In other cases the heel is first affected. Although exercise greatly increases 
the suffering, it is, as a rule, worse at night. The pain may be intermittent 
or continuous. The skin is often not only hyperaemic, but is often marbled 
or mottled in appearance. Elevation of the part, by decreasing the conges- 
tion, diminishes the pain. 

Etiology. — The causes of the malady are several. In rare instances it 
seems to depend upon lesions in the spinal cord, in others it apparently 
depends upon diabetes mellitus, and in still others arteriocapillary fibrosis 
seems to be the underlying factor. 

Diagnosis. — Before determining the diagnosis of erythromelalgia it is 
essential that gout and diseases of the soft and hard tissues of the foot be 
excluded. In the vast majority of cases the symptoms will probably be due 
to such causes, for true erythromelalgia is a very rare malady indeed, and 
but few cases have been recorded. 

Treatment. — Treatment often fails to give much relief. The part should 
be kept in an elevated posture as much as possible, cool lotions may be 
applied to it, and if the patient be lithsemic the alkalies and salicylates 
should be given. 

MIGRAINE. 

Definition. — Much confusion exists as to the exact nature of the condition 
which is called migraine. By all authors it is used to describe a condition 
of severe pain, more or less limited to one side of the head, often accompanied 
by some disturbance of vision in one or both eyes, and by nausea and vomit- 
ing, which often do not develop until toward the end of the attack. Certain 
clinicians have expressed the belief that migraine is an hereditary affection, 
and even go so far as to regard it as a manifestation of nervous instability 
not far removed from epilepsy. This, however, is certainly incorrect in 
the vast majority of cases. It may be true that certain neurotic individuals 
who are subject to hysterical or epileptic manifestations often suffer from 
migraine. But, on the other hand, it cannot be denied that in the majority 
of instances the condition is a toxic neurosis due to the manufacture and 
retention in the body of abnormal products of metabolism. These products 
are chiefly the result of a disturbed action of the liver, either in the sense 
that the liver fails to destroy poisons which are absorbed from the intestines, 
or in the sense that it develops substances which it does not produce when 
in health. As a matter of fact migraine, as a toxic condition, is rarely the 
result of any disorder of function in a single organ, but is produced by 
several causes, an undue development of poison, a deficient action of the 
liver in destroying these poisons, and a torpid condition of the kidneys, 
whereby toxins are not speedily eliminated. It naturally follows that in high- 
strung, nervous individuals, and in those who have neurotic tendencies, 
these toxic products can readily disturb the functions of the sensory nerves 
of the head and so produce a seizure. 

Among the active causes in provoking an attack of migraine, aside from 
the effects of autointoxication, there can be no doubt that nervous tire, or 
exhaustion, aids materially in causing an attack, particularly if in addition 



1078 DISEASES OF THE NERVOUS SYSTEM 

to such stress there is added undue sexual activity, or other forms of abuse. 
All these factors diminish the nervous energy which supports vital processes 
and so tend to cause perversions of metabolism, and at the same time they 
diminish the resistance of the nervous and vascular system to the action of 
such poisons. 

The disease occurs most frequently in women and rarely develops 
before the age of puberty. It is particularly prone to attack those who 
have a gouty ancestry. Certain schools of ophthalmologists have strongly 
urged the view that all cases of migraine are due to errors of refraction. 
There can be no doubt that in many instances this cause of nervous 
exhaustion is a potent factor. The important point for the physician to 
remember in studying this malady is that various causes may be responsible 
for it; and if the patient is to be permanently relieved, one or more of these 
causes must be discovered and removed. 

Symptoms. — The mode of onset of an attack varies greatly. Some patients 
state that for several days prior to a paroxysm they feel generally out-of-sorts 
and anything but well. Often the chief symptom is mental depression. 
Other patients have no premonitory symptoms whatever. Arising in the 
morning in perfect health, they are seized at some time during the day 
with blurring of the vision in one or both eyes, soon followed by a sharp 
attack of pain, or pain may be the first and only symptom, and its onset 
may be so sudden and severe as to completely incapacitate the patient. To 
this form of migraine the terms "fulgurating" or "fulminant" have been 
applied. In most cases the pain exists chiefly in one side of the head, and 
involves the supraorbital region and the eyeball. When it is fully developed 
the entire head may suffer. The character of the pain is throbbing and the 
sensation in the head is tense. Not rarely photophobia is present, and in 
some cases vision may be so much interfered with that actual hemianopsia 
is described by the patient. In addition to the pain the patient not infre- 
quently has some vertigo, is mentally heavy and dull, and not rarely slightly 
aphasic. 

After the attack has lasted from one to several hours the patient quite 
frequently becomes nauseated and then vomits. As a rule, the stomach does 
not contain undigested food; on the contrary, digestion seems to have gone 
on with undue rapidity. The material vomited is usually small in amount 
and excessively acrid and acid. I am firmly convinced that this fluid is the 
result of an attempt on the part of the stomach to eliminate poisonous 
materials, just as this organ eliminates oxydimorphine in morphine poison- 
ing. If the vomiting persists for any length of time bilious materials may 
be brought up by reason of the drawing of bile through the pylorus in the 
act of retching. It is a question whether this vomiting is the result of the 
action of the poison which produces the symptoms, or whether it is in large 
part due to the severity of the pain which, when it affects the eyeball, closely 
resembles the sickening pain produced by an injury to the testicle. During 
an attack the patient's face is usually pallid and betokens severe pain, 
having an anxious and hunted expression or one of profound depression. 
vSometimes the radial pulse is small and hard, and not rarely the temporal 
artery on the affected side stands out like a whipcord. The attacks rarely 



MIGRAINE 1079 

come oftener than once a week, and sometimes much more rarely than this, 
unless the patient by errors in diet and by various excesses produces the 
provoking condition frequently. Sometimes patients state that the attack 
comes on in the midst of perfect health. Thus, I have heard a patient 
remark that she felt so well that she was sure she was going to be sick the 
next day, as it had been her experience that a sensation of well-being was 
not rarely followed by a nervous explosion. In rare cases a certain degree 
of paralysis of the extraocular muscles may be present during the attack. 
In still more rare instances the face is flushed instead of being pallid. Not 
rarely during the attack the urine is scanty and high colored, but as the 
attack subsides the urine is frequently passed in large quantities and is 
exceedingly limpid. Speedy recovery usually follows the vomiting of the 
acrid fluid already named. 

Treatment. — The treatment depends upon the underlying cause of the 
malady. All excesses as to eating and sexual activity must be prevented. 
If the patient is run down and neurasthenic, a vacation or a rest cure is 
essential. If the kidneys fail to excrete a sufficient quantity of urinary solids 
per day, the various potassium salts, such as the acetate, citrate, or bitar- 
trate of potassium, must be given in 5 or 10 grain doses three or four times 
a day, in copious draughts of water to increase urinary elimination. If 
there are any evidences that the liver is persistently or occasionally inactive, 
its function should be stimulated by the use of calomel, blue mass, or podo- 
phyllin. Many of these cases do very well if 5 to 10 grains of blue mass are 
taken every week or ten days, and then followed by a saline purge. In those 
instances in which the patient leads a sedentary life, active out-door exercise 
to ensure perfect oxidation processes in the body are essential. In those 
patients who suffer from gastrointestinal catarrh, a dose of Hunyadi or 
Apenta water, taken hot and in sips, before breakfast, will often be efficient 
not only in moving the bowels, but preventing the attacks. Often diluting 
one of these waters one-half with hot water makes it an efficient purgative. 
The use of salol in the dose of 5 to 10 grains a day as an intestinal antiseptic 
is often advantageous. 

Of all forms of preventive treatment, that which is devoted to the in- 
creased activiy of the intestines, the liver, and the kidneys is of most impor- 
tance. If the patient is gouty, or suffers from that condition commonly but 
erroneously called "uricacidsemia," not only should the treatment just 
recommended be employed , but the use of other more active salicylates, such 
as the salicylate of strontium in 5 or 10 grain doses three times a day, are 
advisable. If errors in refraction exist, carefully fitted glasses should be 
provided, and if the nasal mucous membrane is hypertrophied or other 
abnormalities exist in this region, they should be treated. For the relief 
of the attack many measures have been suggested. In those instances 
where the patient has prodromal symptoms, a brisk saline cathartic, such as 
Seidlitz powder, citrate of magnesia, or Rochelle salt, should be given, with 
the idea of sweeping out from the bowels poisonous material. This may 
be followed in half an hour to an hour by 2 grains of caffeine with 10 grains 
of bromide of sodium. The best way to give this is in granular effervescent 
salts. In some instances a small dose of phenacetin or acetanilid should 



1080 DISEASES OF THE NERVOUS SYSTEM 

be added. If high arterial tension is present, nitroglycerin is valuable. 
For the relief of the pain when it is very severe phenacetin, antipyrin, and 
acetanilid are useful, but it must always be remembered that the stomach 
is, as a rule, excreting rather than absorbing, and that the mere administra- 
tion of a palliative at this time may be fruitless for this reason. Under these 
circumstances it may be necessary to give these drugs by the rectum, or to 
empty the stomach by vomiting or by the use of the stomach tube before 
they are administered. Sometimes the stomach can be stimulated to absorp- 
tion by -fa grain of strychnine. In certain cases the use of a full dose, 10, 15, 
or 20 drops, of the tincture of gelsemium with a grain of an active extract of 
cannabis indica gives the greatest relief. The use of cologne-water contain- 
ing 5 to 10 grains of menthol to the ounce applied over the course of the 
painful nerve may give much relief. In many instances it is impossible for 
any of these remedies to do good unless the patient will lie down in a quiet 
and dark room for several hours. 



SUNSTROKE. 

Definition. — Sunstroke, more accurately called heatstroke, insolation, or 
thermic fever, and by the French coup de soleil, is a condition of the body 
produced by exposure to great heat. In rare instances the temperature of 
the patient does not rise, but falls, and to this condition is given the name 
heat exhaustion. 

Etiology. — The chief factor in producing heatstroke is the presence of 
great heat associated, as a rule, with marked humidity of the atmosphere. 
It is important to bear in mind the fact that exposure to the rays of the sun 
is not necessary for the development of heatstroke. Cases are constantly 
met with in which the illness of the patient is due to artificial heat, and heat- 
stroke may occur in the night as well as in the day if the atmosphere is hot 
and moist. Dry heat is better borne by all persons than is moist heat, 
probably because evaporation on the skin proceeds rapidly in dry air, and so 
the body is cooled by the function of perspiration, whereas in a moist atmos- 
phere the imperfect evaporation results in an accumulation of heat in the 
body. For this reason heatstroke is very rare on the western plains of the 
United States, where the temperature in summer often reaches 105° in the 
shade, whereas in Philadelphia, where the air is humid, heatstroke is exceed- 
ingly common when the thermometer registers a temperature of 90°. In the 
one case evaporation is so rapid that the heat of the body is kept at a normal 
level, whereas in the latter case the perspiration lies on the skin in great beads. 
A second factor in producing heatstroke is the use of alcoholic drinks in any 
form. There can be no doubt that all such beverages greatly predispose to 
the development of this state. So, too, renal disease and a feeble heart may 
act as predisposing factors. Loss of sleep and torpidity of the bowels are 
also possessed of an evil influence. 

Certain French clinicians have asserted, with notable facts in support of 
their views, that sunstroke is really a form of infection which develops under 
the atmospheric states already named. 



SUNSTROKE 1081 

Pathology and Morbid Anatomy. — While a very considerable number of 
clinicians in America and in the East Indies described sunstroke symp- 
tomatically in the early part of the last century, it was not till H. C. Wood 
collated our knowledge and enriched it by further experimentation that the 
profession began to fully grasp the facts concerning its production and the 
lesions which ensued. 

The pathology of the disorder resides in the inability of the heat-regulating 
mechanism of the body to maintain a normal body temperature. The 
primary difficulty lies in a decreased power of the body to carry out an 
efficient heat dissipation, and this is followed by an unrestrained heat pro- 
duction, due, in Wood's opinion, to failure of the inhibitory heat centres, in 
the pons, to check oxidation processes. With diminished heat dissipation 
and increased heat production it is not difficult to perceive why the tem- 
perature of the body rises until a state of hyperpyrexia is reached. 

The morbid anatomy consists in changes in the tissues which in turn per- 
mit decomposition to set in very rapidly, being preceded by well-marked 
rigor mortis. The veins of the brain and lungs are found distended with 
fluid blood, and everywhere the blood fails to clot as it does in the vessels 
of the ordinary cadaver. If an autopsy is made very soon after death, the 
left ventricle is found in firm systole, but the right ventricle is distended with 
blood. The liver and kidneys are also found to be intensely engorged. 

Symptoms. — The symptoms of sunstroke consist, in the preliminary stage, 
in oppression and dizziness. If these evidences of heat are ignored, the stage 
of sudden unconsciousness develops, and is often ushered in by a convulsion 
which may be exceedingly violent. In other cases no convulsion develops, 
but deep stupor with stertorous breathing comes on. The face is at first livid 
and later deeply cyanotic, the great vessels of the neck and upper extremities 
being distended. The temperature of the patient speedily rises to a height 
never seen in any other disease, sometimes reaching 112° or more, the 
average being from 105° to 110°. The pupils may be contracted or widely 
dilated. If the fever cannot be reduced and the cardiac and pulmonary 
congestion are not relieved, death ensues within twelve to thirty-six hours. 
When improvement takes place, a relapse some hours later often ensues. A 
patient who has sunstroke may subsequently become very ill and die from 
a secondary meningitis. Persons who have had sunstroke are very suscep- 
tible to high temperatures, and when exposed in after years may be greatly 
distressed by an atmospheric temperature as low as 80°, if the air is moist. 

Diagnosis. — There are only two other states that resemble heatstroke, 
namely, uraemia and apoplexy. The first can be excluded by the absence 
of hyperpyrexia and albumin in the urine. The second is excluded by the 
same lack of temperature, except in those cases in which the pons is involved, 
when the fever may be high, but pontile hemorrhage is usually speedily fatal 
and the paralysis severe. Sunstroke and uraemia may, however, exist 
simultaneously. The history of the patient will exclude epilepsy which is 
also excluded by the high fever. 

Prognosis. — The prognosis depends on the height of the fever and the 
resistance which it offers to treatment. Do what we will a large number of 
these cases die. 



1082 DISEASES OF THE NERVOUS SYSTEM 

Treatment. — The treatment of sunstroke, if it is to be followed by satis- 
factory results, must be bold and vigorous. In most cases three things are 
essential : First, that the temperature must be reduced until it is at a safe 
level, by the application of cold water or ice. This is best carried out by 
stripping the patient, laying him upon a canvas cot, and then directing a 
stream of cold water upon his body from a hose, the patient being actively 
and vigorously rubbed at the same time by one or more attendants, with the 
object of producing reaction, of overcoming internal congestion, of bringing 
the blood to the surface, whereby it may be cooled, and of increasing the 
dissipation of heat, for frictions increase the dissipation of heat during the 
application of cold nearly fifty per cent. During this procedure ice should 
be applied to the head constantly. In other instances, the patient may be 
immersed in a tub of cold water, and if necessary pieces of ice may be placed 
in this water. If the tub is used, active frictions are as essential as in the 
case just stated. Care should be taken that the temperature, when it once 
begins to fall, does not drop too rapidly, so that the patient passes into hypo- 
thermia and collapse. If the patient is robust and there is evidence of 
venous engorgement, free venesection should be practised. Many physicians 
of large experience believe that venesection is of almost equal importance 
with the use of cold. Venesection should be followed by hypodermo- 
clysis or by the intravenous injection of normal salt solution. By these two 
measures engorgement of the right side of the heart is diminished and 
toxsemia combated. If the circulation on the left side of the heart seems 
failing, hypodermic injections of Hoffmann's anodyne and strychnine may 
be administered. The use of alcohol should be avoided. If the bowels are 
confined, citrate of magnesia should be given in full purgative dose to relieve 
them, and where the patient is unconscious and unable to swallow so large 
a dose, J of a grain of elaterium may be used not only to move the bowels, 
but diminish cerebral congestion. The violent headache which often follows 
sunstroke may, in some instances, yield to the ordinary coal-tar products 
combined with the use of bromide of sodium and caffeine. Where it does 
not do so, and there are any evidences of meningeal or cerebral congestion, 
free venesection should be practised, not only for the relief of pain, but in 
order to prevent the development of secondary meningitis. This is a matter 
of very great importance, but is often treated as of little moment. 

In the after-treatment of the patient it is essential that the temperature 
should be carefully watched, as it nearly always has a tendency to rise a 
second time. Such a tendency should be combated by the application of 
cold to the head, and by cold bathing if actual hyperpyrexia develops. Per- 
fect rest in bed for a number of days after the sunstroke should be insisted 
upon, and the patient should be warned that any exposure to heat for several 
days will be liable to produce another attack. 

HEAT EXHAUSTION. 

Heat exhaustion is a condition produced by the same causes as heatstroke, 
but instead of hyperpyrexia developing the temperature becomes subnormal, 
the patient's skin may be bedewed with a cold sweat, and all the evidences 



PERIODICAL PARALYSIS 1083 

of severe collapse may be present. This condition is to be treated by immers- 
ing the patient in hot water, and by the application about his body, after the 
removal from the bath, of hot bottles or hot bricks to maintain body tem- 
perature. A failing circulation should be supported by hypodermic injec- 
tions of Hoffmann's anodyne and atropine. Care should be taken that cold- 
ness of the extremities is not mistaken for true heat exhaustion, for it some- 
times happens that the extremities are cold in thermic fever, although the 
temperature of the body may be far above normal. This point must be 
determined by taking the rectal temperature. If the rectal temperature is 
found to be very high, the treatment for heatstroke should be instituted and 
the circulation equalized by active rubbing. A hot bath in such a case is 
not advisable. 

FACIAL HEMIATROPHY. 

This is a condition in which one side of the face undergoes a slowly pro- 
gressive wasting. As a rule it begins between the ages of ten and twenty 
years. The cause is unknown, although it is without doubt due to some 
localized degenerative change in the nervous system. In an autopsy upon 
a case of this character Mindel found degeneration of the trifacial nerve in 
its efferent fibres and atrophy of the substantia nigra. 

When the malady first develops, the skin of the affected part begins to be 
thin and glossy and seems to be stretched. The fine hairs fall out and the 
sebaceous glands atrophy, so that the part is unduly dry. After that the 
subcutaneous tissues atrophy so that the natural fulness of the face is dimin- 
ished, and, in the later stages of the affection, even the underlying bone may 
be atrophied or absorbed. The muscular tissues escape the atrophy to a 
greater extent, and do not undergo degenerative changes. The eye may 
become sunken from wasting of the orbital part, and the pupil may be in a 
state of mydriasis. Usually the condition is painless, but local spasm of the 
muscles of the part may occur. No treatment is of any avail in arresting 
the progress of the disease. 

PERIODICAL PARALYSIS. 

This term is applied to an extraordinary condition of paralysis involving 
widely distributed groups of muscles in the arms, legs, and trunk, which 
develops rapidly in apparently healthy individuals without any apparent 
exciting cause. Not rarely several members of a family are affected by the 
malady. The patient may go to bed in perfect health and wake to find him- 
self paralyzed, or the paralysis develops after a preliminary sense of weak- 
ness in the affected parts. As a rule, the legs suffer chiefly. Very rarely the 
muscles of the neck are affected, but the cranial nerves always escape. 
The reflexes are minus, and the muscles and nerve trunks lose their 
reaction to faradic stimulation. The paralysis lasts from a few hours to a 
day, and speedy and perfect recovery ensues, but relapses frequently take 
place 

The condition is apparently a form of autointoxication, and is said to be 
benefited by the use of alkaline diuretics. 



INDEX. 



ABDOMINAL facies in ascites, 650 
Abducens nerve, paralysis of, 1022 
Abscess of brain, 941 

in bronchiectasis, 387 
in erysipelas, 192 
hepatic, 653. See Hepatic abscess 
of liver in dysentery, 232 
of lung, 423 

in croupous pneumonia, 148, 151, 
157 
of mediastinum, 452, 455 
parotid, 551 
perinephritic, 737 

treatment of, 737 
peritoneal, 643 
pulmonary, in septicaemia, 195 

in typhoid fever, 42 
in smallpox, 82 
of spleen, 764 
Acetone in urine, test for, 799 
Achylia-gastrica nervosa, 604 
Acquired idiocy, 928 
Acromegaly, 837 

definition of, 837 
diagnosis of, 839 

from gigantism, 839 
from leontiasis ossea, 839 
from myxoedema, 839 
from osteitis deformans, 839 
from pulmonary hypertrophic 
osteo-arthropathy, 839 
etiology of, 837 
symptoms of, 837 
Actinomycosis, 273 
cerebral, 274 
definition of, 273 
diagnosis of, 275 
etiology of, 274 
morbid anatomy of, 274 
pathology of, 274 
ray fungus in, 273 
streptothrix actinomyces in, 273 
symptoms of, 274 
treatment of, 275 
Acute anterior poliomyelitis, 970 
Addison's disease, 760 

anaemia in, 761 
asthenia in, 761 
atrophic changes in, 760 
definition of, 760 
diagnosis of, 762 

from diabetes bronze\ 762 



Addison's disease, diagnosis of, from hyper- 
trophic cirrhosis of liver, 
762 
from pregnancy, 762 
from prolonged use of arsenic, 
762 
etiology of, 760 
history of, 760 
languor in, 761 
morbid anatomy of, 760 
pathology of, 760 
pigmentation of skin in, 761, 762 
prognosis in, 763 
symptoms of, 761 
treatment of, 763 
tuberculosis in, 760 
Adenitis, cervical, 300 

tropical, 226 
Adenoma of kidney, 732 
of pancreas, 695 
of thyroid gland, 751 
Adhesive pericarditis, chronic, 463 
Adiposis dolorosa, 836 
Adrenal apoplexy, 761 
iEstivo-autumnal parasite of malarial fever, 

866 
African lethargy, 879. See Sleeping sickness. 
Agraphia, 931 

Ague cake in malarial fever, 868, 875 
Ainhum, 841 

treatment of, 841 
Albuminuria, 741 

in acute diffuse nephritis, 701 
of adolescence, 741 
cyclic, 741 

in diabetes mellitus, 796 
in diphtheria, 176, 177 
orthostatic, 741 
in pneumonic plague, 223 
tests for, 742 
in typhoid fever, 41 
in ulcerative endocarditis, 487 
in yellow fever, 216 
Albuminuric neuroretinitis, 714 
papillitis, 714 

retinitis in chronic parenchymatous 
nephritis, 706 
degenerative, 714 
hemorrhagic, 714 
typical, 714 
Albumosuria, myelopathic, 746 
Alcoholism, 843 

( 1085 ) 



1086 



INDEX 



Alcoholism, acute, symptoms of, 843 
treatment of, 843 
chronic, 844 

morbid anatomy of, 845 
symptoms of, 845 
treatment of, 845 
dietetic, 846 
definition of, 843 
etiology of, 843 
Alexia, 931 

Algid form of yellow fever, 216 
Alimentary canal, tuberculosis of, 334 
Allochiria in locomotor ataxia, 962 
Alopecia, syphilitic, 284 
Amaurosis, ursemic, 722 
Ambh r opia, in whooping-cough, 122 
Amimia, 931 
Amceba, dysenteriae, 229 
Amoebic abscess of liver, 654 

dysentery, 227 
Amok, 1066 

Amphoric breathing, 319 
Amyloid degeneration of heart, 474 
disease of kidney, 718 
liver, 667 
Amyotrophic lateral sclerosis, 980 
Anaemia, 773 

in Addison's disease, 761 

brickmakers', 887 

in chronic lead poisoning, 854 

definition of, 773 

in diphtheria, 180 

essential, 775 

in gastric ulcer, 582 

infantum, 785 

blood changes in, 785 
definition of, 785 
treatment of, 785 
, miners', 887 
pernicious, 777 

blood changes in, 778 
definition of, 777 
diagnosis of, 779 
etiology of, 777 
morbid anatomy of, 778 
prognosis in, 779 
symptoms of, 778 
treatment of, 779 
Porto Rican, 887 
primary, 775 
secondary, 773 
causes of, 773 
diagnosis of, 774 
symptoms of, 774 
treatment of, 774 
in septicaemia, 194 
splenic, 765 

blood in, 766 

clinical characteristics of, 766 
definition of, 765 
diagnosis of, 766 
etiology of, 765 
morbid anatomy of, 765 
pathology of, 765 
prognosis in, 766 



Anaemia, splenic, spleen in, 765 
symptoms of, 765 
treatment of, 766 
in sprue, 244 
in syphilis, 284 
in typhoid fever, 34 
tunnel, 888 
in uncinariasis, 890 
Anaesthesia in hysteria, 1049 
Anaesthetic leprosy, 349 
Aneurysm, 534 

of abdominal aorta, 542 

cardiac, 479 

definition of, 534 

"dissecting," 534 

embolic, 534 

etiology of, 534 

false, 534 

frequency of, 535 

fusiform, 534 

haematemesis in, 605 

of hepatic artery, 543 

morbid anatomy of, 534 

mycotic, 534 

pathology of, 534 

of renal artery, 543 

sacculated, 534 

of splenic artery, 543 

of superior mesenteric artery, 543 

of thoracic aorta, 536 

complications of, 538 
diagnosis of, 539 
prognosis in, 540 
sequelae of, 537, 538 
symptoms of, 536 
treatment of, 540 
operative, 541 
TufneU, 540 
varicose, 534 
Aneurysmal varix, 534 
Angina Ludovici, 552 
pectoris, 523 

definition of, 523 
diagnosis of, 525 
etiology of, 523 
pathology of, 523 
prognosis in, 525 
symptoms of, 524 
treatment of, 525 
Angiomata, cavernous, of liver, 668 

of kidney, 732 
Angioneurotic oedema, 1075 
definition of, 1075 
diagnosis of, 1076 
prognosis of, 1076 
treatment of, 1076 
Angiosclerosis, 532 

Animal parasites, diseases due to, 863 
Ankle clonus in lateral sclerosis, 979 
Ankylosis in gonorrhceal arthritis, 187 
Ankylostomiasis, 887 
Ankylostomum duodenale, 887 
Annular stricture of oesophagus, 561 
Anorexia nervosa, 604 
Anthracosis, 41 1 



INDEX 



1087 



Anthrax, 257 

bacillus of, 257 
definition of, 257 
diagnosis of, 260 
etiology of, 257 
frequency of, 258 
lesion of, 259 
morbid anatomy of, 258 
oedema, malignant, 259 
pathology of, 258 
prevention of, 258 
prognosis in, 260 
symptoms of, 259 
treatment of, 261 
Antirabic serum, 265 
Antisepsis, intestinal, in typhoid fever, 56 
Anuria, 737 

treatment Of, 737 
Aorta, abdominal, aneurysm of, 542 

thoracic, aneurysm of, 536 
Aortic regurgitation, 508 

Corrigan pulse in, 510 
definition of, 508 
diagnosis of, 512 
Duroziez sign in, 512 
etiology of, 508 
murmur in, 511 
ox-heart in, 509 
pathology of, 508 
physical signs of, 509, 511 
pistol-shot sound in, 512 
prognosis in, 512 
Quincke's pulse in, 510 
symptoms of, 509 
trip-hammer pulse in, 511 
water-hammer pulse in, 511 
stenosis, 504 

definition of, 504 
diagnosis of, 507 
etiology of, 505 
physical signs of, 506 
prognosis in, 507 
symptoms of, 506 
Aphasia, 930 

in apoplexy, 920 
in brain tumor, 934 
conduction, 931 
definition of, 930 
symptoms of, 930 

transitory, in croupous pneumonia, 160 
Aphemia, 931 
Aphonia, hysterical, 1050 
in smallpox, 83 
in tuberculous laryngitis, 375 
Aphthae tropicae, 242 
Aphthous stomatitis, 546 
Apoplectiform attack, 913 
bulbar paralysis, 913 
type of yellow fever, 216 
Apoplexy, 913 
adrenal, 761 
aphasia in, 920 
astereognosis in, 920 
athetosis in, 921 
bed-sores in, 920 



Apoplexy, contractures in, 921 
definition of, 913 
in diabetes mellitus, 797 
diagnosis of, 922 

from acute alcoholism, 922 
from coma of diabetes, 922 

of uraemia, 922 
from embolism of cerebral vessels, 

922 
from epilepsy, 922 
from general paralysis of insane, 

923 
from opium poisoning, 922 
from sunstroke, 923 
from syncope, 922 
from thrombosis of cerebral vessels, 
922 
etiology of, 913 
frequency of, 913 
hemianaesthesia in, 920 
hemianopsia in, 920 
hemiplegia in, 919 
Hutchinson's pupil in, 921 
ingravescent, 922 
muscular atrophy in, 921 
ocular symptoms of, 919 
paralysis in, 919, 920 
pathology of, 914 
prognosis in, 923 
pulse in, 918 
reflexes in, 919 
sequelae of, 921 
stertorous breathing in, 918 
symptoms of, 917 

premonitory, 917 
treatment of, 921 
unconsciousness in, 919 
uraemic, 923 
Appendicitis, 615 
abscess in, 619 
catarrhal, 617 
definition of, 615 
diagnosis of, 621 

from hepatic colic, 621 
from intestinal obstruction, 621 
from ovarian inflammation, 621 
from renal colic, 621 
from tuberculosis, 621 
from typhoid fever, 621 
etiology of, 615 
gangrenous, 617 
McBurney's point, 620 
morbid anatomy of, 617 
muscular rigidity in, 620 
obliterative, 617 
pathology of, 617 
perforative. 617 
prognosis in, 622 
symptoms of, 619 
treatment of, 622 
in typhoid fever, 30, 39 
ulcerative, 617 
vomiting in, 620 
Apraxia, 931 



1088 



INDEX 



Aran-Duchenne type of chronic anterior 

poliomyelitis, 975 
Argyll-Robertson pupil in dementia par- 
alytica, 952 
in disseminated sclerosis, 956 
in locomotor ataxia, 962 
Arhythmia, 522 
Arsenical poisoning, 850 

chronic, etiology of, 850 
prognosis in, 851 
pseudotabes in, 851 
symptoms of, 851 
treatment of, 851 
Arteries, diseases of, 528 
Arteriocapillary fibrosis, 529 
Arteriosclerosis, 529 
definition of, 529 
etiology of, 529 
morbid anatomy of, 530 
pathology of, 530 
symptoms of, 533 
treatment of, 533 
Arteritis, syphilitic, 281 
Artery of cerebral hemorrhage, 915 
Arthritis in cerebrospinal fever, 137 
in croupous pneumonia, 161 
deformans, 818 

definition of, 818 
diagnosis of, 822 
etiology of, 819 
Hay garth's nodosities in, 820 
Heberden's nodes in, 821 
morbid anatomy of, 820 
prognosis in, 822 
symptoms of, 820 
treatment of, 822 
gonorrhceal, 186 

ankylosis in, 187 
chronic, 186 
endocarditis in, 187 
symptoms of, 186 
treatment of , 188 
infections, in cholera, 209 
in mumps, 118 

in rheumatic fever, acute, 199 
rheumatoid, 818 

in bronchiectasis, 386 
septic, in scarlet fever, 103 
in smallpox, 83 
in typhoid fever, 44 
Articular rheumatism, acute, 196. See 

Rheumatic fever, acute. 
Ascariasis, 884 

symptoms of, 885 
treatment of, 885 
Ascaris lumbricoides, 884 
Ascending myelitis, 983 

paralysis, acute, 1000 
Ascites, 650 

definition of, 650 
diagnosis of, 652 

from hepatic enlargement, 652 
from ovarian cyst, 652 
from splenic enlargement, 652 
dyspnoea in, 651 



Ascites, etiology of, 650 

paracentesis abdominis in, 653 
physical signs of, 650 
symptoms of, 650 
treatment of, 653 
Asiatic cholera, 204 
Aspiration pneumonia, 398 
Astasia-abasia, 1067 
definition of, 1067 
symptoms of, 1067 
Astereognosis in apoplexy, 920 
Asthenia in Addison's disease, 761 
Asthma, bronchial, 390 

Charcot-Leyden crystals in, 392 
Curschmann's spirals in, 392 
definition of, 390 
diagnosis of, 393 

from pulmonary cedema, 393 
etiology of, 390 
Harrison's groove in, 392 
morbid anatomy of, 391 
pathology of, 391 
pigeon-breast in, 392 
prognosis of, 394 
sputum in, 392 
symptoms of, 392 
treatment of, 394 

bronchitis tent in, 396 
cardiac, 391 
renal, 391 
Asymmetrical stricture of oesophagus, 561 
Ataxia, familv, 967 
Friedreich's, 967 
hereditary, 967 
locomotor, 958 

Marie's cerebellar hereditary, 970 
Atheroma, 531 
Athetosis in apoplexy, 921 
Athyrea, 756 
Atonic dilatation of oesophagus, 562 

gastrectasis, 578 
Atriplicism, 860 

treatment of, 860 
Atrophic cirrhosis of liver, 659 
emphysema, 413 
enteritis of tropics, 242 
nasal catarrh, 366 
paralysis, acute, 970 
rhinitis, 365 

spinal paralysis, chronic, 974 
Atrophy of heart, 474 
of liver, red, 666 

yellow, acute, 670 
muscular, progressive, 974 
of peroneal type, 1037 
in apoplexy, 921 
optic, 1014 
Auctioneers' sore throat, 555 
Auditory nerve, disease of, 1028 
deafness in, 1028 
tinnitus in, 1028 
vertigo in, 1029 
Aura in epilepsy, 1054, 1056 
Autumnal catarrh, 367 
fever, 17 



INDEX 



1089 



BABINSKI reflex in amyotrophic lateral 
sclerosis, 981 
in lateral sclerosis, 979 
Bacillary dysentery, 227 
Bacillus aerogenes capsulatus in pneumo- 
pericardium, 467 

of amoebic dysentery, 227, 231 

of anthrax, 257, 

of Asiatic cholera, 204, 207 

coli communis in typhoid, 18 

of diphtheria, 172 

dysenteriae, 18 

of Eberth, 17 

leprae, 345 

mallei in glanders, 272 

para-colon, 18 

pertussis Eppendorf, 119 

pestis, 219, 220 

of Pfeiflfer in influenza, 125, 126 

of tetanus, 267 

of tuberculosis, method of staining, 322 

typhosus, 17 

of typhoid fever, 17 
Banti's disease, 767 
Barlow's disease, 831 

Barrel-shaped chest in chronic hypertrophic 
tonsillitis, 559 
in emphysema, 413 
Basedow's disease, 751 
Basilar meningitis, 301 
Bath, Brand, in typhoid fever, 53 
Baths, Nauheim, in myocarditis, 478 
Bed-sores in typhoid fever, 33 
Beef- worm, 901 
Benign goitre, 749 
Beriberi, 249, 1007 

acute pernicious, 255 

blood in, 256 

cardiac changes in, 255 

definition of, 249 

diagnosis of, 256 

distribution of, 250 

etiology of, 250, 251 

forms of, 254 

frequency of, 252 

incubation of, 252 

mild, 255 

morbid anatomy of, 253 

pathology of, 253 

prognosis in, 256 

prophylaxis of, 253 

rudimentary, 255 

symptoms of, 254 

treatment of, 256 

urine in, 256 
Bile-ducts, catarrh of, acute, 671 
chronic, 673 
treatment of, 673 

constriction of, 674 

inflammations of, suppurative, 673 

diagnosis of, 674 

symptoms of, 674 

treatment of, 674 

occlusion of, 674 

congenital, 674 

69 



Bilharzia disease, 904, 905 
diagnosis of, 907 
distribution of, 905 
etiology of, 905 
haematuria in, 906 
pathology of, 906 
prognosis in, 907 
schistosoma haematobium in, 905 
symptoms of, 906 
treatment of, 907 
Biliary calculi, 677 
colic, 679 

passages, malignant growths of, 683 
tract, diseases of, 671 
Bilious fever, 874 

remittent fever, 874 
Bilocular heart, 527 

stomach, 598 
Birth palsy, 1007 
"Black" measles, 112 
smallpox, 81 

vomit in j^ellow fever, 216 
-water fever, 875 
Bladder, tuberculosis of, 340 
Blepharofacial spasm, 1027 
Blepharospasm, 1027 
Blindness, word-, 931 
Blood in beriberi, 256 

in cerebrospinal fever, 138 
changes in anaemia infantum, 785 

in pneumonic plague, 223 
in chlorosis, 775 
in diabetes mellitus, 794 
in diphtheria, 176 
diseases of, 773 
in Hodgkin's disease, 768 
in malarial fever, changes in, 867 
in pernicious anaemia, 778 
in septicaemia, 194 
-spitting in mitral regurgitation, 497 
in splenic anaemia, 766 
in splenomedullary leukaemia, 781 
in stools, tests for, 584 
in typhoid fever, 25, 33 
in urine, 738 
in yellow fever, 214 
Blue line on gums in chronic lead poisoning, 

853 
Boas' reagent, 593 

test meal in gastric cancer, 593 
Boils in typhoid fever, 34 
Bone-marrow in malarial fever, 868 
Bones, syphilis of, 286 
Bossy frontals in rickets, 827 
Bothriocephalus cordatus, 903 
cristatus, 903 
latus, 903 
Bouquet fever, 131 
Bovine tuberculosis, 291 
Bowel, hemorrhage from, in typhoid fever, 
36 
treatment of, 57 
obstruction of, 623 

by congenital malformations, 624 
by fecal impaction, 624 



1090 



INDEX 



Bowel, obstruction of, by foreign bodies, 
624, 628 
by internal strangulation, 624, 626 
by intussusception, 624 
by stricture, 624 
by tumors, 624 
by volvulus, 627 
perforation of, in typhoid fever, 30, 
37 
diagnosis of, 38 
treatment of, 58 
Bradycardia, 522 
Brain, abscess of, 941 

in bronchiectasis, 387 
definition of, 941 
diagnosis of, 943 
etiology of, 941 
morbid anatomy of, 942 
pathology of, 942 
prognosis in, 944 
symptoms of, 942 
treatment of, 944 
cancer of, 932 
diseases of, 913 
echinococcus cyst of, 932 
fibroma of, 932 
glioma of, 932 
gumma of, 932 
hemorrhage into, 913 
neuroma of, 932 
osteoma of, 932 
sarcoma of, 932 
softening of, in croupous pneumonia, 

160 
syphilis of, 285 
tabes of, 952 
tubercle of, 932 
tuberculosis of, 343 
tumors of, 932 

aphasia in, 934 
diagnosis of, 939 

from localized meningitis, 939 
etiology of, 932 
frequency of, 932 
headache in, 933 
morbid anatomy of, 932 
optic neuritis in, 934 
paralysis in, 934 

bilateral, 934, 935 
crossed, 934 
pathology of, 932 
prognosis in, 940 
symptoms of, 933 
table of cerebral localizing symp- 
toms in, 938 
treatment of, 940 
surgical, 941 
vascular, 932 
vertigo in, 933 
vomiting in, 933 
Weber's syndrome in, 934 
Brand bath in typhoid fever, 53 
Breakbone fever, 131 
Breathing, stertorous, in apoplexy, 918 
Brickmakers' anaemia, 887 



Bright's disease, acute, 700 

chronic, 703 
Bromatotoxismus, 855 
Bronchi, diseases of, 377 
Bronchial asthma, 390 
Bronchiectasis, 383 

brain abscess in, 387 
complications of, 386 
cough in, 385 

in croupous pneumonia, 158 
definition of, 383 
diagnosis of, 386 

from pulmonary tuberculosis, 386 
etiology of, 383 
forms of, 383 
haemoptysis in, 386 
morbid anatomy of, 383 
pathology of, 383 
prognosis in, 387 
pulmonary gangrene in, 387 

osteoarthropathy in, 387 
rheumatoid arthritis in 386 
sputum in, 385 
symptoms of, 385 
treatment of, 387 
Bronchitis actinomycotica, chronic, 274 
capillary, 402 
catarrhal, acute, 377 

definition of, 377 
distribution of, 377 
etiology of, 378 
morbid anatomy of, 380 
pathology of, 380 
prevention of, 380 
symptoms of, 380 
treatment of, 381 
chronic, 382 

definition of, 382 
treatment of, 382 
in croupous pneumonia, 149 
fibrinous, 388 

definition of, 388 
diagnosis of, 390 

from diphtheria, 390 
etiology of, 388 
pathology of, 388 
prognosis of, 390 
symptoms of, 389 
treatment of, 390 
in influenza, 126 
in measles, 110, 111 
in smallpox, 83 
tent in bronchial asthma, 396 
in whooping-cough, 123 
Bronchocele, 749 
Bronchopneumonia, 397 
complications of, 404 
definition of, 397 
diagnosis of, 404 

from acute bronchitis, 404 
from croupous pneumonia, 404 
from malarial infection, 405 
from tuberculous infection, 40 
in diphtheria, 176, 178, 179 
distribution of, 397 



INDEX 



iHQI 



Bronchopneumonia, duration of, 403 

etiology of, 397 

frequency of, 39S 

in measles, 110, 112 

morbid anatomy of, 399 

pathology of, 399 

prevention of, 398 

prognosis of, 405 

in scarlet fever, 103 

in smallpox, 83 

symptoms of, 400 

treatment of, 406 

types of, 398 

in whooping-cough, 122 
Brown induration of heart, 474 
Bubo, climatic, 226 

parotid, 551 

tropical. 226 
Buboes in bubonic plague, 222 
Bubonic plague, 219 
Buccal psoriasis, 550 
Bucket fever, 131 
Bulbar paralysis, 977 

apoplectiform, 913 
Bulimia, 604 



CACHEXIA, miners', 887 
in pellagra, 858 
Caecum, tuberculosis of, 336 
Caisson disease, 1001 

treatment of, 1002 
palliative, 1002 
prophylactic, 1002 
Calcareous degeneration of heart, 474 
Calculi, biliary, 677 
Calculus, coral, of kidney, 733 
"hemp-seed," of kidney, 734 
mulberry, of kidney, 734 
pancreatic, 693 
renal, 733 
Cancer of brain, 932 
of kidney, 732 
of oesophagus, 563 
of peritoneum, 649 
of stomach, 588 
Cancrum oris, 548 
Canker, 548 

Capillary bronchitis, 402 
Capsular cirrhosis of liver, 665 
Jircinoma of biliarv ducts, 683 
of gall-bladder," 683 
of liver, 668 
in lung, 428 
of mediastinum, 452 
of thyroid gland, 751 
•cinosarcoma of thyroid gland, 751 
iac aneurysm, 479. See Heart, aneu- 
rysm of. 
sthma, 391 
langes in beriberi, 255 

in croupous pneumonia, 149 
in yellow fever, 214 
ipli cations in rheumatic fever, 200, 
31 



Cardiac defects, congenital, 527 

dilatation, 468, 471. Sec Heart, dila- 
tation of. 
hypertrophy, 468, 469. See Heart, 

hypertrophy of. 
palpitation, 521 
valvular anomalies, 528 
Cardiospasm, 601 

treatment of, 602 
Caseative nephritis, 725 
Cataract in diabetes mellitus, 797 
Catarrh, autumnal, 367 

of bile-ducts, acute, 671 

chronic, 673 
gastric, acute, 564. See Gastric ca- 
tarrh, 
nasal, atrophic, 366 

definition of, 366 
etiology of, 366 
pathology of, 366 
prognosis of, 366 
symptoms of, 366 
treatment of, 366 
chronic, 365 

definition of, 365 
etiology of, 365 
pathology of, 365 
' symptoms of, 365 
treatment of, 366 
suffocative, acute, 400, 402 
Catarrhal appendicitis, 617 
bronchitis, acute, 377 

chronic, 382 
cholecystitis, 675 
dysentery, acute, 227 
enteritis, 609 
laryngitis, acute, 369 

chronic, 371 
pneumonia, 397 
pyelonephritis, 726 
stomatitis, 546 
Cerebral actinomycosis, 274 
embolism, 9l3 
hemorrhage, 913 

artery of, 915 
meningitis, 946 
paralysis, infantile, 925 
syphilis, 285, 286 
thrombosis, 913 
Cerebritis, acute, 944 

definition of, 944 
diagnosis of, 945 
etiology of, 944 
morbid anatomy of, 944 
pathology of, 944 
prognosis of, 945 
symptoms of, 945 
treatment of, 945 
Cerebrospinal fever, 134 
arthritis in, 137 
blood in, 138 
complications of, 139 
croupous pneumonia in, 139 
definition of, 134 
delirium in, 137 



1092 



INDEX 



Cerebrospinal fever, diagnosis of, 139 

from croupous pneumonia, 140 
diplococcus intracellularis 

meningitides in, 134 
from influenza, 140 
lumbar puncture as aid to, 140 
from tuberculous meningitis, 

140 
from typhoid fever, 139 
of Weichselbaum in, 134, 139 
eruption in, 137 
etiology of, 135 
fever in, 138 
forms of, 138 
chronic, 138 
intermittent, 138 
malignant, 138 
moderate, 137 
typhoid, 138 
frequency of, 136 
headache in, 137 
herpes in, 137 
history of, 135 
incubation of, 137 
Kernig's sign in, 138 
morbid anatomy of, 136 
pathology of, 136 
prevention of, 136 
prognosis of, 142 
respiration in, 137 

Cheyne-Stokes, 137 
sequelae of, 139 
symptoms of, 137 
treatment of, 142 
meningitis, 134 
Cervical adenitis, 300 
Cervicobrachial neuritis, 1006 
Cestodes, 900 
Ceylon sour mouth, 242 
Chalicosis, 411 
Chancre, 280, 283, 284 

leprous, 348 
Charcot joint in locomotor ataxia, 963 
Charcot-Leyden crystals, 392 

in distomatosis of lung, 908 
in uncinariasis, 890 
Charcot-Marie-Tooth form of progressive 

muscular atrophy, 1037 
Cheyne-Stokes respiration in cerebrospinal 

fever, 137 
Chicken-breast in rickets, 828 
Chickenpox, 90. See Varicella. 
Chickpea disease, 859 
Chigger, 911 

treatment of, 911 
Chloroma, 784 
Chlorosis, 775 
blood in, 775 
complications of, 776 
definition of, 775 
diagnosis of 776 

from pernicious anaemia, 776 
Egyptian, 887 
etiology of, 775 
florida, 776 



Chlorosis, pathology of, 775 
prognosis in, 777 
symptoms of, 776 
tarda, 775 
treatment of, 777 
tropical, 888 
Cholangitis, acute, 671 

diagnosis of, 672 
acute, etiology of, 671 
prognosis in, 672 
symptoms of, 671 
treatment of, 672 
chronic, 673 

treatment of, 673 
suppurative, 673 

diagnosis of, 674 

from catarrhal cholangitis, 674 
from hepatic abscess, 674 
symptoms of, 674 
treatment of, 674 
Cholecystitis, acute, 675 
definition of, 675 
diagnosis of, 676 

from acute appendicitis, 676 

pancreatitis, 676 
from gastric ulcer, 676 
from hepatic colic, 676 
from intestinal obstruction, 
676 
etiology of, 675 
morbid anatomy of, 675 
symptoms of, 676 
treatment of, 677 
catarrhal, 671 
in typhoid fever, 40 
Cholelithiasis, 677 
colic in, 679 
complications of, 680 
Courvoisier's law in 681 
definition of, 677 
diagnosis of, 680 

from appendicitis, 680 

from gastralgia, 680 

from gastric crises of ataxia, 680 

ulcer, 681 
from pleurisy, 681 
from renal stone, 681 
enlargement of gall-bladder in, 680 
etiology of, 677 
jaundice in, 678 
pathology of, 677 
perforation in, 680 
sequelae in, 680 
symptoms of, 678 
treatment of, 681 
in typhoid fever, 41 
urine in, 679 
Cholera, 204 

arthritis, infectious, in, 209 
Asiatic, 204 
bacillus of, 204, 207 
collapse in, 208 
complications of, 209 
definition of, 204 
diagnosis of, 209 



INDEX 



1093 



Cholera, diarrhoea in, 207 
distribution of, 204 
etiology of, 204 
facial expression in, 208 
gangrene in, 208, 209 
history of, 204 
incubation in, 207 
infantum, 613 

definition of, 613 

etiology of, 613 

morbid anatomy of, 613 

pathology of, 613 

prognosis in, 614 

symptoms of, 613 

treatment of, 614 
liver in, 206 

morbid anatomy of, 206 
nephritis in, 209 
oedema of lungs in, 209 
parotitis in, 209 
pathology of, 206 
prevention of, 205 

inoculations for, 205 
prognosis in, 209 
purging in, 208 
sequelae of, 209 
sicca, 209 
stools in, 208 
symptoms of, 207 
treatment of, 210 

irrigation of bowel in, 211 
variations in symptoms of, 208 
visceral changes in, 206 
vomiting in, 208 
Cholerine, 208 
Chondroma in lung, 428 
Chorea, acute, 1043 

in acute rheumatic fever, 201 
electrical, 1047 
gravidarum, 1043 
hereditary, 1046 

prognosis in, 1047 

symptoms of, 1046 

treatment of, 1047 
Huntington's, 1047 
insaniens, 1045 
minor, 1043 

complications of, 1045 

definition of, 1043 

diagnosis of, 1045 

from hysteria, 1045 
from infantile cerebral palsy 
1045 

duration of, 1045 

endocarditis in, 1045 

etiology of, 1043 

exciting causes of, 1043 

frequency of, 1044 

hysteria in, 1045 

mental state in, 1045 

morbid anatomy of, 1044 

movements in, 1044 

pathology of, 1044 

prognosis in, 1045 

symptoms of, 1044 



Chorea minor., treatment of, 1046 
paralytic, 1045 
Sydenham's, 1043 
Chvostek's sign in gastric tetany, 576 

of tetany, 1065 
Chyluria, 744 

" Cinder-sifting" kidney, 696 
Circulatory disturbances in kidney, 698 

system, diseases of, 457 
Circumscribed peritonitis, 643 
Cirrhosis of kidney, 710 

of liver, 658 
Claw-hand in chronic anterior poliomyelitis, 

975 
Clergymen's sore throat, 555 
Climatic bubo, 226 

definition of, 226 
symptoms of, 226 
treatment of, 227 
Coffee-ground vomit 605 
Coin sound in hydropneumothorax, 451 
Cold bathing in typhoid fever, 52 
Colic, biliary, 679 

in chronic lead poisoning, 854 
painters', 854 
renal, 735 
Colica pictonum, 854 
Colitis, 636 
acute, 636 

symptoms of, 637 
treatment of, 637 
croupous, 638 

treatment of, 638 
follicular, 638 
mucous, 637 

definition of, 637 
treatment of, 637 

counterirritation in, 638 
diet in, 638 
rest in, 637 
nodular, 638 
pseudomembranous, 639 
Collapse in cholera, 208 
"Collar of brawn" in scarlet fever, 99 
Colloid goitre, 750 
Colon, dilatation of, 639 

by foreign bodies, 640 
by gas, 639 

treatment of, 640 
idiopathic, 640 
by obstruction, 640 
Coma in chronic parenchymatous nephritis, 
706 
diabetic, 796, 797 
in uraemia, 721 
vigil in typhoid fever, 43 
Comma bacillus of Asiatic cholera, 204, 207 
Compensatory emphysema, 413 
Compression of spinal cord, 993 
Conduction aphasia, 931 
Condylomata, syphilitic, 284 
Confluent smallpox, 81 
Congenital cardiac defects, 527 
hydronephrosis, 728 
malformations of bowel, 624 



1094 



INDEX 



Congenital myxcedema, 758 

stenosis of pylorus, 595, 597 
wryneck, 1033 
Congestion of lungs, 425 
definition of, 425 
diagnosis of, 427 

from catarrhal pneumonia, 

427 
from croupous pneumonia, 

427 
from pleural effusion, 428 
dyspnoea of, 427 
etiology of, 425 
hypostatic, 426 
pathology of, 425 
prognosis of, 428 
symptoms of, 427 
treatment of, 428 
Conjunctiva, diphtheria of, 179 
Conjunctival hemorrhages in whooping- 
cough, 122 
Conjunctivitis in measles, 113 
Constitutio lymphatica, 770 
Contracted kidney, 710 
Contractures in apoplexy, 921 
Convulsions in acute anterior poliomyelitis, 
972 
in chronic lead poisoning, 853 
in croupous pneumonia, 155 
in epilepsy, 1054 
in hysteria, 1048 

in infantile cerebral paralysis, 927 
in mumps, 118 
in typhoid fever, 44 
in uraemia, 721 
in yellow fever, 215 
Cor bovinum in aortic regurgitation, 509 
Corrigan pulse in aortic regurgitation, 510 
Corvza in measles, 110 
"acute, 363 

definition of, 363 
diagnosis of, 364 
diplococcus coryzse in, 363 
etiology of, 363 
morbid anatomy of, 363 
pathology of, 363 
symptoms of, 363 
transmission of, 363 
treatment of, 364 
Coup de soleil, 1080 
Courvoisier's law, 681 
Cracked-pot sound, 319 
Cramp, flute-players', 1072 
pianists', 1072 
telegraphers', 1072 
violinists', 1072 
writers', 1072 
Cranial nerves, diseases of, 1012 
Craniotabes, 827 
Crawcraw, 894 
Cretinism, 758 

definition of, 758 
diagnosis of, 759 
prognosis in, 759 
symptoms of, 758 



Cretinism, treatment of, 759 

thyroid gland in, 759 
Crisis in croupous pneumonia. 155 
Croup, false, 374 

spasmodic, 374 
Croupous colitis, 638 

pharyngitis, 555 

pneumonia, 143. See Pneumonia, 
croupous. 
Curschmann's spirals, 392 
Cyclasterion scarlatinalis, 97 
Cyanosis in croupous pneumonia, 151 

in mitral regurgitation, 497 

in cedematous laryngitis, 373 
Cyclic albuminuria, 741 

vomiting, 607 
Cylindrical stricture of oesophagus, 561 
Cynanche gangrenosa, 552 
Cyst, hydatid, of spleen, 764 
Cystadenoma of pancreas, 694 
Cystic adenoma of peritoneum, 649 

disease of kidney, 730 
of liver, 668 

epithelioma of pancreas, 694 

goitre, 749 
Cysticercus mediocanellata, 901 
Cystitis in typhoid fever, 42 
Cysts of mediastinum, 453 

of pancreas, 694 
Cytoryctes vaccinse as a cause of smallpox, 

71 
Cytoscopy in pleurisy with effusion, 440 



DACTYLITIS, syphilitic, 286 
Dandy fever, 131 
Deafness, 1028 
word-, 931 
Delirium in acute rheumatic fever, 201 
in cerebrospinal fever, 137 
cordis in diphtheria, 179 
in croupous pneumonia, 152, 154, 156 
ferox in typhus fever, 64 
in relapsing fever, 70 
in smallpox, 79 
in typhoid fever, 28, 43 
Dementia paralytica, 950 

Argyll-Robertson pupil in, 952 
definition of, 950 
diagnosis of, 953 
etiology of, 951 
morbid anatomy of, 951 
pathology of, 951 
prognosis in, 954 
symptoms of, 952 
treatment of, 954 
Dengue, 131 

chill in, 132 
crisis in, 132 
definition of, 131 
desquamation in, 133 
diagnosis of, 133 

from influenza, 133 
from rotheln, 133 
from scarlet fever, 133 



INDEX 



1095 



Dengue, diagnosis of, from syphilitic rose- 
ola, 133 
distribution of, 131 
eruption in, 133 
erythema in, 132 
history of, 131 
pathology of, 131 
prognosis in, 133 
relapse in, 133 
symptoms of, 132 
treatment of, 133 
Dentition in rickets, 828 
Dermatobia cyaniventris, 912 
Dermoid cyst in lung, 428 

of mediastinum, 453 
Descending myelitis, 983 
Desquamation in dengue, 133 
in scarlet fever, 104, 108 
Desquamative nephritis, chronic, 704 
Dhobie itch, 909 

definition of, 909 
etiology of, 909 
treatment of, 910 
types of, 909 
Diabetes insipidus, 806 

definition of, 806 
diagnosis of, 807 
etiology of, 806 
morbid anatomy of, 806 
prognosis in, 807 
symptoms of, 806 
treatment of, 807 
urine in, 807 
mellitus, 789 

albuminuria in, 796 
blood changes in, 794 
carbuncles in, 795 
coma in, 796, 797 
complications of, 795 
dyspeptic, 796 
nervous, 796 
ocular, 797 
pulmonary, 796 
definition of, 789 
diagnosis of, 797 

blood tests in, 798 
urinary tests in, 799 
distribution of, 789 
dyspeptic symptoms in, 796 
emaciation in, 795 
etiology of, 790 
frequency of, 789 
gangrene in, 795 
glycosuria in, 794, 795 
kidney changes in, 793 
KussmauTs coma in, 797 
morbid anatomy of, 793 
nervous system in, changes in, 793 
pathology of, 790 
prognosis in, 800 
sequelae of, 795 
symptoms of, 794 
treatment of, 801 

dietetic, 801, 802, 803 
medicinal, 804 



Diabetes mellitus, urine in, 795 

"phosphatic," 745 
Diarrhoea, 608 
alba, 242 
in cholera, 207 
hill, 240 

definition of, 240 
etiology of, 240 
pathology of, 241 
symptoms of, 241 
treatment of, 241 
in influenza, 127 
in measles, 112 
serous, 608 

causes of, 608 
treatment of, 608 
Simla, 241 
in sprue, 243 
in typhoid fever, 27, 30 
Diazo reaction of urine in typhoid fever, 50 
Dibothriocephalus latus, 901, 903 
Dietl's crises in movable kidney, 697 
Digestive tract, diseases of, 545 
Dilatation of colon, 639 
of oesophagus, 561 
of stomach, 572 
acute, 578 
Dilatation of the stomach, paralytic, 578 
Diphtheria, 171 

albuminuria in, 176, 177 
anaemia in, 180 
antitoxin, 183, 184 

administration of, 184 
disagreeable effects of, 185 
results of administration, 185 
bacillus of, 172 
blood in, 176 

bronchopneumonia in, 176, 178, 179 
complications of, 179 
of conjunctiva, 179 
definition of, 171 
"delirium cordis" in, 179 
diagnosis of, 180 

bacteriological, 180 
from tonsillitis, 181 
distribution of, 172 
emphysema in, 176 
etiology of, 172 

glandular enlargement in, 176, 177 
heart failure in, 179 

lesions in, 175 
hemorrhage in, 180 
kidney lesions in, 176 
laryngeal, 178 
local lesion of, 174 
lymphatic enlargements in, 176 
in measles, 113 
morbid anatomy of, 174 
myositis, acute, in, 175 
nasal, 178 
nephritis in, 176 

nervous manifestations of, 176, 177 
neuritis in, 176, 1010 
paralysis, facial, in, 180 

local or widespread, in, 179 



1096 



INDEX 



Diphtheria, paralysis of phrenic nerve in, 179 
pathology of, 174 
poliomyelitis, anterior, acute in, 176 
prognosis of, 182 
prophylaxis of, 182 
sequelae of, 179 
sore throat in, 177 
spleen in, 176 
symptoms of, 176 
transmission, mode of, 172 
treatment of, 183 
local, 185 
serum, 183, 184 
visceral lesions of, 175 
Diphtheritic dysentery, 227 

gastritis, 568 
Diplegia, spastic, 926 
Diplococcus coryzse, 363 

of Weichselbaum in cerebrospinal fever, 
134 
Diplopia in kubisagari, 362 

in locomotor ataxia, 963 
Diptera, infection by larvae of, 911 
Dipylidium caninum, 901 
"Dissecting aneurysm," 534 
Disseminated myelitis, 983 

sclerosis, 954 
Distomatosis, 904 
of liver, 908 

symptoms of, 909 
of lung, 904, 907 

pathology of, 908 
prognosis of, 908 
symptoms of, 908 
treatment of, 908 
Diverticula of oesophagus, pressure, 561 

traction, 561 
Dracontiasis, 896 
Dracunculus medinensis, 896 
Drop-foot in chronic anterior poliomyelitis, 

975 
Dropsy in mediastinal tumor, 454 
Dry mouth, 551 

pleurisy, 432 
Dubini's disease, 1047 
Duchenne's type of ascending paralysis, 

975 
Ductless glands, diseases of, 749 
Dum dum fever, 883 
Dumb rabies, 264 

Duodenal ulcer, 628. See Ulcer, duodenal. 
Duroziez sign in aortic regurgitation, 512 
Dwarf tapeworm, 901 
Dysbasia, 1068 
Dysentery, 227 
amoebic, 227 

diagnosis of, 231 
hepatic abscess in, 232 

changes in, 231 
intestinal perforation in, 234 
pathology of, 231 
peritonitis in, 234 
symptoms of, 233 
bacillary, 227 

pathology of, 230 



Dysentery, bacillary, Shiga's bacillus in, 230 

specific treatment of, 238 
catarrhal, 227 

pathology of, 232 

symptoms of, 234 
definition of, 227 
diagnosis of, 234 
diphtheritic, 227 

pathology of, 232 

symptoms of, 234 
etiology of, 227 
frequency of, 230 
morbid anatomy of, 230 
pathology of, 230 
prevention of, 229 
prognosis in, 235 
stools in, 233 
symptoms of, 232 
treatment of, 236 

diet in. 236 

local, 238 
Dysphagia in dilatation of oesophagus, 
562 
in tuberculous laryngitis, 375 
Dyspnoea in acute pernicious beriberi, 255 
in ascites, 652 

in croupous pneumonia, 151 
in emphysema of lung, 417 
in exophthalmic goitre, 754 
in Hodgkin's disease, 768 
in mitral regurgitation, 497 
in pleurisy with effusion, 437 
in pneumothorax, 450 
in uraemia, 722 
Dystrophy, muscular, 1035 

definition of, 1035 

Erb's juvenile, 1036 

etiology of, 1035 

Landouzy-Dejerine type of, 1037 

morbid anatomy of, 1035 

pathology of, 1035 

treatment of, 1037 



EARACHE in smallpox, 83 
Echinococcic strumitis, 749 
Echinococcus cyst of brain, 932 
exogena, 903 
multilocularis, 903 
Eclampsia, 1062 
infantile, 1062 

diagnosis of, 1063 
prognosis in, 1063 
treatment of, 1063 
puerperal, 1063 

treatment of, 1063 
Ectopia cordis, 528 
Eczema of tongue, 549 
Effusion, pericardial, 461 

pleural, 436 
Egyptian chlorosis, 887 
Ehrlich's reaction in typhoid fever, 50 
Electrical chorea, 1047 
Elephantiasis, 895 
Elephantoid fever in filariasis, 895 



INDEX 



1097 



Embolic aneurysm, 534 
Embolism, cerebral, 913 

in croupous pneumonia, 162 
in typhoid fever, 35 
Embryocardia in typhoid fever, 34 
Emphysema in diphtheria, 176 
of lungs, 413 

acute, 413, 419 
atrophic, 413 

barrel-shaped chest in, 413 
chronic, 413 
compensatory, 413, 419 
definition of, 413 
diagnosis of, 417 
dyspnoea in, 417 
etiology of, 413 
frequency of, 413 
hvpertrophic, 413 
interstitial, 413, 419 
morbid anatomy of, 413 
pathology of, 413 
physical signs of, 415 
prognosis in, 417 
senile, 413 
small-lunged, 420 

treatment of, 420 
subjective signs of, 417 
surgical, 413 
symptoms of, 415 
treatment of, 418 
venesection in, 419 
in whooping-cough, 122 
Emprosthotonos in tetanus, 269 
Empyema, 430, 443 

complications of, 446 
in croupous pneumonia, 157 
definition of, 443 
diagnosis of, 446 

from serous effusion, 446 
etiology of, 443 
micro-organisms in, 444 
necessitatis, 446 
perforation in, 446 
physical signs of, 446 
prognosis in, 447 
sepsis in, 446 
in septicaemia, 195 
symptoms of, 445 
in typhoid fever, 43 
treatment of, 447 

aspiration in, 447 
Encephalitis, acute, 944 
Encephalomyelitis, 983 
Encephalopathia saturnina, 853 
Endarteritis, obliterative, 532 

in typhoid fever, 26 
Endemic hasmaturia, 904 
haemoptysis, 904 
multiple neuritis, 249 
Endocarditis, 482 
acute, 482 

complications of, 485 
diagnosis of, 485 
etiology of, 482 
malignant, 482 



Endocarditis, acute, morbid anatomy of, 
484 
pathology of, 484 
prognosis in, 485 
symptoms of, 484 
in tonsillitis, 557 
treatment of, 485 
benign, 482 
chronic, 488 

valvular disease as result of, 489 
in croupous pneumonia, 149, 159 
definition of, 481 
gonorrhceal, 187 
mural, 482 
papillary, 482 

in rheumatic fever, acute, 200 
simple, 482 

tuberculous vegetative, 343 
ulcerative, 485 

albuminuria in, 487 
cerebral type of, 487 
complications of, 487 
definition of, 485 
diagnosis of, 488 
in erysipelas, 192 
etiology of, 486 
haematuria in, 487 
malarial type of, 487 
morbid anatomy of, 486 
pathology of, 486 
prognosis in, 488 
septic form of, 487 
splenic enlargement in, 487 
symptoms of, 486 
treatment of, 488 
serum in, 488 
typhoid type of, 487 
valvular, 482 
verrucous, 482 
Endothelioma of kidney, 732 
in lung, 428 
of thyroid gland, 751 
Enteric fever, 17. See Typhoid fever. 

intussusception of bowel, 624 
Enteritis, atrophic, of tropics, 242 
catarrhal, 609 

symptoms of, 609 
treatment of, 609 
Enteroptosis, 632 

definition of, 632 
diet in, 635 
etiology of, 632 
symptoms of, 634 
treatment of, 634 
surgical, 635 
Ephemeral fever, 351 
Epidemic gangrenous proctitis, 239 
definition of, 239 
etiology of, 239 
pathology of, 240 
symptoms of, 240 
treatment of, 240 
parotitis, 117 
roseola, 115 



I Epididymitis in typhoid fever, 42 



1098 



INDEX 



Epilepsy, 1052 

apoplexy in, 1058 

aura in, 1054, 1056 

complications of, 1057 

convulsions in, 1054 

cry in, 1054 

definition of, 1052 

diagnosis of, 1058 

from alcoholic epilepsy, 1058 
from hysteria, 1058, 1059 
from petit mal, 1059 
from syncope, 1059 
from tetanus, 1059 
from uraemia, 1059 

etiology of, 1052 

Jacksonian, 1061 

localized, 1061 

minor, 1061 

motor paralysis in, 1057 

pathology of, 1054 

prognosis in, 1060 

risus sardonicus in, 1055 

spinal, 1039. See Paramyoclonus multi- 
plex. 

symptoms of, 1054 

traumatisms in, 1057 

treatment of, 1061 
Epiphysitis, syphilitic, 286 
Epistaxis, 369 

etiology of, 369 

in leprosy, 348 

treatment of, 369 
Epithelioma, cystic, of pancreas, 694 
Erb's juvenile muscular dystrophy, 1036 

sign in gastric tetany, 576 
of tetany, 1065 
Ergotism, 856 
Erosive gastritis, 569 
Eructation, nervous, 603 
Eruption in cerebrospinal fever, 137 

in dengue, 133 

in frambesia, 359 

in leprosy, 348 

in measles, 111 

in pellagra, 858 

in rubella, 116 

in scarlet fever, 100 

in smallpox, 75, 77 

in tick fever, 355 

in varicella, 91 

in verruga, 361 
Erysipelas, 189 

abscess in, 192 

complications of, 191 

definition of, 189 

endocarditis in, 192 

etiology of, 189 

facial, 191 

frequency of, 189 

incubation of, 190 

migrans, 191 

morbid anatomy of, 190 

pathology of, 190 

pericarditis in, 192 

pleuritis, purulent in, 192 

prognosis in, 192 



Erysipelas, sequelae of, 191 

in smallpox, 83 

symptoms of, 190 

treatment of, 192 
local, 192 

in typhoid fever, 34 

in varicella, 92 
Erythema in acute rheumatic fever, 201 

in dengue, 133 
Erythromelalgia, 1076 

definition of, 1076 

diagnosis of, 1077 

etiology of, 1077 

treatment of, 1077 
Esbach's method for quantitative estima- 
tion of albumin in urine, 742 
Essential emphysema, 413 
Ewart's sign of pericardial effusion, 461 
Exhaustion, heat, 1082 
Exophthalmic goitre, 751 
Exophthalmos in exophthalmic goitre, 

753 
Exudative nephritis, 701 
Eyeballs, protrusion of, in exophthalmic 
goitre, 753 

FACIAL erysipelas, 191 
expression in cholera, 208 

in typhoid, 27 
hemiatrophy, 1083 
nerve, paralysis of, 1025 

diagnosis of, 1026 
etiology of, 1025 
prognosis in, 1027 
symptoms of, 1026 
treatment of, 1027 
spasm, 1027 

prognosis in, 1028 
treatment of, 1028 
Fallopian tubes, tuberculosis of, 342 
False aneurysm, 534 

croup, 374 
Family ataxia, 967 
Famine fever, 68 
Farcv, 272 
buds, 273 
chronic, 273 
Fatty degeneration of heart, 473 

liver, 668 
Febricula, 351 

definition of, 351 
diagnosis of, 351 
etiology of, 351 
symptoms of, 351 
treatment of, 351 
Febris recurrens, 68 

Fecal impaction as cause of intestinal ob- 
struction, 624 
Fehling's solution, 799 
Fetid stomatitis, 546 
Fibrinous bronchitis, 388 
pericarditis, 459 
pleurisy, 430 
pneumonia, 143 
Fibroma of brain, 932 



INDEX 



1099 



Fibroma in lung, 428 

of mediastinum, 453 
Fibromata of kidney, 732 
Filaria nocturna, 892 

sanguinis hominis, 892 
Filariasis, 892 

definition of, 892 
elephantiasis in, 895 
filaria Demarquaii in, 892 
diurna in, 892 
loa in, 892 
Magalhaesi in, 892 
microscopic demonstration of, 891 
nocturna in, 892, 893 
Ozzardi in, 892 
perstans in, 892 
hsematochyluria in, 895 
lymph scrotum in, 896 
morbid anatomy of, 894 
pathology of, 894 
symptoms of, 895 
treatment of, 896 
varicose groin glands in, 896 
Fingers, club-shaped, in mitral regurgita- 
tion, 497 
Flatulence in sprue, 243 
Flea, sand, 911 
Floating kidney, 696 
Fluke, lung, 904 
Flukes, 904 

Flute-players' cramp, 1072 
Follicular colitis, 638 
pharyngitis, 556 
stomatitis, 546 
Food poisoning, 855 
Foot-and-mouth disease, 356 

definition of, 356 
Foramen ovale, persistence of, 527 
Forchheimer's spots in rubella, 116 
Foreign bodies in bowel, 624, 628 
Frambesia, 358 

definition of, 358 
diagnosis of, 360 

from syphilis, 360 
from verruga, 360 
eruption in, 359 
etiology of, 358 
incubation of, 359 
prognosis of, 360 
symptoms of, 359 
treatment of, 360 
tropica, 358 
Friedreich's ataxia, 967 

definition of, 967 
diagnosis of, 969 

from hereditary cerebellar 
ataxia, 969 
etiology of, 967 
gait in, 968 
inco-ordination in, 968 
morbid anatomy of, 967 
pathology of, 967 
prognosis in, 970 
speech in, 969 
symptoms of, 968 



Friedreich's ataxia, treatment of, 970 

disease, 967, 1039. See Paramyoclonus 
multiplex. 
Fulminant migraine, 1078 
Fulminating purpura, 786 
Fungus foot of India, 275 
Funnel chest in chronic hypertrophic tonsil- 
litis, 559 
Fusiform aneurysm, 534 



GAIT m Friedreich's ataxia, 968 
in locomotor ataxia, 961 
Galactotoxismus, 857 
Gall-bladder, carcinoma of, 683 
diagnosis of, 685 
etiology of, 683 
carcinoma of, jaundice in, 684 
inflammation of, acute, 675 
morbid anatomy of, 683 
pathology of, 683 
prognosis in, 685 
symptoms of, 683 
treatment of, 685 
malignant growths of, 683 
perforation of, 680 
Gallstone crepitus, 680 
Gallstones, 677 
Gangrene in cholera, 208, 209 
diabetic, 795 
of lung, 420 

cough in, 422 

in croupous pneumonia, 148, 157 
diagnosis of, 422 
etiology of, 420 
frequency of, 420 
morbid anatomy of, 421 
odor of breath in, 421 
pathology of, 421 
septic diarrhoea in, 422 
sputum in, 422 
symptoms of, 421 
treatment of, 422 
surgical, 423 
pulmonary, in bronchiectasis, 387 
in Raynaud's disease, 1075 
of skin in smallpox, 83 
in typhoid fever, 33 
Gangrenous appendicitis, 617 
pancreatitis, 689 
proctitis, epidemic, 239 
pyelonephritis, 726 
stomatitis, 548 
Gastralgia, 603 
Gastrectasis, 572 
acute, 578 

diagnosis of, 578 

from acute indigestion, 578 
from volvulus, 578 
etiology of, 578 
lavage in, 579 
morbid anatomy of, 578 
prognosis in, 579 
symptoms of, 578 
treatment of, 579 



1100 



INDEX 



Gastrectasis, atonic, 578 

toxic, 578 
Gastric cancer, 588 

diagnosis of, 592 

from gastric ulcer, 593 
from pernicious anaemia, 592 
microscopic, 594 
test meal in, 593 
duration of, 594 
etiology of, 589 
hsematemesis \n, 592, 605 
mode of spreading, 589 
morbid anatomy of, 589 
Oppler-Boas bacillus in, 594 
prognosis in, 594 
symptoms of, 591 
treatment of, 595 
vomiting in, 592 
catarrh, acute, 564 

definition of, 564 
diagnosis of, 565 
etiology of, 564 
symptoms of, 564 
treatment of, 565 
chronic, 568 

changes in yellow fever, 215 
crises in locomotor ataxia, 962 
dilatation, 572 
acute, 578 
definition of, 572 
diagnosis of, 576 
etiology of, 572 
morbid anatomy of, 573 
pathology of, 573 
physical signs of, 574 
symptoms of, 573 
treatment of, 576 
vomiting in, 573 
fever, 17 
ectasy, 572 
hyperperistalsis, 602 

treatment of, 602 
juice, hypersecretion of, 604 

hyposecretion of, 604 
neuralgia, 603 
neuroses, 601 
tetany, 575 

Chvostek's sign in, 576 
Erb's sign in, 576 
Trousseau's sign in, 575 
Turck's gyromele in, 575 
ulcer, 579 

anaemia in, 582 
classes of, 580 
chronic, 582 
definition of, 579 
diagnosis of, 584 

from duodenal ulcer, 584 

tests for blood in stools, 
584 
from gallstone colic, 584 
from gastric cancer, 584 
from gastric crises of loco- 
motor ataxia, 584 
from gastric neuralgia, 584 



Gastric ulcer, etiology of, 579 
frequency of, 579 
gastroenterostomy in, 587 
hsematemesis in, 582, 604 
hemorrhage in, treatment of, 587 
hour-glass contraction in, 581 
morbid anatomy of, 580 
pathology of, 580 
perforation in, 583 
prognosis in, 585 
symptoms of, 581 
treatment of, 586 
dietetic, 586 
surgical, 587, 588 
in typhoid fever, 36 
Gastritis, catarrhal, acute, 564 
chronic, 568 
definition of, 568 
diagnosis of, 570 

from gastric cancer, 570 
diet in, 572 
etiology of, 568 
lavage in, 571 
morbid anatomy of, 569 
pathology of, 569 
prognosis in, 570 
symptoms of, 569 
tongue in, 570 
treatment of, 570 
diphtheritic, 568 
erosive, 569 
mycotic, 568 
phlegmonous, 566 

definition of, 566 
diagnosis of, 567 
etiology of, 567 
symptoms of, 567 
treatment of, 568 
polyposa, 569 
toxic, acute, 565 

diagnosis of, 566 
etiology of, 565 
morbid anatomy of, 566 
symptoms of, 566 
treatment of, 566 
Gastrodiaphany, 575 
Gastrodynia, 603 
Gastrointestinal paralysis, 578 
Gastroptosis, 632 
Gastrorrhagia, 604 

Genito-urinary complications of typhoid 
fever, 41 
system, tuberculosis of, 338 
Geographical tongue, 549 
Gerhard's test for acetone in urine, 800 
German measles, 115. See Rubella. 
Gibralter fever, 245 
Gingko poisoning, 861 
Gland, thymus, diseases of, 772 
Glanders, 271 

bacillus mallei in, 272 
chronic, 273 
definition of, 271 
diagnosis of, 273 

from carbuncles, 273 



INDEX 



1101 



Glanders, diagnosis of, from multiple ab- 
scesses, 273 
etiology of, 272 
morbid anatomy of, 272 
pathology of, 272 
symptoms of, 273 
treatment of, 273 
Glands, ductless, diseases of, 749 

suprarenal, diseases of, 760 
Glandular enlargement in bubonic plague, 
222 
in diphtheria, 176, 177 
in rubella, 116 
in scarlet fever, 99, 103 
in whooping-cough, 122 
fever, 353 

definition of, 353 
diagnosis of, 353 
etiology of, 353 
glandular enlargements in, 353 
nephritis, acute, in, 353 
prognosis in, 354 
symptoms of, 353 
treatment of, 354 
tuberculosis, 299 
Glaucoma, hemorrhagic, in chronic inter- 
stitial nephritis, 715 
Glenard's disease, 632 
Glioma of brain, 932, 933 
Globus in hysteria, 1050 
Glomerular nephritis, 700 
Glomerulo nephritis, chronic, 704 
Glosso-labio-laryngeal paralysis, 977 
Glossopharyngeal nerve, paralysis of, 1030 
Glottis, spasm of, in tetanus, 269 
Glycosuria, 794, 795 
Goitre, 749 

benign, 749 
colloid, 750 
cystic, 749 
definition of, 749 
etiology of, 750 
exophthalmic, 751 
definition of, 751 
dyspncea in, 754 
etiology of, 752 
exophthalmus in, 753 
frequency of, 752 
Mobius' sign in, 753 
morbid anatomy of, 752 
nervous symptoms of, 754 
pathology of, 752 
prognosis in, 755 
Stelwag's sign in, 753 
symptoms of, 753 
tachycardia in, 753 
treatment of, 755 
tremor in, 754 
von Graefe's sign in, 753 
hyperplastic, 749 
lingual, 750 
malignant, 749 
mixed, 749 
neoplastic, 749 
parenchymatous, 749 



Goitre, simple, 749 

symptoms of, 750 

treatment of, 750 

vascular, 749 
Gold-dust complaint, 412 
Gonorrhceal arthritis, ankylosis in, 187 
chronic, 186 
symptoms of, 186 
temporary, 186 
treatment of, 188 

endocarditis, 187 

infection, 186 

diagnosis of, 187 
prognosis of, 188 

pyaemia, 186 

rheumatism, 187 
Gout, 808 

acute, 813 

symptoms of, 813 

cardiovascular changes in, 812 

chronic, 814 

symptoms of, 814 

definition of, 80S 

diagnosis of, 815 

from arthritis deformans, 816 

etiology of, 808 

frequency of, 809 

irregular, symptoms of, 814 

joint changes in, 811 

morbid anatomy of, 811 

pathology of, 809 

prognosis in, 816 

retrocedent, 815 

symptoms of, 813 

treatment of, 816 
dietetic, 817 
Gouty lesions in chronic lead poisoning, 853 
Grain shovellers' disease, 411 
Grand mal, 1052 
Granular kidney, 710 

meningitis, 301 
Graves' disease, 751 
Green sickness, 776 
Grindstone consumption, 412 
Ground itch, 889 
Guinea-worm, 896 

definition of, 896 

disease, 896 

distribution of, 896 

symptoms of, 897 

treatment of, 898 
Gull's disease, 756 
Gumma of brain, 932, 933 
Gummata, syphilitic, 281, 284 



H^EMAMCEBA malarias, 863 
in man, 865 
in mosquito, 867 
Haematemesis, 604 
in aneurysm, 605 

diagnosis of, from haemoptysis, 607 
in gastric cancer, 592, 605 

ulcer, 582, 604 
in haemophilia, 605 



1102 



INDEX 



Hsematemesis in hepatic cirrhosis, 605 
in purpura, 605 
in smallpox, 605 
in yellow fever, 605 
Hsematinuria, 739 

treatment of, 740 
Haematitis, suppurative, 780 
Haematochyluria in filariasis, 895 
Hsematuria, 738 

in bilharzia disease, 906 
causes of, 738 
endemic, 904 
in movable kidney, 697 
treatment of, 738 
in ulcerative endocarditis, 487 
Hsemoglobinuria, 739 

in croupous pneumonia, 155 
in malarial fever, 877 
Haemopericardium, 467 
Haemophilia, 787 

definition of, 787 
epistaxis in, 788 
etiology of, 787 
hsematemesis in, 605 
morbid anatomy of, 788 
pathology of, 788 
prognosis in, 788 
symptoms of, 788 
treatment of, 788 
Haemoptysis, 607 

in bronchiectasis, 386 
endemic, 904, 907 
parasitic, 904, 907 
in pulmonary tuberculosis, 316 
Hammerer's palsy, 1072 
Hanot's cirrhosis of liver, 664 
Harrison's groove in rickets, 828 
Haut mal, 1052 
Hay fever, 367 

definition of, 367 
distribution of, 367 
etiology of, 367 
morbid anatomy of, 367 
pathology of, 367 
prognosis of, 368 
symptoms of, 367 
treatment of, 368 
Haygarth's nodosities in arthritis defor- 
mans, 820 
Head tetanus, 271 
Heart, aneurysm of, 479 
causes of, 480 
forms of, 479 
symptoms of, 481 
atrophy of, 474 
bilocular, 527 
brown induration of, 474 
congenital defects of, 527 
degeneration of, amyloid, 474 
calcareous, 474 
fatty, 474 
hyaline, 474 
parenchymatous, 473 
dilatation of, 468, 471 
causes of, 471 



Heart, dilitation of, definition of, 468 
physical signs of, 472 
prognosis in, 472 
symptoms of, 471 
treatment of, 472 
diseases of, 468 
failure in diphtheria, 179 
in typhoid fever, 35 
hypertrophy of, 468, 469 
definition of, 468 
diagnosis of, 470 

from cardiac dilatation, 470 
from pericardial effusion, 470 
from tobacco heart, 470 
physical signs of, 469 
prognosis in, 470 
symptoms of, 469 
treatment of, 471 
-muscle, changes in, in typhoid fever,26 
neuroses of, 521 

definition of, 521 
treatment of, 522 
palpitation of, 521 
fragmentation of, 474 
pulmonary valves of, disease of, 515 
segmentation of, 474 
-sounds in typhoid fever, 34 
trilocular, 527 
tuberculosis of, 343 
valves of, mechanism of, 490 
valvular anomalies of, 528 
disease of, chronic, 489 
causes of, 489 
treatment of, 516 
valves affected in, 489 
wounds of, 481 
Heat exhaustion, 1082 
Heatstroke, 1080 

Heat test for albumin in urine, 742 
Heberden's nodes in arthritis deformans, 

821 
Hematoma of dura mater, 947 
Hemiansesthesia in apoplexy, 920 

in hysteria, 1049 
Hemianopsia, 1015 
in apoplexy, 920 
binasal, 1015 
bitemporal, 1015 
homonymous, 1015 
Hemiatrophy, facial, 1083 
Hemiplegia in apoplexy, 919 
in croupous pneumonia, 160 
in malarial fever, 876 
pneumonique, 159 
spastic, 925 
in typhoid fever, 44 
in uraemia, 722 
Hemorrhage, cerebral, 913 
in diphtheria, 180 
in duodenal ulcer, 630 
from lungs, 607 
into pancreas, 695 
in pneumonic plague, 223 
in pulmonary tuberculosis, 316 
retinal, in malarial fever, 876 



INDEX 



1103 



Hemorrhage into spinal cord, 990 
definition of, 990 
diagnosis of, 991 
etiology of, 990 

prognosis of, 991 

symptoms of, 990 

treatment of, 991 

membranes, 991 
from stomach, 604 

symptoms of, 605 
subconjunctival in whooping-cough, 

122 
in typhoid fever, 30, 36, 37 

diagnosis of, 36 

symptoms of, 36 

treatment of, 57 
Hemorrhagic affections of newborn, 786 
albuminuric retinitis, 714 
cysts of pancreas, 694 
glaucoma in chronic interstitial neph- 
ritis, 715 
internal pachymeningitis, 947 
measles, 112 
nephritis, 701 
pancreatitis, acute, 695 
peritonitis, 643 
smallpox, 81 
Henoch's purpura, 786 
Hepatic abscess, 653 

amcebse dysenteriae in, 656 

diagnosis of, 657 

from emp3^ema, 658 

from infection of gall-ducts, 

657 
from malarial infection, 657 

in dysentery, 232 

etiology of, 653 

fever in, 656 

morbid anatomy of, 654 

multiple, 655 

pathology of, 654 

prognosis in, 658 

pyaemic, 654 

single large, 654 

symptoms of, 656 

traumatic, 653 

treatment of, 658 

tropical, 654 
artery, aneurysm of, 543 
bloodvessels, affections of, 666 
changes in croupous pneumonia, 149 

in yellow fever, 215 
cirrhosis, 658. See Liver, cirrhosis of. 

haematemesis in, 605 
congestion, 666 

fever of Charcot, intermittent, 679 
tuberculosis, 338 
Hepatitis, acute, 653 

definition of, 653 

etiology of, 653 
Hepatization of lung, 426 

in croupous pneumonia, 147 
Hereditary ataxia, 967 

Marie's cerebellar, 970 
ataxic paraplegia, 967 



Hereditary chorea, 1046 

syphilis, 286 
Herpes in cerebrospinal fever, 137 
in croupous pneumonia, 151 
in typhoid fever, 31 
Hill diarrhoea, 240 

definition of, 240 
etiology of, 240 
pathology of, 241 
symptoms of, 241 
treatment of, 241 
Hip, spontaneous dislocation of , in typhoid 

fever, 44 
Hippocratic facies in acute peritonitis, 644 
in cholera, 208 
in yellow fever, 216 
Hob-nail liver, 659 
Hodgkin's disease, 767 

blood changes in, 768 
bronzing of skin in, 768 
definition of, 767 
diagnosis of, 769 

from true leukaemia, 769 
from tuberculous lymph 
glands, 769 
dyspnoea in, 768 
etiology of, 767 
morbid anatomy of, 767 
oedema in, 768 
pathology of, 767 
prognosis in, 770 
symptoms of, 767 
treatment of, 770 
Hoffman's sign of tetany, 1065 
Hookworm disease, 888 
Horseshoe kidney, 696 
Hour-glass stomach, 598. See Stomach, 

hour-glass. 
Hunger typhus, 61 
Huntington's disease, 1046 
Hutchinson's pupil in apoplexy, 921 

teeth in syphilis, 286 
Hyaline degeneration of heart, 474 
Hybrid scarlet fever, 115 
Hydatid cyst of mediastinum, 453 
of peritoneum, 649 
of spleen, 764 
Hydrocephalus, 927 
Hydronephrosis, 728 
acquired, 728 
congenital, 728 
definition of, 728 
diagnosis of, 729 
etiology of, 728 
pathology of, 728 
prognosis of, 729 
in tuberculosis of kidney, 342 
symptoms of, 729 
treatment of, 729 
Hydropericardium, 466 
prognosis of, 466 
symptoms of, 466 
treatment of, 467 
Hydrophobia, 261 
definition of, 261 



1104 



INDEX 



Hydrophobia, diagnosis of, 265 

from pseudohydrophobia, 265 
from tetanus, 265 

distribution of, 262 

etiology of, 262 

frequency of, 262 

morbid anatomy of, 262 

pathology of, 262 

prevention of, 262 

prognosis of, 265 

symptoms of, in animals, 263 
in man, 264 

treatment of, 265 
b} r serum, 265 
Hydropneumothorax, 449 

coin sound in, 451 

in croupous pneumonia, 157 

metallic tinkling in, 451 

physical signs of, 451 

Skodaic resonance in, 451 
Hydrotherapy in typhoid fever, 52 
Hydrothorax, 448 
Hyperemia of kidney, acute, 699 
chronic, 699 

of liver, 666 
Hyperhsemocytosis in scarlet fever, 99 
Hymenolipsis nana, 901 
Hyperesthesia of stomach, 603 
Hypernephromata of kidney, 732 
Hyperperistalsis, gastric, 602 
Hyperplastic goitre, 749 

tuberculosis, chronic, 296 
Hypertrophic cirrhosis of liver, 663 

emphysema, 413 

pulmonar}' osteoarthropathy, 810 

rhinitis, 365 

stenosis of pylorus, 595 

tonsillitis, chronic, 558 
Hypertrophy, pseudomuscular, 1035 
Hypo derrnocly sis in cholera infantum, 614 
Hvpoglossal nerve, disease of, 1034 
Hysteria, 1047 

anaesthesia in, 1049 

aphonia in, 1050 

convulsion in, 1048 

in chorea minor, 1045 

definition of, 1047 

diagnosis of, 1051 

from organic nervous disease, 1051 

disturbances of special sense in, 1049 

etiology of, 1047 

globus in, 1050 

hemianesthesia in, 1049 

major, 1048 

merycismus in, 1050 

ovarian tenderness in, 1050 

paralysis of motion in, 1050 

pathology of, 1048 

prognosis in, 1051 

pseudo-angina in, 1050 

symptoms of, 1048 
sensory, 1049 

tachycardia in, 1050 

treatment of, 1051 
Hysteroepilepsy, 1051 



ICE, infection by, in typhoid fever, 18 
" Iced liver," 464 
Ichthyosis lingualis, 550 
Ichthyotoxismus, 856 
Icterus neonatorum, 686 
Idiocy, acquired, 928 
Idiopathic dilatation of colon, 640 

muscular spasm, 1064 
Ileocecal intussusception of bowel, 625 
Ileocolic intussusception of bowel, 625 
Ileocolitis of childhood, 609 
definition of, 609 
diagnosis of, 612 

from typhoid fever, 612 
etiology of, 609 
morbid anatomy of, 610 
pathology of, 610 
prognosis in, 612 
symptoms of, 611 
treatment of, 612 
Incarcerated kidney, 696 
Incoordination in Friedreich's ataxia, 968 

in locomotor ataxia, 961 
"India-rubber bottle stomach," 589 
Indicanuria, 745 
test for, 746 
Indurative mediastinopericarditis, 463 
Infantile cerebral paralysis, 925 

eclampsia, 1062. See Eclampsia, infan- 
tile, 
palsy, acute, 970 
spinal paralysis, 970 
scurvy, 831 
Infarct of spleen, 764 

in septicaemia, 195 
Infarction of lung in typhoid fever, 42 
Infection, diseases due to specific, 17 

latent malarial, 878 
Inflammation of bile-ducts, suppurative, 
673 
of liver, 653 
of salivary glands, 551 
Influenza, 125 

bacillus of Pfeiffer in, 125, 126 
bronchitis in, 126 
chill in, 126 
complications of, 128 

cardiac, 128 
definition of, 125 
diagnosis of, 128 
diarrhoea in, 127 
endemic-epidemic, 125 
etiology of, 125 
fever in, 126 
history of, 125 
incubation in, 126 
jaundice in, 127 
kidneys in, 128 
meningitis, 127 
mental disturbances in, 127 
nervous manifestations of, 127 
pleurisy in, 127 
pneumonia in, 127 
prophylaxis of, 130 
pulmonary congestion in, 127 



INDEX 



1105 



Influenza, sequelae of, 128 
symptoms of, 126 
toxic neuritis in, 127 
treatment of, 129 
vera, 125 
vomiting in, 127 
Infusoria, parasitic, 909 
Ingravescent apoplexy, 922 
Inoculation preventive in plague, 224 
Insolation, 1080 

Insomnia in croupous pneumonia, 155 
in typhoid fever, 26 
treatment of, 58 
in uraemia, 722 
Insular sclerosis, 954 
Intermittent fever, diagnosis of, 872 
from septicaemia, 872 
from tuberculosis, 872 
from ulcerative endocarditis, 
872 
prognosis of, 872 
treatment of, 872 
hepatic fever of Charcot, 679 
malarial fever, 863 
Interstitial emphysema, 413 
neuritis, 1003 
nephritis, chronic, 710 
Intestinal amcebiasis, 227 

antisepsis in typhoid fever, 56 
changes in yellow fever, 216 
hemorrhage in typhoid fever, 36 

treatment of, 57 
perforation in typhoid fever, 37 

treatment of, 58 
myiasis, 912 
obstruction, 623 
acute, 623 
causes of, 623 
chronic, 623 

by congenital malformations, 624 
diagnosis of, 624 
prognosis of, 624 
symptoms of, 624 
treatment of, 624 
definition of, 623 
by foreign bodies, 624, 628 
by internal strangulation, 624, 626 

symptoms of, 627 
by intestinal paralysis, 624, 627 
by intussusception, 624 
etiology of, 625 
frequency of, 625 
pathology of, 625 
prognosis in, 626 
symptoms of, 625 
treatment of, 626 
by volvulus, 627 

prognosis in, 627 
symptoms of, 627 
treatment of, 627 
ulcers in paratyphoid fever, 59 
Intestines, diseases of, 608 
tuberculosis of, 335 

chronic hyperplastic, 336 
Intoxications, 843 

70 



Intubation in acute catarrhal laryngitis, 371 

in cedematous laryngitis, 374 
Intussusception, 624 

acute, 625 

enteric, 625 

etiology of, 625 

frequency of, 625 

ileocaecal, 625 

ileocolic, 625 

pathology of, 625 

prognosis in, 626 

retrograde, 625 

subacute, 625 

symptoms of, 625 

treatment of, 626 

ultra-acute, 625 
Iritis, syphilitic, 284 
Itch, dhobie, 909 



JACKSONIAN epilepsy, 1061 
Japanese river fever, 357 

definition of , 357 
etiology of, 358 
fever in, 358 
symptoms of, 358 
treatment of, 358 
Jaundice in acute pancreatitis, 689 
in cancer of gall-bladder, 684 
in cholelithiasis, 678 
in croupous pneumonia, 155 
in influenza, 127 
in newborn, 686, 786 
in relapsing fever, 69 
in typhoid fever, 40 
in yellow fever, 216 
Joint complications in typhoid fever, 44 
Joints in gout, changes in, 811 

inflammation of, in acute rheumatic 

fever, 199 
in verruga, 361 



KAKKE, 1007 
Kala-azar, 883 

definition of, 883 
etiology of, 883 
morbid anatomy of, 884 
pathology of, 884 
symptoms of, 884 
treatment of, 884 
Keratitis in measles, 113 

syphilitic, 286 
Kernig's sign in cerebrospinal fever,, 138 
Kidney, adenoma of, 732 
alveolar, 732 
papillary, 732 
amyloid disease of, 718 
definition of, 718 
etiology of, 718 
pathology of, 719 
prognosis in, 719 
symptoms of, 719 
treatment of, 719 
urine in, 719 



1106 



INDEX 



Kidney, angiomata of, 732 
cancer of, 732 
chronic contracted, 710 
" cinder-sifting," 696 
circulatory disturbances in, 698 
cirrhosis of, 710 
contracted, 710 
in croupous pneumonia, 149 
cystic disease o^, 730 
cysts of, congenital, 730 
echinococcus, 731 
multiple, 730 
single, 730 
symptoms of, 731 
in diabetes mellitus, changes in, 793 
diseases of, 696 
endothelioma of, 732 
fibromata of, 732 
floating, 696 
granular, 710 
horseshoe, 696 
hyperemia of, acute, 699 
treatment of, 699 
chronic, 699 

albuminuria in, 699 
diagnosis of, 699 
symptoms of, 699 
treatment of, 699 
hypemephromata of, 732 
incarcerated, 696 
in influenza, 128 
large white, 705 
lipomata of, 732 

in malarial fever, changes in, 868 
malformations of, 696 
movable, 696 

diagnosis of, 697 
Dietl's crises in, 697 
etiology of, 697 
hematuria in, 697 
symptoms of, 697 
treatment of, 698 
papilloma of, 732 
sarcoma of, 732 
in scarlet fever, 99 102 
sclerotic, 710 
small white, 705 
stone in, 733 

suppuration of, in septicaemia, 195 
tuberculosis of, 341 
tumors of, 732 

malignant, hsematuria in, 733 
symptoms of, 733 
in typhoid fever, changes in, 26 
in typhus fever, 63 
Klebs-Loeffler bacillus of diphtheria, 172 
Knee-jerks in locomotor ataxia, 961 
Knife-grinders' rot, 412 
Kopf -tetanus, 271 
Koplik's spots in measles, 111 
Korsakoff's disease, 1009 
Kreotoxismus, 856 
Kubisagari, 362 

diplopia in, 362 
paresis in, 362 



Kubisagari, ptosis in, 362 

treatment of, 362 
KussmauTs coma in diabetes mellitus, 
797 



LACQUER poisoning, 860 
treatment of, 861 
La grippe, 125. See Influenza. 
Landouzy-Dejerine type of muscular 

dystrophy, 1037 
Landry's paralysis, 1000 
Large-lunged emphysema, 413 
Larval plague, symptoms of, 223 
Laryngeal diphtheria, 178 
tuberculosis, 314 
ulceration in typhoid fever, 42 
Laryngitis, catarrhal, acute, 369 
definition of, 369 
diagnosis of, 370 
etiology of, 369 
intubation in, 371 
pathology of, 370 
prognosis of, 371 
symptoms of, 370 
tracheotomy in, 371 
treatment of, 371 
chronic, 371 

diagnosis of, 372 
pathology of, 372 
symptoms of, 371 
treatment of, 372 
cedematous, 372 

cyanosis in, 373 
definition of, 372 
diagnosis of, 373 

from foreign body, 373 
from laryngeal crises in loco- 
motor ataxia, 373 
etiology of, 372 
intubation in, 374 
pathology of, 373 
prognosis in, 373 
symptoms of, 373 
tracheotomy in, 374 
treatment of, 373 
in smallpox, 83 
spasmodic, 374 

definition of, 374 
etiology of, 374 
treatment of, 374 
syphilitic, 376 

diagnosis of, 377 

from tuberculous ulceration, 
377 
etiology of, 376 
prognosis of, 377 
symptoms of, 377 
treatment of, 377 
tuberculous, 375 

aphonia in, 375 
cough in, 375 
definition of, 375 
diagnosis of, 376 

from carcinoma of larynx, 376 



IXDEX 



1107 



Laryngitis, tuberculosis, diagnosis of, from 
syphilitic laryngitis, 376 
dysphagia in, 375 
etiology of, 375 
lesion in, 376 
pathology of, 375 
prognosis of, 376 
symptoms of, 375 
treatment of, 376 
Larvnx, diseases of, 369 
Latah, 1066 
Lateral sclerosis, 978 

amyotrophic, 980 
Lathyrism, 859 

definition of, 859 
etiology of, 859 
history of, 859 
symptoms of, 859 
treatment of, 860 
Lavage in chronic gastritis, 572 
Lead poisoning, 851 
acute, 851 
chronic, 851 

anaemia in, 854 
blue line on gums in, 853 
colic in, 854 
convulsions in, 853 
diagnosis of, 854 

from acute poliomvelitis, 

854 
from chronic .poliomev- 

litis, 854 
from epilepsy, 854 
from pressure palsy, 854 
etiology of, 852 
gouty lesions in, 853 
morbid anatomy of, 852 
neuritis in, 853 
optic neuritis in, 853 
pathology of, 852 
prevention of, 852 
prognosis in, 854 
squint in, 853 
symptoms of, 853 
treatment of, 854 
wrist-drop in, 853 
Leathery stomach, 589 
Leontiasis, 349 
ossea, 840 
Leprosy, 344 

anaesthetic, 349 
bacillus of, 345 
clinical forms of, 347 
definition of, 344 
diagnosis of, 349 
distribution of, 344 
epistaxis in, 348 
eruptions in, 348, 349 
etiology of, 345 
incubation period in, 348 
leontiasis in, 349 
leprous chancre in, 348 
manner of infection in, 345 
mixed, 349 
morbid anatomy of, 347 



Leprosy, nodules in, 348 
prognosis in, 350 
prophylaxis of, 351 
symptoms of, 347 
treatment of, 350 
tuberculous, 348 
Leptomeningitis, 948 
diagnosis of, 949 
morbid anatomy of ? A 9 
pathology of, 949 
symptoms of, 949 
treatment of, 950 
Lethargy, African, 879 
Leucocythaemia, 780 
Leucocytosis in typhoid fever, 

33 
Leukaemia, 780 

definition of, 780 
diagnosis of, 783 
etiologv of, 781 
lymphatic, 780, 782 

symptoms of, 783 
morbid anatomy of, 781 
myelogenous, 780 
pathology of, 781 
prognosis in, 783 
splenomedullary, 780, 781 
blood changes in, 781 
spleen in, 782 
symptoms of, 783 
treatment of, 784 
Leukoplakia buccalis, 550 
Lingual goitre, 750 
Lipomata of kidney, 732 
Lithiasis, 411 
Lithuria, 746 
Little's disease, 929 
Liver, abscess of, 653 

diagnosis of, 657 
in dysentery, 232 
etiology of, 653 
multiple, 655 
pathology of, 654 
prognosis of, 658 
pyaemic, 654 
single large, 654 
symptoms of, 656 
traumatic, 653 
treatment of, 658 
tropical, 654 
amyloid, 667 

symptoms of, 667 
treatment of, 667 
angiomata, cavernous, of, 668 
carcinoma of, 668 

secondary, 668 
changes in, in typhoid fever, 25 
in cholera, 206 
cirrhosis of, 658 
atrophic, 659 

etiology of, 660 
hepatic coma in, 662 
morbid anatomy of, 660 
pathology of, 660 
physical signs of, 662 



1108 



INDEX 



Liver, cirrhosis of, atrophic, prognosis in, 
662 
symptoms of, 661 
treatment of, 662 
capsular, 665 
definition of, 658 
hypertrophic, 659, 663 
definition of, 663 
diagnosis of, 664 
etiology of, 663 
Hanot's type of, 664 
morbid anatomy of, 663 
pathology of, 663 
prognosis in, 664 
symptoms of, 664 
treatment of, 664 
syphilitic, 664 

treatment of, 665 
congestion of, 666 

nutmeg appearance in, 666 
symptoms of, 667 
treatment of, 667 
cystic disease of, 668 
diseases of, 653 
distomatosis of, 908 
hyperemia of, 666 
fatty, 668 
flukes, 908 

varieties of, 905 
"iced," 464 
inflammation of, 653 
in malarial fever, changes in, 868 
red atrophy of, 666 
sarcoma of, 668 
syphilis of, 281 
tuberculosis of, 338 
tumors of, 668 

diagnosis of, 669 

from echinococcus cyst, 669 
from gumma, 669 
from hypertrophic cirrhosis, 
669 
prognosis in, 669 
symptoms of, 669 
treatment of, 669 
in typhoid fever, changes in, 40 
yellow atrophy of, a.cute, 670 
definition of, 670 
diagnosis of, 670 
etiology of, 670 
morbid anatomy of, 670 
pathology of, 670 
prognosis in, 671 
symptoms of, 670 
treatment of, 671 
Lobar pneumonia, 143 
Lobular pneumonia, 397 
Localized epilepsy, 1061 

peritonitis, 643 
"Lock-jaw" in tetanus, 269 
Locomotor ataxia, 958 

allochiria in, 962 
Argyll-Robertson pupil in, 962 
Charcot joint in, 963 
crises in, 962 



Locomotor, ataxia, definition of, 958 
diagnosis of, 964 

from caries of vertebrse, 964 
from cerebellar tumor, 964 
from general paralysis of in- 
sane, 964 
from paraplegia, 964 
from peripheral neuritis, 964 
diplopia in, 963 
etiology of, 958 
gait in, 961 

girdle sensations in, 962 
inco-ordination in, 961 
knee-jerk in, 961 
lightning pains in, 962 
morbid anatomy of, 958 
ocular symptoms of, 962 
optic atrophy in, 963 
pathology of, 958 
perforating ulcer of foot in, 964 
prognosis in, 964 
Romberg's symptom in, 961 
symptoms of, 960 
treatment of, 965 
baths in, 966 
electrical, 966 
WestphaPs symptom in, 961 
Loculated peritonitis, 643 
Lu cilia macellaria, 911 
Ludvig's angina, 552 

symptoms of, 552 
treatment of, 552 
Lues, 276 

venerea, 276 
Lumbar puncture as aid to diagnosis of 

cerebrospinal fever, 140 
"Lumpy jaw," 274 
Lung, abscess of, 423 

in croupous pneumonia, 148, 157 
congestion of, 425 
diseases of, 397 
distomatosis of, 904, 907 
emphysema of, 413 
fever, 143 
flukes, 907 
gangrene of, 420 

in croupous pneumonia, 148, 162 
hemorrhage from, 607 
hypostatic congestion of, in typhoid 
fever, 42 
in typhus fever, 63 
infarction of, in typhoid fever, 42 
oedema of, in cholera, 209 
syphilis of, 281 
tumors in, 428 
Lupinosis, 859 

Lymph nodes, syphilitic, 283 
scrotum in filariasis, 896 
Lymphadenoma of mediastinum, 452 
Lymphatic areas of stomach, 590 
constitution, 770 
glands, tuberculosis of, 299 
involvement in diphtheria, 176 
leukaemia, 780, 782 
system, diseases of , 749 



INDEX 



1109 



Lymphoma of mediastinum, 452 
Lyssa, 261 



McBURNEY'S point, 620 
Macular syphilide, 284 
Madura foot, 275 
Maidismus, 857 
Malarial fever, 863 

aestivo-autumnal, parasite of, 866 
ague cake in, 868, 875 
blood changes in, 867 

examination in, 869 
bone-marrow in, 868 
chill in, 869 
chronic, 863 

changes in. 868 
comph cations of, 875 

nervous, 876 
definition of, 863 
distribution of, 863 
etiology of, 864 

mosquito as, 864 
hemiplegia, 876 
hepatic changes in, 868 
intermittent, 863 
morbid anatomy of, 867 
nephritic changes in, 868 
pathology of, 867 
pernicious, 863, 875 

symptoms of, 875 
Plasmodium, 863 
prevention of, 867 
quartan, parasite of, 866 
remittent, 863 
retinal hemorrhages in, 876 
sequelae of, 875 
splenic changes in, 868 

enlargement in, 876 
symptoms of, 870 
tertian, parasite of, 865 
infection, latent, 878 
Malformations, congenital, of bowel, 624 

of kidney, 696 
Malignant anthrax oedema, 259 
goitre, 749 

growths of gall-bladder and biliary 
ducts, 683 
of spleen, 764 
of vertebrae, 994 
Mali-mali, 1066 
Malta fever, 245 

complications of, 249 
definition of, 245 
diagnosis of, 247 
distribution of, 245 
duration of, 248 
etiology of, 246 
fever in, 247 
incubation of, 247 
micrococcus melitensis in, 245 
pathology of, 246 
prognosis of, 248 
spleen in, 246 
symptoms of, 247 



Malta fever, treatment of, 248 

Mania in uraemia, 722 

Marie's cerebellar hereditary ataxia, 970 

disease, 837 
Measles, 108 

bacteriology of, 109 

"black," 112 

bronchitis in, 110, 111 

bronchopneumonia in, 110, 112 

chill in, 110 

complications of, 112 
nervous, 113 

conjunctivitis in, 113 

coryza in, 110 

diagnosis of, 113 

diarrhoea in, 112 

diphtheria in, 113 

distribution of, 108 

eruption of, 111 

etiology of, 108 

fever in, 111 

frequency of, 110 

German, 115. See Rubella. 

hemorrhagic, 112 

incubation of, 109 

keratitis in, 113 

"Koplik's spots" in, 111 

meningitis in, 113 

morbid anatomy of, 110 

noma in, 112 

pathology of, 110 

prevention of, 109 

prognosis in, 113 

respiratory form of, 111 

sequelae of, 112 

stomatitis in, 112 

symptoms of, 110 

transmission of, mode of, 109 

treatment of, 114 

variations of, 111 

vomiting in, 112 

whooping-cough in, 113 
Mediastinal glands, tuberculosis of, 

300 
Mediastinopericarditis, indurative, 463 
Mediastinum, abscess of, 452, 455 

carcinoma of, 452 

dermoid cyst of, 453 

diseases of, 452 

fibroma of, 453 

hydatid cyst of, 453 

lymphadenoma of, 452 

lymphoma of, 452 

sarcoma of, 452 

teratoma of, 453 

tumors of, 452 

abdominal effusion in, 454 
dropsy in, 454 
dyspnoea in, 454 
pain in, 455 
symptoms of, 453 
Medina worm, 896 
Mediterranean fever, 245 
Melanuria, 746 
Membranous oesophagitis, 560 



1110 



INDEX 



Meniere's disease, 1029 

treatment of, 1030 
Meningeal tuberculosis, acute, 301 
Meningitis in acute rheumatic fever, 201 
basilar, 301 
cerebral, 946 

definition of, 946 
etiology of, 946 
cerebrospinal, 134 
in croupous pneumonia, 149, 159 
granular, 301 
in influenza, 127 
in measles, 113 
in mumps, 118 
spinal, 997 

chronic, 999 

diagnosis of, 999 
etiology of, 999 
symptoms of, 999 
treatment of, 999 
definition of, 997 
diagnosis of, 998 
etiology of, 997 
morbid anatomy of, 997 
pathology of, 997 
prognosis in, 998 
symptoms of, 997 
treatment of, 998 
in typhoid fever, 43, 44 
Meningoencephalitis, 950 
Mental disturbances in influenza, 127 

state in chorea minor, 1045 
Merycismus, 603 

in hysteria, 1050 
Mesenteric artery, superior, aneurysm of, 
543 
glands, tuberculosis of, 300 
Metallic tinkling in hydropneumothorax, 

451 
Metastatic pneumonia, 408 
Micrococcus lanceolatus in pneumonia, 143, 
147 
melitensis in Malta fever, 245 
rheumaticus in acute rheumatic fever, 
198 
Microsporon minutissimus in dhobie itch, 

909 
Migraine, 1077 

definition of, 1077 
fulgurating, 1078 
fulminant, 1078 
symptoms of, 1078 
treatment of, 1079 
Miliary fever, 356 

definition of, 356 
etiology of, 357 
prognosis in, 357 
symptoms of, 357 
treatment of, 357 
tubercle, 295 
tuberculosis, acute, 297 
Milk, infection by, in typhoid fever, 18 
sickness, 352 

definition of, 352 
symptoms of, 352 



Milk sickness, treatment of, 352 
Miners' anaemia, 887 
cachexia, 887 
disease, 887 
phthisis, 412 
Minor epilepsy, 1061 
Mitral regurgitation, 494 

blood-spitting in, 497 
club-shaped fingers in, 497 
cyanosis in, 497 
diagnosis of, 498 
dyspncea in, 496 
oedema in, 497 
pathology of, 494 
physical signs of, 497 
prognosis in, 498 
symptoms of, 495 
objective, 497 
subjective, 496 
stenosis, 499 

definition of, 499 
diagnosis of, 503 

from adhesive pericarditis, 504 
from Flint's murmur, 503 
from tricuspid stenosis, 503 
etiology of, 499 
pathology of, 499 
physical signs of, 500 
prognosis in, 504 
Mobius' sign in exophthalmic goitre, 753 
Monilia Candida in thrush, 547 
Monoplegia in croupous pneumonia, 160 

in uraemia, 722 
Morbilli, 108. See Measles. 
Morbus maculosus neonatorum, 787 
Morphinism, 848 
chronic, 848 

symptoms of, 848 
treatment of, 849 
Morvan's disease, 989 
Motor neuritis, 1008 
Mountain fever, 354 

Mouth breathing in chronic hypertrophic 
tonsillitis, 559 
diseases of, 545 
dry, 551 

lesions in sprue, 243 
putrid sore, 546 
Movable kidney, 696 

spleen, 764 
Movements in chorea minor, 1044 

in paralysis agitans, 1041 
Mucomembranous enteritis, 637 
Mucous colitis, 637 
patches, 550 

in syphilis, 284, 286 
Muguet, 547 
Multiple neuritis, 1007 
endemic, 249 
myoclonus, 1039 
sclerosis, 954 
serositis, 464 
Mumps, 117 

arthritis in, 118 
complications of, 117 



INDEX 



1111 



Mumps, convulsions in, 118 
definition of, 117 
etiology of, 117 
fever in, 117 
incubation of, 117 
meningitis in, 118 
orchitis in, 117 
pancreatitis in, 118 
pathology of, 117 
sequelae of, 117 
symptoms of, 117 
treatment of, 118 
Mural endocarditis, 482 
Mu3ca vomitoria, 912 

Muscle changes in croupous pneumonia, 149 
Muscles, diseases of, 1035 
Muscular atrophy, peroneal type of, 1037 
definition of, 1037 
etiology of, 1037 
morbid anatomy of, 1038 
pathology of, 1038 
prognosis in, 1038 
symptoms of, 1038 
treatment of, 1038 
in apoplexy, 921 
progressive, 974, 1037 

Charcot-Marie-Tooth form of, 

1037 
neural, of Hoffman, 1037 
contractions in paramyoclonus multi- 
plex, 1039 
dystrophies, 1035 

definition of, 1035 
Erb's juvenile, 1036 
etiology of, 1035 
Landouzy-Dejerine type of, 1037 
morbid anatomy of, 1035 
pathology of, 1035 
treatment of, 1037 
rheumatism, 824 
rigidity in paralysis agitans, 1042 

in tetanus, 268 
spasm, idiopathic, 1064 
tremors in typhoid fever, 27 
Mycetoma, 275 

treatment of, 276 
Mycotic aneurysm, 534 

gastritis, 568 
Myelitis, 983 
acute, 983 

etiology of, 983 
morbid anatomy of, 983 
paraplegia in, 984 
pathology of, 983 
prognosis in, 985 
symptoms of, 984 
treatment of, 985 
ascending, 983 
central, 983 
chronic, 985, 988 

definition of, 985 
diagnosis of, 986 
etiology of, 985 
morbid anatomy of, 986 
pathology of, 986 



Myelitis, chronic, prognosis in, 986 
symptoms of, 986 
treatment of, 986 
definition of, 983 
descending, 983 
disseminated, 983 
subacute, 983 
transverse, 983 
Myelogenous leukaemia, 780 
Myelomalacia, 987 
Myelopathic albumosuria, 746 
Myiasis, 911 

intestinal, 912 
Myocarditis, 476 
acute, 476 
chronic, 476 
definition of, 476 
Nauheim baths in, 478 
physical signs of, 477 
prognosis in, 477 
in rheumatic fever, acute, 201 
in smallpox, 83 
symptoms of, 477 
treatment of, 477 
in typhoid fever, 35 
in typhus fever, 63 
Myocardium, degeneration of, 473 
amyloid, 474 
calcareous, 474 
fatty, 473 
hyaline, 474 
parenchymatous, 473 
prognosis of, 475 
symptoms of, 474 
disease of, 473 
tuberculosis of, 343 
Myoclonus, 1039. See Paramyoclonus mul- 
tiplex, 
epilepticus, 1039 
multiple, 1039 
Myomalacia cordis in syphilis, 281 
Myositis, acute, in diphtheria, 175 

in typhoid fever, 45 
Myotonia congenita, 1038 
definition of, 1038 
symptoms of, 1038 
Myriachit, 1066 
Mytilotoxismus, 856 

treatment of, 856 
Myxcedema, 756 
congenital, 758 
definition of, 756 
etiology of, 756 
frequency of, 757 
morbid anatomy of, 756 
pathology of, 756 
prognosis in, 757 
symptoms of, 757 
treatment of, 757 

thyroid gland in, 757 



N 



ASAL catarrh, atrophic, 366 
chronic, 365 
diphtheria, 178 



1112 



INDEX 



Nasha fever, 245 

symptoms of, 245 
Nauheim baths in myocarditis, 478 
Neapolitan fever, 245 
Nematodes, 884 
Neoplastic goitre, 749 
Nephritic changes in yellow fever, 215 
Nephritis, acute, in glandular fever, 353 
caseative, 725 
in cholera, 209 
desquamative, chronic, 704 
diffuse, acute, 700 

definition of, 700 
diagnosis of, 702 
etiology of, 700 
morbid anatomy of, 700 
oedema in, 701 
pathology of, 700 
prognosis of, 702 
symptoms of, 701 
treatment of, 702 
urine in, 701 
chronic, 704 
in diphtheria, 176 
exudative, 701 
glomerular, 700 
hemorrhagic, 701 
interstitial, chronic, 703, 710 

hemorrhagic glaucoma in, 715 
Hirschberg's vessels in, 715 
pathology of, 710 
prognosis in, 716 
retinal detachment in, 715 

lesions in, 714 
symptoms of, 710 
cerebral, 713 
circulatory, 713 
respiratory, 713 
treatment of, 717 
climatic, 718 
dietetic, 717 
medicinal, 717 
urine in, 712 
parenchymatous, chronic, 703, 704 
coma in, 706 
definition of, 703 
diagnosis of, 707 
dropsy in, 705 
etiology of, 703 
frequency of, 704 
morbid anatomy of, 705 
pathology of, 705 
prognosis in, 707 
retinitis in, 706 
symptoms of, 705 
treatment of, 707 
dietetic, 707 
urine in, 706 
in scarlet fever, 99, 102 
syphilitic, 281 
tubular, chronic, 704 
in typhoid fever, 41 
in varicella, 92 
Nephrolithiasis, 733 
colic in, 735 



Nephrolithiasis, definition of, 733 
diagnosis of, 735 

from acute appendicitis, 735 
from gallstone colic, 735 
from hydronephrosis, 735 
from neuralgia, 735 
from twist of ureter, 735 
etiology of, 733 
frequency of, 734 
pathology of, 733 
prognosis in, 735 
symptoms of, 735 
treatment of, 736 
urine in, 735 
Nerve, abducens, paralysis of, 1022 
auditory, diseases of, 1028 
facial, diseases of, 1024 
glossopharyngeal, paralysis of, 1030 
hypoglossal, diseases of , 1034 
oculomotor, diseases of, 1018 
olfactory, diseases of, 1012 
optic, diseases of, 1012 
paralysis of, 1018 
pathetic, paralysis of, 1020 
trifacial, paralysis of, 1020 
vagus, diseases of 1030 
Nerves, cranial, diseases of, 1012 
diseases of, 1003 
inflammation of, 1003 
Nervous complications of acute rheumatic 
fever, 201 
of typhoid fever, 43 
diseases, functional, 1038 
disorders of gastric secretion, 604 
eructation, 603 
exhaustion, 1068 
manifestations in influenza, 127 
system in diabetes mellitus, changes in, 
793 
diseases of, 913 
Neuralgia, gastric, 603 
Neurasthenia, 1068 
definition of, 1068 
diagnosis of, 1069 
etiology of, 1068 
prognosis of, 1069 
symptoms of, 1068 
treatment of, 1069 
Neuritis, 1003 

cervicobrachial, 1006 
prognosis in, 1006 
treatment of, 1006 
in croupous pneumonia, 161 
definition of, 1003 
diagnosis of, 1004 
in diphtheria, 176 
endemic multiple, 249 
etiology of, 1003 
interstitial, 1003 
morbid anatomy of, 1003 
motor, 1008 
multiple, 1007 

definition of, 1007 
diagnosis of, 1010 
etiology of, 1007 



INDEX 



1113 



Neuritis, multiple, prognosis in, 1010 
symptoms of, 1007 
treatment of, 1011 
obstetrical, 1007 
optic, 1012 

in brain tumor, 934 
in chronic lead poisoning, 853 
symptoms of, 1013 
treatment of, 1014 
parenchymatous, 1003 
pathology of, 1003 

periaxial, of Gombault in lead poison- 
ing, 853 
peripheral, 1007 

in chronic arsenical poisoning, 1009 
lead poisoning, 853, 1009 
prognosis in, 1004 
retrobulbar, 1013 
symptoms of, 1001 
toxic, in influenza, 127 ' 
treatment of, 1004 
in typhoid fever, 44 
Neuroma of brain, 932 
Neuroretinitis, albuminuric, 714 

in syphilis, 285 
Neuroses, gastric, 601 
of heart, 521 
occupation, 1072 
traumatic, 1070 

definition of, 1070 
etiology of, 1071 
paralyses in, 1071 
symptoms of, 1071 
treatment of, 1072 
Neurotic atrophy, 1037 
Newborn, hemorrhagic affections of, 786 

jaundice in, 686, 786 
Nitric acid test for albumin in urine, 742 
Nodding spasm, 1034 
Nodular colitis, 638 
Nodules, leprous, 348 
Noma, 548 

in measles, 112 
Nose, diseases of, 363 
Nummular sputum in tuberculosis, 316 
Nutrition, diseases of, 789 
Nystagmus in disseminated sclerosis, 956 



OBESITY, 833 
definition of, 833 
etiology of, 833 
symptoms of, 833 
treatment of, 834 
dietetic, 835 
Obliterative appendicitis, 617 
Obstetrical neuritis, 1007 
Obstruction, intestinal, 623 
Occupation neuroses, 1072 
Ocular complications of diabetes mellitus, 
797 
muscles, disturbances of motility of, 

1022 
symptoms in apoplexy, 919 

in disseminated sclerosis, 956 



Ocular symptoms in locomotor ataxia, 962 
Oculomotor nerve, diseases of, 1018 
paralysis of, 1018 

diagnosis of, 1019 
prognosis in, 1019 
symptoms of, 1019 
(Edema in acute diffuse nephritis, 701 
angioneurotic, 1075 
in Hodgkin's disease, 768 
of larynx, 372 
of lungs in cholera, 209 
malignant anthrax, 259 
in mitral regurgitation, 497 
(Edematous laryngitis, 372 
(Esophagismus, 562 
Oesophagitis, 560 
chronic, 560 
membranous, 560 
in typhoid fever, 35 
(Esophagus, cancer of, 563 
prognosis in, 563 
symptoms of, 563 
treatment of, 564 
dilatation of, 561 
atonic, 562 
diagnosis of, 562 
diffuse, 561 
dysphagia in, 562 
etiology of, 561 
localized, 561 
symptoms of, 562 
treatment of, 562 
diseases of, 560 
spasms of, 562 

treatment of, 563 
stricture of, organic, 561 
annular, 561 
asymmetrical, 561 
cylindrical, 561 
multiple, 561 
single, 561 
symmetrical, 561 
symptoms of, 561 
treatment of, 561 
tuberculosis of, 334 
ulceration of, in typhoid fever , 35 
Oidium albicans in thrush, 547 
Olfactory nerve, diseases of, 1012 
Ophthalmoplegia, 1023 
etiology of, 1024 
externa, 1023 
interna, 1023 
pathology of, 1024 
symptoms of, 1024 
treatment of, 1024 
Opisthotonos in tetanus, 269 
Oppler-Boas bacillus in gastric cancer, 594 
Optic atrophy, 1014 

in diabetes mellitus, 797 
diagnosis of, 1015 
etiology of, 1014 
in locomotor ataxia, 963 
pathology of, 1014 
prognosis in, 1015 
symptoms of, 1014 



1114 



INDEX 



Optic atrophy, treatment of, 1015 
nerve, inflammation of, 1012 
neuritis in brain tumor, 934 

in chronic lead poisoning, 853 
Orchitis in mumps, 117 
in typhoid fever, 42 
Oroya fever, 361 
Orthostatic albuminuria, 741 
Osteitis deformans, 839 
Osteoarthritis, 818 

Osteoarthropathy, pulmonary, in bronchi- 
ectasis, 387 
hypertrophic, 840 
in pulmonary tuberculosis, 318 
Osteoma of brain, 932 

in lung, 428 
Osteomyelitis in typhoid fever, 44 
Otitis media, acute, in typhoid fever, 44 
in croupous pneumonia, 162 
in scarlet fever, 99, 103 
Ovaries, tuberculosis of, 342 
Ox-heart in aortic regurgitation, 509 
Oxaluria, 745 
Oxyuris vermicularis, 885 
Oysters, infection by, in typhoid fever, 18 
Ozaena, 365, 366 



PACHYMENINGITIS, 947 
cervical, hypertrophic, 996 
diagnosis of, 947 
interna, 947 

morbid anatomy of, 948 
pathology of, 948 
symptoms of, 948 
morbid anatomy of, 947 
pathology of, 947 
prognosis in, 947 
symptoms of, 947 
treatment of, 947 
Paget' s disease, 839 
Painters' colic, 854 
Palpitation of heart, 521 
Palsy, acute infantile, 970 
birth, 1007 
hammerers', 1072 
scriveners', 1072 

shaking, 1040. See Paralysis agitans. 
Pancreas, adenoma of, 695 
carcinoma of, 695 
cystadenoma of, 694 
cystic epithelioma of, 694 
cysts of, 694 

hemorrhagic, 694 
hydatid, 694 
proliferation, 694 
pseudo-, 694 
retention, 694 
diseases of, 687 
gumma of, 695 
hemorrhages into, 695 
sarcoma of, 695 
tumors of, 695 
Pancreatic calculus, 693 

symptoms of, 693 



Pancreatic calculus, treatment of, 694 
cysts, 694 

diagnosis of, 695 
prognosis in, 695 
symptoms of, 694 
treatment of, 695 
tumors, 695 
Pancreatitis, 687 
acute, 687 

constipation in, 689 
diagnosis of, 689 

from fulminating appendicitis 

690 
from intestinal obstruction, 

689 
from perforation of duodenum 
689 
of gastric ulcer, 689 
from rupture of gall-bladder, 

690 
from suppurative cholecyst- 
itis, 690 
etiology of, 687 
fat-necrosis in, 688 
jaundice in, 689 
morbid anatomy of, 688 
pathology of, 688 
prognosis in, 690 
symptoms of, 688 
treatment of, 690 
chronic, 687, 691 

diagnosis of, 692 

from cancer of head of pan- 
creas, 692 
from gallstones in common 

duct, 692 
from subphrenic abscess, 692 
interacinar, 691 
interlobular, 691 
interstitial, 691 
intralobular, 691 
prognosis in, 692 
symptoms of, 692 
treatment of, 693 
definition of, 687 
gangrenous, 689 
hemorrhagic, acute, 695 
in mumps, 118 
subacute, 687 

symptoms of, 690 
treatment of, 691 
suppurative, 688 
Pani-Ghao, 889 
Papillary endocarditis, 482 
Papillitis, 1013 

albuminuric, 714 
Papilloma of kidney, 732 
Paracentesis abdominis in ascites, 653 

thoracic in pleurisy with effusion, 440, 
441 
Paracholecystitis, 675 
Paralysis of abducens nerve, 1022 
agitans, 1040 

definition of, 1040 
diagnosis of, 1042 



IXDEX 



111.") 



Paralysis agitans, diagnosis of, from multi- 
ple sclerosis, 1042 
from senile tremor, 1042 
etiology of, 1040 
movements in, 1041 
muscular rigidity in, 1042 
pathology of, 1041 
prognosis in, 1042 
symptoms of, 1041 
treatment of, 1042 
tremor in, 1041 
ascending, acute, 1000 

definition of, 1000 
diagnosis of, 1001 
etiology of, 1000 
morbid anatomv of, 1000 
pathology of, 1000 
prognosis in, 1001 
symptoms of, 1000 
treatment of, 1001 
atrophic, acute, 970 
of bowel, 627 
in brain tumor, 934 
bulbar, 977 

apoplectiform, 913 
diagnosis of, 977 
etiology of, 977 
morbid anatomy of, 977 
pathology of, 977 
prognosis in, 977 
symptoms of, 977 
treatment of, 977 
cerebral, infantile, 925 

convulsions in, 927 
definition of, 925 
deformities in, 927, 928 
diagnosis of, 928 

from amaurotic family 

idiocy, 929 
from hereditary spastic 
spinal paralysis, 929 
etiology of, 926 
lesions in, 926 
morbid anatomy of, 926 
paralysis in, 928 
pathology of, 926 
prognosis in, 929 
symptoms of, 927 
in diphtheria, 176, 178, 179 
of facial nerve, 1024 
gastrointestinal, 578 
general, of insane, 950 
glosso-labio-laryngeal, 977 
glossopharyngeal nerve, 1030 
of internal and external muscles of eye- 
ball, 1023 
Landry's, 1000 
monoplegic, in croupous pneumonia, 

160 
of oculomotor nerve, 1018 
of pathetic nerve, 1020 
periodical, 1083 

of spinal accessory nerve, 1034 
atrophic, chronic, 974 
infantile, 970 



Paralysis, spinal spastic, syphilitic, 980 
of trifacial nerve, 1020 
in whooping-cough, 122 
Paralytic chorea, 1045 

dilatation of stomach, 578 
Paramyoclonus multiplex, 1039 
definition of, 1039 
diagnosis of, 1040 

from chorea. 1040 
from electrical chorea, 1040 
from hysterical spasm, 1040 
from "maladie des tics con- 
vulsifs," 1040 
etiology of, 1039 
muscular contractions in, 1039 
prognosis in, 1040 
treatment of, 1040 
Paraphasia, 931 

Paraplegia in acute myelitis, 984 
ataxic, hereditary, 967 
senile, 987 

symptoms of, 987 
treatment of, 987 
spastic, 978 
Parasites, animal, diseases due to, 863 
Parasitic haemoptysis, 904 
infusoria, 909 
stomatitis, 547 
strumitis, 749 
Parasyphilitic affections, 283 
Paratyphoid fever, 59 

bacteriology of, 59 
complications of, 60 
diagnosis of, 60 
intestinal ulcers in, 59 
pathology of, 59 
prognosis of, 61 
splenic enlargement in, 59 
symptoms of, 60 
treatment of, 61 
Parenchymatous degeneration of heart, 
473 
goitre, 749 
neuritis, 1003 
Paresis, 950 

in kubisagari, 362 
Parkinson's disease, 1040 See Paralysis 

agitans. 
Parotid abscess, 551 

bubo, 551 
Parotitis, epidemic, 117- See Mumps, 
in cholera, 209 
chronic indurative, 552 
in croupous pneumonia, 162 
in scarlet fever. 103 
suppurative interstitial, 551 
in typhoid fever, 35 
Parry's disease, 751 
Pathetic nerve, paralysis of, 1020 

symptoms of, 1020 
Pectoriloquy, 319 
"Peg" teeth in syphilis, 286 
Peliomata in typhoid fever, 32 
Peliosis rheumatica, 786 
Pellagra, 857 



1116 



INDEX 



Pellagra, cachexia in, 858 
definition of, 857 
diarrhoea in, 858 
eruption in, 858 
etiology of, 857 
pathology of, 858 
symptoms of, 858 
nervous, 858 
treatment of, 859 
Pemphigus contagiosus, 910 

neonatorum in syphilis, 286 
Peptic ulcer, 579 

Perforation of bowel in typhoid fever, 37, 38 
in duodenal ulcer, 629 

symptoms of, 630 
in empyema, 446 
of gall-bladder, 680 
in gastric ulcer, 583 
Perforative appendicitis, 617 
Pericardial effusion in croupous pneumonia, 
153 
diagnosis of, 461 

from aortic aneurysm, 462 
from cardiac dilatation, 462 

hypertrophy, 462 
from pleural effusion, 462 
physical signs of, 461 
tuberculosis, 304 
" Pericarditic pseudocirrhosis of liver," 464 
Pericarditis, acute, 457 

definition of, 457 
diagnosis of, 461 

from phthisis, 461 
etiology of, 457 
forms of, 459 
frequency of, 458 
pathology of, 459 
physical signs of, 460 
prognosis in, 462 
saddle-leather sound in, 460 
symptoms of, 459 
treatment of, 462 
chronic, 463 

adhesive, 463 

definition of, 463 
diagnosis of, 465 
pathology of, 463 
physical signs of, 465 
prognosis in, 466 
pulsus paradoxus in, 466 
symptoms of, 465 
treatment of, 466 
in croupous pneumonia, 149, 158 
in erysipelas, 192 
externa et interna, 465 
in rheumatic fever, acute, 201 
serofibrinous, acute, 457 

symptoms of, 461 
in typhoid fever, 34 
Pericardium, diseases of, 457 

tuberculosis of, 304 
Pericholecystitis, 675 
Perihepatitis, 665 
Perinephritic abscess, 737 
Perineuritis, 1003 



Periodic rhinitis, 367 
Periodical paralysis, 1083 
Peripheral neuritis, 1007 
Peristaltic unrest, 602 
Peritoneal abscess, 643 

tuberculosis, 304 
Peritoneum, cancer of, 649 
cystic adenoma of, 649 
diseases of, 641 
hydatid cyst of, 649 
sarcoma of, 649 
tuberculosis of, 304 
Peritonitis, acute, 641 

complications of, 644 
definition of, 641 
diagnosis of, 645 

from acute hemorrhagic pan- 
creatitis, 645 
from gallstone colic, 645 
from hysteria, 645 
from intestinal obstruction, 

645 
from perforation of stomach, 

645 
from typhoid fever, 645 
etiology of, 641 
Hippocratic facies in, 644 
micro-organisms in, 641 
morbid anatomy of, 642 
pathology of, 642 
prognosis in, 645 
sequelae of, 644 
symptoms of, 643 
treatment of, 646 

counterirritation in, 647 
tympany in, 644 
adhesive, sclerotic, chronic, 648 
in amoebic dysentery, 232 
chronic, 647 
circumscribed, 643 
hemorrhagic, 643 
localized, 643 
loculated, 643 
putrid, 643 
in scarlet fever, 103 
septic, 642 
tuberculous, 304 
in typhoid fever, 36, 57 
diagnosis of, 37 
Pernicious anaemia, 777 

malarial fever, 863, 875 
Pertussis, 119. See Whooping-cough. 
Pestis minor, 223 
Petechiae in relapsing fever, 68 
in smallpox, 79 
in typhoid fever, 34 
in typhus fever, 64 
Petechial fever, 134 
Petit mal, 1061 

Peyer's patches in typhoid fever, 23 
Pharyngitis, acute, 552 

definition of, 552 
etiology of, 552 
pathology of, 553 
prognosis in, 553 



INDEX 



1117 



Pharyngitis, acute, symptoms of, 553 
treatment of, 553 
local, 554 
chronic, 555 

etiology of, 555 
pathology of, 555 
symptoms of, 555 
treatment of, 555 
croupous, 555 

etiology of, 555 
treatment of, 555 
follicular, 556 

etiology of, 556 
treatment of, 556 
phlegmonous, 554 
in typhoid fever, 34 
ulcerative, 554 

etiology of, 554 
symptoms of, 554 
treatment of, 554 
Pharynx, diseases of, 552 

tuberculosis of, 334 
Phlebosclerosis, 532 
Phlebitis in typhoid fever, 35 
Phlegmonous gastritis, 566 

pharyngitis, 554 
"Phosphatic diabetes," 745 
Phosphaturia, 745 
Phthisis, syphilitic, 282 

ventriculi, 569 
Pianists' cramp, 1072 
Pigeon-breast, 392 

in chronic hypertrophic tonsillitis, 559 
Pin-worm, 885 
Pistol-shot sound in aortic regurgitation, 

512 
Plagiomonas urinaria, 909 
Plague, 219 

bacillus of, 220 
bubonic, 219, 222 
buboes in, 222 
fever in, 222 

glandular enlargements in, 222 
symptoms of, 222 
vomiting in, 222 
definition of, 219 
diagnosis of, 225 
distribution of, 219 
etiology of, 220 
frequency of, 222 
larval, symptoms of, 223 
mode of transmission of, 221 
pathological anatomy of, 224 
pneumonic, albuminuria in, 223 
blood changes in, 223 
hemorrhage in, 223 
relapses in, 223 
sputum in, 223 
symptoms of, 223 
prognosis in, 225 
prophylaxis of, 223 
protective inoculation in, 224 
septicsemic, symptoms of, 223 
symptoms of, 222 
treatment of, 225 



Plasmodium malaria?, 863 
of malarial fever, 863 
Pleura, diseases of, 430 
Pleural effusion, 436 
bloody, 449 
purulent, 443 
Pleurisy, 430 
chronic, 448 

definition of, 448 
primitive dry, 448 
in croupous pneumonia, 149, 156 
definition of, 430 
dry, 430, 432 

cough in, 434 
diagnosis of, 434 

from intercostal neuralgia,434 
from muscular soreness, 434 
from muscular rheumatism, 
434 
fever in, 434 
friction sound in, 433 

pleuropericardial, 433 
physical signs of, 433 
prognosis in, 435 
symptoms of, 433 
treatment of, 435 
etiology of, 430 
fibrinous, 430 
forms of, 430 
frequency of, 432 
in influenza, 127 
purulent, 430 

in erysipelas, 192 
serofibrinous, 430 
in smallpox, 83 
tuberculous, 303, 430 
in typhoid fever, 43 
with effusion, 436 

cytoscopy in, 440 
diagnosis of, 438 

from hydatid cyst of 

liver, 439 
from hypostatic conges- 
tion, 439 
from new-growths in 

lung, 439 
from pleurisy with thick- 
ening, 439 
from pneumonia, 439 
from pneumothorax, 439 
from pulmonary oedema, 

439 
from subphrenic abscess, 

439 
from tubercular consoli- 
dation, 439 
duration of, 438 
dyspnoea in, 437 
paracentesis thoracis in, 440, 

441 
physical signs of, 437 
posture in, 437 
prognosis in, 440 
symptoms of, 436 
treatment of, 440 



1118 



INDEX 



Pleurisy with effusion, treatment of, blisters 
in, 442 
diaphoretics in, 442 
diuretics in, 442 
purges in, 442 
tapping in, 441 
Pleuritis, 430. See Pleurisy. 
Plumbism, 851. See Lead poisoning. 
Pneumogastric nerve, disease of, 1030 
symptoms of, 1032 
treatment of, 1032 
Pneumonia, aspiration, 398 
catarrhal, 397 
croupous, 143 

abscess in, 148, 162 
aphasia, transitory, in, 160 
arthritis in, 161 
brain softening in, 160 
bronchiectasis in, 158 
bronchitis in, 149 
cardiac changes in, 149 
in cerebrospinal fever, 139 
chill in, 150 
complications of, 156 
congestion of lung in, 147 
convulsions in, 155 
cough in, 151 
crisis in, 155 

protracted, 156 
cyanosis in, 151 
definition of, 143 
delirium in, 152, 154 
diagnosis of, 163 

from acute pulmonary tuber- 
culosis, 163 
from appendicitis, 163 
from catarrhal pneumonia, 163 
from hypostatic congestion cf 

lung, 163 
from pleurisy with effusion, 

163 
from pulmonary infarction, 
163 
distribution of, 145 
duration of, 162 
dyspnoea in, 151 
embolism in, 161 
empyema in, 157 
endocarditis in, 149, 159 
engorgement of lung in, 147 
etiology of, 144 
frequency of, 146 
gangrene in, 148, 162 
gray hepatization in, 147 
hemoglobinuria in, 155 
headache in, 151 
hemiplegia in, 159 
hemiplegie pneumonique, 160 
hepatic changes in, 149 
hepatization in, gray, 147 

red, 147 
herpes in, 151 

hydropneumothorax in, 157 
incubation of, 150 
in infants, 146 



Pneumonia, croupous, insomnia in, 155 

jaundice in, 155 

meningitis in, 149, 159 

micrococcus lanceolatus in, 143, 
145 

monoplegia in, 160 

morbid anatomy of, 147 

muscle changes in, 149 

nephritic changes in, 149 

nervous symptoms of, 154 

neuritis in, 161 

otitis media in, 162 

pain in, 150 

paralysis, monoplegic, 160 

parotitis in, 162 

pathology of, 147 

pericardial effusion in, 153 

pericarditis in, 149, 158 

physical signs of, in first stage, 151 
in well-developed stage, 152 

pleurisy in, 149, 156 

pneumococcus of Fraenkel, 143 

prevention of, 146 

prognosis in, 163 

pseudocrisis in, 156 

pulse in, 150, 151, 152 

rales redux in, 156 

red hepatization in, 147 

relapse in, 162 

renal changes in, 149 

respirations in, 150, 151 

sputum in, 151 

sweating in, 155 

symptoms of, 150 

in developed stage, 151 
in stage of onset, 150 
of resolution, 155 

tongue in, 154 

treatment of, 166 

tympanites in, 154 

unusual changes in lung in, 148 

urine in, 153 

varieties of, 162 

venous thrombosis in, 162 
fibrinous, 143 
in influenza, 127 
lobar, 143 
lobular, 397 
metastatic, 408 

abscess in, 410 

definition of, 408 

embolism in, 409 

etiology of, 409 

pathology of, 409 

prognosis in, 411 

sputum in, 409 

symptoms of, 410 

treatment of, 411 
pysemic, 410 
in typhoid fever, 29, 41 
Pneumonic plague, symptoms of, 223 
Pneumonitis, 143 
Pneumonoconiosis, 411 
definition of, 411 
etiology of, 411 






INDEX 



1119 



Pneumonoconiosis, pathology of, 412 
prognosis in, 412 
symptoms of, 412 
treatment of, 412 
Pneumopericardium, 467 

bacillus aerogenes capsulatus in, 467 
prognosis of, 468 
symptoms of, 467 
treatment of, 468 
Pneumothorax, 449 
definition of, 449 
diagnosis of, 451 

from diaphragmatic hernia, 451 
from emphysema, 451 
from pyopneumothorax subphren- 
icus, 451 
dyspnoea in, 450 
etiology of, 450 
physical signs of, 450 
prognosis in, 451 
in pulmonary tuberculosis, 318 
symptoms of, 450 
syncope in, 451 
treatment of, 452 
in whooping cough, 122 
Podagra, 808 
Poisoning, alcoholic, 843 
acute, 843 
chronic, 844 
arsenical, 850 
by cheese, 857 
by coast orach, 860 
by ergot, 856 
by fermented maize, 857 
by fish, 856 
food, 855 

by gingko tree, 861 
by impure milk, 857 
lacquer, 860 
lead, acute, 851 
chronic, 851 
by meat, 856 
morphine, chronic, 848 
by mussels, 856 
Poker back, 821 
Polioencephalitis superior of Wernicke, 

945 
Poliomyelitis, 983 

anterior, acute, 970 

convulsions in, 972 
definition of, 970 
diagnosis of, 973 
in diphtheria, 176 
etiology of, 970 
morbid anatomy of, 971 
paralysis in, 972 
pathology of, 971 
prognosis in, 973 
symptoms of, 972 
treatment of, 973 
chronic, 974 

Aran-Duchenne type of, 975 
claw-hand in, 975 
definition of, 974 
diagnosis of, 976 



Poliomyelitis, anterior, chronic, diagnosis 
of, from amyotrophic 
lateral sclerosis, 976 
from muscular dystrophy 

976 
from neuritis, 976 
from syringomyelia, 976 
drop-foot in, 975 
etiology of, 975 
morbid anatomy of, 975 
pathology of, 975 
prognosis in, 976 
symptoms of, 975 
treatment of, 976 
Polyneuritis, 1007 
Polyuria in typhoid fever, 42 
Porencephaly. 926 
Pork-worm, 901 
Portal vein, thrombosis of, 666 
Porto Rican anaemia, 887 
Posture in pleurisy with effusion, 437 
Potassium ferrocyanide test for albumin in 

urine, 742 
Potters' rot, 411 
Pox, 276 

Pregnancy, typhoid fever complicating, 45 
Prevention of tetanus, 268 
Primitive dry pleurisy, 448 
Proctitis, epidemic gangrenous, 239 
Progressive muscular atrophy, 974 
Proliferation cysts of pancreas, 694 
Prophylaxis against diphtheria, 182 

plague, 223 
Pseudoangina in hysteria, 1050 
Pseudo crisis in croupous pneumonia, 156 
Pseudocysts of pancreas, 694 
Pseudohydrophobia, 265 
Pseudoleukemia, 767 
Pseudolyssaphobia, 265 
Pseudomembranous colitis, 639 

pyelonephritis, 726 
Pseudomuscular hypertrophy, 1035 

prognosis in, 1036 
Pseudotabes, arsenical, 851 
Psilosis, 242 
Psoriasis, buccal, 550 
Psorospermiasis, 879 
Ptosis in kubisagari, 362 
Ptyalism, 550 
Puerperal eclampsia, 1063 
"Puking fever," 352 
Pulex penetrans, 911 
Pulmonary abscess, 423 

diagnosis of, 424 
etiologv of, 423 
multiple, 423 
prognosis in, 425 
in septicaemia, 195 
symptoms of, 424 
treatment of, 425 
in typhoid fever, 41 
complications of rheumatic fever, acute 

200 
congestion, 425 

in influenza, 127 



1120 



INDEX 



Pulmonary emphysema, 413 
gangrene, 420 

in bronchiectasis, 387*" 
oedema in cholera, 209 
osteoarthropathy in bronchiectasis, 378 
hypertrophic, 840 
in pulmonary tuberculosis, 318 
regurgitation, 516 
stenosis, 516 
tuberculosis, 309 
valves of heart, diseases of, 515 
Pulsus paradoxus in chronic adhesive peri- 
carditis, 466 
Purpura, 785 

causes of, 785 
fulminating, 786 
haematemesis in, 605 
hemorrhagica, 786 
Henoch's, 786 
micro-organisms in, 785 
in rheumatic fever, acute, 201 
rheumatica, 786 
treatment of, 787 
Purulent pericarditis, 459 
pleural effusion, 443 
pleurisy, 430 
Pus in urine, 744 
Putrid fever, 61 

peritonitis, 643 
sore mouth, 546 
Pyaemia, 193. See Septicaemia. 

gonorrhceal, 186 
Pyaemic abscess of liver, 653 

pneumonia, 410 
Pyelitis, 725 
Pyelonephritis, 725 
catarrhal, 726 
definition of, 725 
diagnosis of, 727 

from aneurysm, 728 
from malarial fever, 727 
from perinephritic abscess, 727 
from suppurative cystitis, 727 
from typhoid fever, 727 
etiology of, 725 
gangrenous, 726 
micro-organisms in, 725 
morbid anatomy of, 726 
pathology of, 726 
prognosis in, 728 
pseudomembranous, 726 
suppurative, 726 
symptoms of, 727 
treatment of, 728 
Pylephlebitis, suppurative, 666 
Pylorospasm, 602 

Pylorus, stenosis of, congenital, 595, 597 
hypertrophic, 595 

definition of, 595 
diagnosis of, 596 

from cicatricial contrac- 
tion, 597 
from gastric cancer, 596 
etiology of, 596 
morbid anatomy of, 596 



Pylorus, stenosis of, hvpertrophic,prognosis 
of, 598 
symptoms of, 596 
treatment of, 598 
Pyopericardium, 459 
Pyonephritis, 725 
Pyonephrosis, 725 

in tuberculosis of kidney, 342 
Pyopneumothorax, 449 
Pyuria, 744 

treatment of, 744 
in typhoid fever, 42 



QUARTAN parasite of malarial fever, 
866 
Quincke's pulse in aortic regurgitation, 510 



RABIES, 261 
dumb, 264 
Rachitic rosary, 827 
Rachitis, 825 
Ragweed fever, 367 

Rales redux in croupous pneumonia, 156 
Rashes in smallpox, 79 
Ray fungus in actinomycosis, 273 
Raynaud's disease, 1075 

definition of, 1075 

etiology of, 1075 

gangrene in, 1075 

treatment of, 1075 
Rectal crises in locomotor ataxia, 962 
Rectum, tuberculosis of, 336 
Red-light treatment of smallpox, 87 
Reflexes in apoplexy, 919 
Regurgitation, aortic 508 
mitral, 494 
pulmonary, 516 
tricuspid, 513 
Relapse in croupous pneumonia, 162 
Relapsing fever, 68 

chill in, 69 

crisis in, 70 

definition of, 68 

delirium in, 70 

distribution of, 68 

etiology of, 68 

fever in, 70 

history of, 68 

incubation in, 68 

jaundice in, 69 

morbid anatomy of, 68 

pathology of, 68 

petechise in, 68 

prognosis of, 70 

relapse in, 68 

spirillum in, 68 

spleen in, 68 

symptoms of, 69 

treatment of, 70 

vomiting in, 69 
Remittent fever, bilious, 874 

complications of, 876 

diagnosis of, 877 



INDEX 



1121 



RcmitttMit fever, hemoglobinuria in, 875 
sequelae of, 875 
symptoms of, 874 
treatment of, 877 
Renal artery, aneurysm of, 543 
asthma, 391 
calculus, 733 

changes in croupous pneumonia, 149 
colic, 735 

disease, acute, in typhoid fever, 30 
tuberculosis, 341 
Respiratory system, diseases of, 363 
Retention cyst of pancreas, 694 
Retinal hemorrhages in malarial fever, 876 
lesions in chronic interstitial nephritis, 
714 
Retinitis, albuminuric, in chronic parenchy- 
matous nephritis, 706 
degenerative, 714 
hemorrhagic, 714 
in puerperal eclampsia, 1063 
typical, 714 
diabetic, 797 
Retrobulbar neuritis, 1013 
Retrocedent gout, 815 
Retrograde intussusception of bowel, 625 
Rheumatic fever, acute, 196 
arthritis in, 199 
bacteriology of, 198 
chorea in, 201 
complications of, 200 
definition of, 196 
delirium in, 201 
diagnosis of, 201 

from arthritis, acute, 202 

septic, 202 
from gonorrhoeal rheum- 
atism, 202 
from monoarticular in- 
flammation, 202 
from osteomvelitis, acute, 
202 
distribution of, 196 
duration of, 200 
endocarditis in, 200 
etiology of, 197 
joints in, 199 
meningitis in, 201 
micrococcus rheumaticus, 198 
morbid anatomy of, 198 
mvocarditis in, 201 
pericarditis in, 200, 201 
prognosis of, 202 
pulmonary complications in, 

201 
purpura rheumatica in, 201 
rheumatic nodules in, 201 
sweating in, 199 
symptoms of, 199 
tongue in, 199 
treatment of, 202 
urine in, 199 
urticaria in, 201 
Rheumatism, acute articular, 196. See 
Rheumatic fever, acute. 
71 



Rheumatism, chronic, 823 
definition of, 823 
etiology of, 823 
morbid anatomy of, 823 
symptoms of, 823 
treatment of, 823 

gonorrhoeal, 187 

muscular, 824 

treatment of, 824 
Rheumatoid arthritis, 818 

in bronchiectasis, 386 
Rhinitis, atrophic, 365 

hypertrophic, 365 

periodic, 367 

syphilitic, 286 
Rice-water stools in Asiatic cholera, 208 
Rickets, 825 

bossy frontals in, 827 

chicken-breast in, 828 

definition of, 825 

dentition in, 828 

diagnosis of, 828 

etiology of, 825 

Harrison's groove in, 828 

morbid anatomy of, 826 

prognosis in, 829 

symptoms of, 827 

treatment of, 829 
Ringworms, 909 
Risus sardonicus in epilepsy, 1054 

in tetanus, 269 
Rock fever, 245 

Romberg's symptom in locomotor ataxia,961 
Rose cold, 367 

rash in rubella, 116 

spots in typhoid fever, 28 
Roseola, epidemic, 115 

in syphilis, 283 
Rotch's sign of pericardial effusion, 461 
Rotheln, 115. See Rubella. 
Round-worm, 884 
Rubella, 115 

definition of, 115 

diagnosis of, 116 

from measles, 116 
from scarlet fever, 116- 

eruption in, 116 

etiology of, 116 

Forchheimer's spots in, 116 

glandular enlargements in, 116 

incubation of, 116 

prognosis in, 116 

"rose rash" of, 116 

symptoms of, 116 

treatment of, 116 
Rubeola notha, 115 
Running amok, 1066 
Rupture of spleen, 764 
Russian tapeworm, 901 



ST. ANTHONY'S FIRE," 189 
St. Gothard's tunnel disease, 887 
St. Vitus' dance, 1043 
Saccharomvces albicans in thrush, 547 



1122 



INDEX 



Sacculated aneurysm, 534 

Saddle-leather sound in acute pericarditis. 

460 
Salivary glands, diseases of, 550 

functional disorders of, 550 
inflammation of, 551 
Salivation, 550 
Sand flea, 911 
Sanduhrmagen, 598 

Sansom's sign of pericardial effusion, 461 
Sarcoma of brain, 932, 933 
of kidney, 732 
of liver, 668 
in lung, 428 
of mediastinum, 452 
of pancreas, 695 
of peritoneum, 649 
of thyroid gland, 751 
Saturnine epilepsy, 853 
Scarlatina, 93 
Scarlet fever, 93 

bacteriology of, 95 
bronchopneumonia in, 103 
"collar of brawn" in, 99 
complications of, 102 
definition of, 93 
desquamation in, 104, 108 
diagnosis of, 103 

from erythema scarlatinif orm, 

104 
from German measles, 104 
from nephritic eruption, 104 
from rash of sepsis, 105 
from rose rash of indigestion, 

104 
from syphilitic rash, 104 
distribution of, 93 
eruption in, 100 

peculiarities of, 100 
etiology of, 93 
fulminant form of, 102 
glandular enlargements in, 99, 103 
hybrid, 115 

hyperhsemocytosis in, 99 
incubation period of, 99 
kidneys in, 99, 102 
malignant, 101 
morbid anatomy of, 98 
mortality of, 105 
nephritis in, 99, 102 
otitis in, 99, 103 
parotitis in, 103 
pathology of, 98 
peritonitis in, 103 
prognosis of, 105 
prophylaxis of, 97 
septic arthritis in, 103 

infections in, 99 
sequelae of, 102 
sore throat in, 99, .100, 101 
" strawberry tongue" in, 104 
suppression of urine in, 101 
surgical, 102 
treatment of, 105 
hygienic, 105 



Scarlet fever, valvular disease of heart in, 103 

vomiting in, 99 
"Schluck-pneumonie," 398 
Schonlein's disease, 786 
Scleroderma, 840 

treatment of, 840 
Sclerosis, disseminated, 954 

Argyll-Robertson pupil in, 956 
definition of, 954 
diagnosis of, 957 

from general paralysis of 

insane, 957 
from hysteria, 957 
from locomotor ataxia, 957 
from paralysis agitans, 957 
from spastic paraplegia, 957 
etiology of, 954 
morbid anatomy of, 955 
nystagmus in, 956 
pathology of, 955 
prognosis in, 957 
symptoms of, 955 
treatment of, 957 
insular, 954 
lateral, 978 

amyotrophic, 980 

Babinski reflex in, 981 
definition of, 980 
diagnosis of, 982 

from bulbar paralysis, 982 
from syringomvelia, 982 
etiology of, 980 
pathology of, 980 
prognosis in, 982 
symptoms of, 981 
treatment of, 982 
ankle clonus in, 979 
Babinski reflex in, 979 
definition of, 978 
diagnosis of, 979 
etiology of, 978 
morbid anatomy of, 978 
pathology of, 978 
prognosis in, 979 
Strumpell's family type of, 978 
symptoms of, 978 
treatment of, 979 
multiple, 954 
Sclerotic kidney, 710 
Scorbutus, 830 
Screw-worm, 911 

treatment of infection by, 912 
Scriveners' palsy, 1072 
Scrofula, 299 
Scurvy, 830 

definition of, 830 
etiology of, 830 
infantile, 831 
morbid anatomy of, 830 
pathology of, 830 
symptoms of, 831 
treatment of, 832 
Seat-worm, 885 
Secondary anaemia, 773 
Secretion, gastric, nervous disorders of, 604 



IXDEX 



1123 



Secretion, gastric, nervous disorders of, 

treatment of, 604 
Segmentation of heart muscle, 474 
Senile emphysema, 413 

paraplegia, 987 
Sepsis in empyema, 446 
Septic arthritis in scarlet fever, 103 
in smallpox, 83 

peritonitis, 642 

pneumonia, 409 
Septicaemia, 193 

anaemia in, 194 

blood in, 194 

chill in, 194 

chronic, 195 

definition of, 193 

diagnosis of, 195 

empyema in, 195 

etiology of, 193 

infarction of spleen in, 195 

morbid anatomy of, 193 

pathology of, 193 

pulmonary abscess in, 195 

subacute, 195 

suppuration of kidney in, 195 

sweating in, 194 

symptoms of, 194 

treatment of, 196 
Septicaemic plague, s\'mptoms of, 223 
Serofibrinous pericarditis, acute, 459, 461 

pleurisy, 430 
Serositis, multiple, 465 
Serous diarrhoea, 608 

membranes, tuberculosis of, 301 
Serum, antirabic, 265 

antitubercle, 331 

treatment of ulcerative endocarditis, 
488 
Seven days' fever, 68 
Sewing spasm, 1072 

Shaking palsy, 1040. See Paralysis agitans 
Shiga's bacillus in dysentery, 230 
Ship fever, 61 
Siderosis, 411 
Simla diarrhoea, 241 
Sitotoxismus, 856 
Skin changes in typhoid fever, 32 

eruptions, syphilitic, 283, 286 

gangrene of, in smallpox, 83 

in Hodgkin's disease, 768 

pigmentation of, in Addison's disease, 
761 
Skod.iic resonance in hvdropneumothorax, 

451 
Sleeping sickness, 879, 881 
diagnosis of, 883 
etiology of, 882 
pathology of, 882 
prognosis in, 883 
symptoms of, 882 
treatment of, 883 
"Slows" in cattle, 352 
Smallpox, 70 

aberrant manifestations of, 81 

abscesses , in, 82 



Smallpox, aphonia in, 8 
backache in, 77 
bed-sores in, 83 
black, 81 
bronchitis in, 83 
bronchopneumonia in, 83 
complications of, 82 
confluent, 81 
cytoryctes vaccinae in, 71 
deafness in, 83 
definition of, 70 
delirium in, 79 
diagnosis of, 84 

from chickenpox, 84 

from measles, 84 

from scarlet fever, 84 

from syphilides, 84 
distribution of, 71 
earache in, 83 
endocarditis in, 83 
eruption in, 75, 77 

development of, 77 

forms of, 78 

on mucous membrane, 79 

stages of, 78 

variations in, 79, 80 
erysipelas in, 83 
etiology of, 71 
forms of, 81 
frequency of, 73 
gangrene of skin in, 83 
haematemesis in, 605 
headache in, 77 
hemorrhagic, 81 
history of, 70 
incubation of, 72 
laryngitis in, 83 

mode of spreading contagion, 71 
morbid anatomy of, 75 
myocarditis in, 83 
pathology of, 75 
pericarditis in, 83 
pleurisy in, 83 
in pregnancy, 83 
prevention of, 73 
prognosis of, 85 
rashes in, 79 
septic arthritis in, 83 
sequelae of, 82 
symptoms of, 77 
treatment of, 86 

red-light, 87 
urine in, 77 

vaccination as a preventive, 73, 88 
varioloid, 82 
Smokers' tongue, 550 
"Snuffles," 286 
Soor, 547 

Sore throat, clergymen's, 555 
in diphtheria, 177 
in scarlet fever, 99, 100, 101 
ulcerated, 554 
Spasm, facial, 1027 

muscular, idiopathic, 1064 
nodding, 1034 



1124 



INDEX 



Spasm of oesophagus, 562 

sewing, 1072 
Spasmodic croup, 374 
laryngitis, 374 
wryneck, 1033 
Spasmus nutans, 1034 
Spastic diplegia, 926 
hemiplegia, 925 
paraplegia, 978 
Speech in Friedreich's ataxia, 969 
Spinal accessory nerve, disease of, 1032 
symptoms of, 1033 
paralysis of, 1034 
cord, compression of, 993 
by aneurysm, 995 
definition of, 993 
by disease of vertebrae, 993 
diagnosis of, 994 
prognosis in, 994 
symptoms of, 994 
treatment of, 994 
etiology of, 993 

by hypertrophic cervical 
pachymeningitis, 996 
symptoms of, 996 
treatment of, 996 
by malignant growths, 994 
hemorrhage into, 990 
definition of, 990 
diagnosis of, 991 
prognosis in, 991 
symptoms of, 990 
treatment of, 991 
inflammation of, 983 
syphilis of, 285, 286 
tuberculosis of, 343 
epilepsy, 1039. See Paramyoclonus 

multiplex, 
membranes, hemorrhage into, 991 
definition of, 991 
etiology of, 991 
extrameningeal, 991 
intrameningeal, 991 
prognosis in, 993 
symptoms of, 992 
treatment of, 993 
meningitis, 997 

chronic, 999 
paralysis, atrophic, chronic, 974 
infantile, 970 
spastic, syphilitic, 980 
syphilis, 285, 286 
Spirillum cholerae Asiatica, 204 

of relapsing fever, 68 
Splanchnoptosis, 632 
Spleen, abscess of, 764 
diseases of, 764 
in diphtheria, 176 
enlargement of, in paratvphoid fever, 

59 
in hepatic cirrhosis, 764 
hvdatid cyst of, 764 
infarct of, 764 

in septicaemia, 195 
in malarial fever, 764 



Spleen in malarial fever, changes in, 868 

malignant growths of, 764 

in Malta fever, 246 

movable, 764 

in relapsing fever, 68 

rupture of, 764 

in splenic anaemia, 765 

in splenomedullary leukaemia, 764, 782 

in typhoid fever, 25, 27, 30, 764 

in typhus fever, 63 

wandering, 764 

treatment of, 765 
Splenic anaemia, 765 

artery, aneurysm of, 543 
Splenization of lung, 426 
Splenomedullary leukaemia, 780, 781 
Splenomegaly, tropical, 883 
Spondylitis deformans, 821 

rhizomelique, 821 
Spotted fever, 61, 134, 354 
Sprue, 242 

anaemia in, 244 

definition of, 242 

diagnosis of, 244 

diarrhoea in, 243 

etiology of, 242 

flatulence in, 243 

mouth lesions of, 243 

pathology of, 242 

predisposing causes of, 242 

prognosis in, 244 

symptoms of, 243 

tongue in, 243 

treatment of, 2 44 
Sputum in bronchial asthma, 392 

in bronchiectasis, 385 

in croupous pneumonia, 151 

in distomatosis of lung, 908 

in metastatic pneumonia, 409 

in pneumonic plague, 223 

in pulmonary gangrene, 422 
tuberculosis, 315, 316 

microscopic examination of, 
322 
Squint in chronic lead poisoning, 853 
St. Anthony's fire, 189 
St. Gothard's tunnel disease, 887 
St. Vitus' dance, 1043. See Chorea minor. 
Status epilepticus, 1056 

lymphaticus, 770 

definition of, 770 
etiology of, 770 
morbid anatomy of, 770 
pathology of, 770 
symptoms of, 771 
tetany of, 771 
treatment of, 771 
Stelwag's sign in exophthalmic goitre, 753 
Stenosis, aortic, 504 

mitral, 499 

pulmonary, 516 

of pylorus, congenital, 595, 597 
hypertrophic, 595 

tricuspid, 515 
Still's disease, 821 



IXDEX 



1125 



See Gastric dilata- 



604 



599 



Stokes-Adams syndrome, 475 
Stomach, bilocular. 598 
cancer of, 58S 
dilatation of, 572. 
tion. 
paralytic, 578 
diseases of, 564 
hemorrhage from, 
hour-glass, 598 

definition of, 598 
etiology of, 599 
morbid anatomy of 
pathology of. 599 
physical signs of, 599 
symptoms of, 599 
treatment of, 601 
Woelfler's "first sign" in, 599 
" second sign" in, 600 
hyperesthesia of, 603 
symptoms of, 603 
lymphatic areas of, 590 
neuroses of, 601 
ulcer of, 579 See Gastric ulcer. 
Stomatitis, 545 
aphthous, 516 
catarrhal, 545 

prognosis of, 546 
symptoms of, 545 
definition of, 545 
fetid, 546 
follicular, 546 
gangrenous, 548 
symptoms of, 
treatment of, 
in measles, 112 
parasitic, 547 

monilia Candida in, 547 
oidium albicans in, 547 
prognosis in, 548 
saccharomyces albicans in, 547 
symptoms of, 547 
treatment of, 548 
ulcerative, 546 

treatment of, 546 
vesicular, 546 
Stone in kidney, 733 
Stools in cholera, 208 
in dysentery, 233 
Strangulation, internal, of bowel, 624, 
"Strawberry tongue" in scarlet fever 
Streptococcus erisipelatus, 189 
Streptothrix actinomvces, 273 
Stricture of bowel, 623 

of oesophagus, organic, 561 
Strongyloides intestinalis, 898 
classification of, 898 
definition of, 898 
diarrhoea in, 900 
distribution of, 898 
emaciation in, 900 
treatment of, 900 
Struma, 749 

colloid, 749 
Strumitis, echinococcic. 749 
parasitic, 749 



549 
549 



626 i 

104 



Strumitis, syphilitic, 749 

traumatic, 749 

tuberculous, 749 
StrumpelTs family type of lateral sclerosis, 
^ 978 
Sudamina in miliary fever, 357 

in typhoid fever, 31 
Suffocative catarrh, acute, 400, 402 
Sunstroke, 1080 

definition of, 1080 

diagnosis of, 1081 

etiology of, 1080 

morbid anatomv of, 1081 

pathology of, 1081 

prognosis in, 1081 

svmptoms of, 1081 

treatment of, 1082 

hydrotherapeutic, 1082 
venesection in, 1082 
Suppression of urine, 737 
Suppuration of kidney in septicaemia, 195 
Suppurative hsematitis, 780 

inflammation of bile-ducts, 673 

pancreatitis, 688 

pyelonephritis, 726 

pylephlebitis, 666 
Suprarenal glands, diseases of, 760 
Surgical emphvsema, 413 

kidney, 727 

scarlet fever, 102 
Sweating sickness, 356 
Sydenham's chorea, 1043, See Chorea 

minor. 
Symmetrical stricture of oesophagus, 561 
Syncope in pneumothorax, 450 
Syphilis, 276 

acquired, 276 

anaemia in, 284 

arteritis in, 281 

of bones, 286 

of brain and spinal cord, 285, 286 

chancre of, 280, 283, 284 

condylomata in, 284 

definition of, 276 

diagnosis of, 286 

distribution of, 276 

etiology of, 277 

frequency of, 279 

gummata in, 281 

headache in, 285 

heart changes in, 281 

hereditary, 276, 286, 289 
epiphysitis in, 286 
eruptions in, 286 
Hutchinson teeth in, 286 
mucous patches in, 286 
rhinitis in, 286 
symptoms of, 286 

iritis in, 284 

lesions of, primary. 280 
secondarv, 280 
tertiary, 280 

of liver, 281 

of lungs, 281 

macular syphilide in, 284 



1126 



INDEX 



Syphilis, morbid anatomy of, 280 

mucous patches in, 284, 286 

of nervous system, 283, 285 

neuroretinitis in, 285 

paralyses in, 285 

pathology of, 280 

prevention of, 279 

prognosis of, 286 

roseola in, 283 

skin eruptions in, 283 

stages of, 276, 280 

symptoms of, 283 

transmission of, 277, 278 

treatment of, 286 
Syphilitic alopecia, 284 

arteritis, 281 

cirrhosis of liver, 664 

condylomata, 284 

dactylitis, 286 

epiphysitis, 286 

eruptions, 283 

gummata, 281, 284 

infantilism, 286 

iritis, 284 

keratitis, 286 

laryngitis, 376 ■ 

lymph nodes, 283 

marasmus, 286 

nephritis, 281 

phthisis, 282 

rhinitis, 286 

spastic spinal paralysis, 980 

strumitis, 749 
Syringomyelia, 988 

claw-hand in, 989 

definition of, 988 

diagnosis of, 989 

etiology of, 988 

history of, 988 

morbid anatomy of, 988 

pathology of, 988 

prognosis in, 990 

symptoms of, 989 

treatment of, 990 



TABES of brain, 952 
mesenterica, 300 
Tache blenatre in typhoid fever, 32 

cerebrale in typhoid fever, 32 
Tachycardia, 521 

in exophthalmic goitre, 753 

in hysteria, 1050 
Taenia confusa, 901 

cucumerina, 903 

echinococcus, 901 

medio canellata, 901 

nana, 901 

saginata, 901 

solium, 901 
Tapeworm, 900 

dog, double-pored, 901 

dwarf, 901 

Russian, 901 

symptoms of, 903 



Tapeworm, treatment of, 904 
Tapping in pleurisy with effusion, 441 
Teeth in syphilis, 286 
Telegraphers' cramp, 1072 
Teratoma of mediastinum, 453 
Tertian parasite of malarial fever, 865 
Testicle, tuberculosis of, 338 
Test, Widal, in typhoid fever, 48 
Test-meal in gastric cancer, 593 
Tests for albumin in urine, 742 

blood, in diabetes mellitus, 798 

for sugar in urine, 799 
Tetanilla, 1064 
Tetanus, 267 

bacillus of, 267 

definition of, 267 

diagnosis of, 269 

from hysteria, 269 

from strychnine poisoning, 269 

from tetany, 269 

distribution of, 267 

emprosthotonos in, 269 

etiology of, 267 

frequency of, 267 

head, 271 

kopf-, 271 

" lock-jaw" in, 269 

morbid anatomy of, 268 

muscular rigidity in, 268 

opisthotonos in, 269 

pain in, 269 

pathology of, 268 

prevention of, 268 

prognosis of, 269 

risus sardonicus in, 269 

spasm of diaphragm in, 269 
of glottis in, 269 

symptoms of, 268 

treatment of, 270 
antitoxin, 270 
Tetany, 1064 

Chvostek's sign of, 1065 

diagnosis of, 1065 

from Jacksonian epilepsy, 1065 
from hysteria, 1065 

Erb's sign of, 1065 

etiolog}^ of, 1064 

gastric, 575 

Chvostek's sign in, 576 
Erb's sign in, 576 
Trousseau's sign in, 575 

Hoffmann's sign of, 1065 

morbid anatomy of, 1064 

pathology of, 1064 

prognosis in, 1065 

in status lymphaticus, 771 

symptoms of, 1064 

treatment of, 1065 

Trousseau's sign of, 1065 
svmptom of, 1065 
Thermic fever, 1080 
Thomsen's disease, 1038 
Thread-worm, 885 
Three-day fever, 131 
Thrombosis, cerebral, 913 



IXDEX 



1127 



Thrombosis in croupous pneumonia, 162 
of portal vein, 666 
in typhoid fever, 35 
venous, in croupous pneumonia, 162 
sinuses, 946 

etiology of, 946 
morbid anatomy of, 946 
pathology of, 946 
prognosis of, 946 
symptoms of, 946 
treatment of ; 946 
Thrush, 547, See Stomatitis, parasitic. 
Thymus gland, diseases of, 772 
Thyreocele, 749 

Thyroid gland, adenoma of, 751 
carcinoma of, 751 
carcinosarcoma of, 751 
diseases of, 749 
endothelioma of, 751 
sarcoma of, 751 
swelling of, 750 
tuberculosis of, 343 
tumors of, 751 
Tic convulsif, 1027 
Tick fever, 354 

albuminuria in, 355 
definition of, 354 
diagnosis of, 355 
etiology of, 354 
fever in, 355 
prognosis of, 356 
pyroplasma hominis in, 354 
rash in, 355 
symptoms of, 355 
treatment of, 356 
Tinnitus, 1028 
Tongue, eczema of, 549 

treatment of, 550 
geographical, 549 
smokers', 550 

strawberry, in scarlet fever, 104 
Tonsillitis, acute, 556 

definition of, 556 
diffuse, 556 
endocarditis in, 557 
etiology of, 556 
follicular, 556 
forms of, 556 
morbid anatomy of, 557 
pathology of, 557 
symptoms of, 557 
treatment of, 558 
hypertrophic, chronic, 558 

barrel-shaped chest in, 559 
definition of, 558 
funnel chest in, 559 
mouth breathing in, 559 
pigeon-breast in, 559 
symptoms of, 559 
treatment of, 559 
Tonsils, diseases of, 556 
tuberculosis of, 334 
Torticollis, 1033 
Toxic gastrectasis, 578 
gastritis, acute, 565 



Tracheotomy in acute catarrhal laryngitis, 
371 

in oedematous laryngitis, 374 
Transverse myelitis, 983 
Traumatic abscess of liver, 653 
neuroses, 1070 
strumitis, 749 
Trematodes, 904 

definition of, 904 
"Trembles" in cattle, 352 
Tremor in exophthalmic goitre, 754 

in paralysis agitans, 1041 
Trichina spiralis, 885 
Trichiniasis, 885 

diagnosis of, 887 
etiology of, 885 
morbid anatomy of, 886 
pathology of, 886 
prognosis in, 887 
symptoms of, 887 
treatment of, 887 
Trichocephalus dispar, 900 
Trichomonas hominis, 909 

vaginalis, 909 
Tricophyton, 909 
Tricuspid regurgitation, 513 
definition of, 513 
diagnosis of, 514 
etiology of, 513 
pathology of, 513 
physical signs of, 514 
prognosis in, 515 
symptoms of, 514 
. stenosis, 515 

diagnosis of, 515 
Trifacial nerve, paralysis of, 1020 

symptoms of, 1020 
Trilocular heart, 527 
Trip-hammer pulse in aortic regurgitation, 

511 
Trommer's test for sugar in urine, 799 
Tropical abscess of liver, 654 
adenitis, 226 
bubo, 226 
chlorosis, 888 
splenomegaly, 883 
Trousseau's sign in gastric tetany, 575 

of tetany, 1065 
Trypanosoma fever, 880 

treatment of, 881 
Trypanosomata, varieties of, 879 
Trypanosomiasis, 879 
definition of, 879 
human, 880 
Tubercle, 295 
of brain, 932 
miliary, 295 
Tuberculin treatment of tuberculosis, 332 
Tuberculosis, 290 

miliary, acute, 297 

bacillus in, 297 
diagnosis of, 298 
prognosis of, 299 
symptoms of, 297 
treatment of, 299 



1128 



INDEX 



Tuberculosis in Addison's disease, 760 
of alimentary canal, 334 
bacillus of, 290 
of bladder, 340 

diagnosis of, 340 

symptoms of, 340 

treatment of, 341 
bovine, 291 
of brain, 343 
of csecum, 336 
of cervical glands, 300 
chronic hyperplastic, 296 
definition of, 290 
etiology of, 290 
of Fallopian tubes, 342 
frequency of, 293 
of genitourinary system, 338 
glandular, 299 

signs of, 300 

treatment of, 300 
of heart, 343 
of intestine, 335 

chronic hyperplastic, 336 

prognosis in, 337 

symptoms of, 336 

treatment of, 337 
of kidneys, 341 

acute, 341 

chronic, 341 

hydronephrosis in, 342 

pyonephrosis in, 342 

symptoms of, 342 
of liver, 338 

of mediastinal glands, 300 
meningeal, acute, 301 

diagnosis of, 302 

from acute meningitis, 

302 
from cerebrospinal men- 
ingitis, 302 
symptoms of, 301 
of mesenteric glands, 300 
mode of infection in, 290 
morbid anatomy of, 295 . 
mortality of, 294 
of myocardium, 343 
of oesophagus, 334 
of ovaries, 342 
pathology of, 295 
of pericardium, 304 

symptoms of, 304 
of peritoneum, 304 

acute miliary, 305 

caseous type of, 306 

chronic fibroid, 306 
symptoms of, 306 
of pharynx, 334 
of pleura, 303 

lesions in, 303 
pneumonic, acute, diagnosis of, 318 

physical signs of, 318 
predisposing causes of, 291, 292 
prevention of, 293 
pulmonary, 309 

amphoric breathing in, 319 



Tuberculosis, pulmonary, bacillus of, 
method of staining, 322 
caseation in, 310 
cavities in, 311 
complications of, 316 
" cracked-pot sound" in, 319 
diagnosis of, 318 

fluoroscope in, 321 

microscopic, 322 

tuberculin in, 321 
haemoptysis in, 316 

prognosis of, 324 

treatment of, 333 
hemorrhage in, 316 
infiltration of Laennec in, 310 
lesions in, 309 
metallic tinkling in, 319 
mode of infection in, 309 
pectoriloquy in, 319 
physical signs of, 318 
pneumothorax in, 318 
prognosis in, 323 
pulmonary osteoarthropathy, 318 
reparation in, 312 
symptoms of, 314 

cough, 316 

dyspnoea, 316 

fever, 314, 315 

laryngeal, 314 

loss of weight, 315 

sputum, 315, 316 

sweating, 315 
treatment of, 324 

antistreptococcic serum in, 
332 

bronchitis in, 330 

climatic, 326 

cough, 331 

diet in, 324 

exercise in, 326 

fever, 330 

medicinal, 329 

night-sweats, 330 

out-door life in, 326 

serum, 331 

special symptoms, 330 

tuberculin in, 332 
types of, 309 

caseating, 309, 310 

chronic, 309 

fibroid, 309, 312 

miliary, 309 

ulcerative, 309 
vascular changes in, 310 
vomiting in, treatment of, 333 
of rectum, 336 
of retroperitoneal glands, 300 
of serous membranes, 301 

acute, 301 

chronic, 301 

treatment of, 308 
of spinal cord, 343 
of stomach, 335 
of testicle, 338 

diagnosis of, 339 



INDEX 



1129 



Tuberculosis of testicle, symptoms of, 339 
treatment of, 339 
of thyroid gland 
of tonsils, 334 

of uterus, 342 
Tuberculous laryngitis, 375 
leprosy, 348 
pleurisy, 303 
strumitis, 749 

vegetative endocarditis, 343 
Tubular nephritis, chronic, 704 
Tumors of bowel as cause of obstruction, 
624 
of brain and its membranes, 932 
of kidney, 732 
of liver, 668 
in lungs, 428 
of mediastinum, 452 
of pancreas, 695 
of thyroid gland, 751 
Tungau, 911 
Tunnel anaemia, 888 
disease, 887 

St. Gothard's, 887 
Tiirck's gyromele in gastric dilatation, 575 
Tympanites, 639 

in croupous pneumonia, 154 
in typhoid fever, 28, 40 
treatment of, 57 
Tympany in acute peritonitis, 644 
Typhoid fever, 17 

albuminuria in, 41 
anaemia in, 34 
antisepsis in, 56 
appendicitis in, 30, 39 
arthritis in, 44 
atypical forms of, 30 
bacillus of, 17 

in blood, 25 
bathing in, 53 
bed-sores in, 33 

treatment of, 58 
blood in, 34 

bloodvessels, lesions of, in, 35 
boils in, 34 

bone complications in, 44 
Brand bath in, 53 

contraindications to, 53 
cardiac failure in, 35 
in children, 30 
chills in, 30, 32 
cholecystitis in, 40 
cholelithiasis in, 41 
circulatory complications in, 34 
cold in, 52 
coma vigil in, 43 
complicating pregnancy, 45 
complications of, 34, 35 
constipation in, 27 

treatment of, 56 
convulsions in, 44 
cystitis in, 42 
definition of, 17 
delirium in, 28, 30 
delusions in, 43 



Typhoid fever, diagnosis of, 45 
diarrhoea in, 27, 30, 36 

treatment of, 56 
diazo reaction of urine in, 50 
diet in, 54 
differentiation of, from other 

fevers, 46, 47 
disinfection of discharges in, 18 
dislocation of hip in, spontaneous, 

44 
distribution of, 17 
Ehrlich's reaction in, 50 
embolism in, 35 
embryocardia in, 34 
empyema in, 43 
endarteritis in, 26 
epididymitis in, 42 
erysipelas in, 34 
etiology of, 17 
facial expression in, 27 
frequency of, 21 
gangrene in, 33 

gastric ulcer in, 36 
genitourinary complications in, 41 
headache in, 27, 30 
heart clot in, 35 

muscle in, changes in, 26 

sounds in, 34 
hemiplegia in, 44 
hemorrhage in, 30, 36 

diagnosis of, 36 

symptoms of, 36 

treatment of, 57 
hepatic complications in, 40 
herpes in, 32 
history of, 17 
hydrotherapy in, 52 
hypostatic congestion of lung in, 

42 
incubation of, 27 
infarction of lung in, 42 
insomnia in, 27 

treatment of, 58 
jaundice in, 40 
joint complications in, 44 
kidneys in, 26 
laryngeal ulceration in, 42 
leukocytosis in, 34 
liver in, 26, 40 
medicines in, 55 
meningitis in, 43, 44 
mesenteric nodes in, 25 
mixed infection in, 32 
mode of infection in, 18 
morbid anatomy of, 23 
mortality of, 22 
muscle, complications in. 44 
muscular tremors in, 28 
myocarditis in, 35 
myositis in, 45 
nephritis in, 41 
nervous complications of, 43 
neuritis in, 44 
nose-bleed in, 26 
oesophagitis in, 35 



1130 



INDEX 



Typhoid fever, oesophagus in, ulceration of, 
35 
orchitis in, 42 
osteomyelitis in, 44 
otitis media, acute, in, 44 
parotitis in, 35 
pathology of, 23 
peliomata in, 32 
pericarditis in, 34 
perforation in, 37 

diagnosis of, 38 

signs of, 38 

treatment of, 58 
peritonitis in, 38 

diagnosis of, 38 
petechias in, 34 
pharyngitis in, 35 
phlebitis in, 35 
pleurisy in, 43 
pneumonia in, 30, 42 
polyuria in, 42 
prevention of, 18 
preventive inoculation in, 20 
prognosis of, 51 
pulmonary abscess in, 42 
pulse in, 27 
pyuria in, 42 
recrudescence in, 31 
renal disease, acute, in, 30 
respiratory complications in, 42 

lesions in, 26 
rose spots in, 28 
sequelae in, 34 
skin changes in, 32 
splenic enlargement in, 25, 27 
stimulants in, 55 
stools in, 36 
stupor in, 28 
sudamina in, 32 
symptoms of, 27 
tache blenatre in, 32 

cerebrale in, 32 
temperature in, 27, 31 
tests in, 48 
thirst in, 27 
thrombosis in, 35 
tongue in, 27 
treatment of, 52 

during convalescence, 59 

medicinal, 55 

special symptoms, 56 
tympanites in, 28, 40 

treatment of, 57 
tvphoid spine in, 44 
ulcer in, 23, 24 
vomiting in, 36 

treatment of, 56 
"Widal's test in, 48 
Tvphus fever, 61 

chill in, 63 
complications of, 65 
definition of, 61 
delirium in, 64 
diagnosis of, 65 
distribution of, 61 



Typhus fever, eruption in, 63, 64 

etiology of, 62 

fever in, 63 

hepatic changes in, 63 

history of, 61 

hypostatic congestion of lungs in, 
63 

intestinal lesions in, 63 

kidneys in, 63 

morbid anatomy of, 63 

myocarditis in, 63 

pathology of, 63 

petechias in, 64 

prevention of, 63 

prognosis of, 66 

pulse in, 64 

relapses in, 65 

retention of urine in, 67 

spleen in, 64 

termination of, 65 

treatment of, 66 
siderans, 64 
Tyrotoxicon, 857 
Tyrotoxismus, 857 



ULCER, duodenal, 628 
diagnosis of, 630 

from acute fat-necrosis, 631 
from gallstone colic, 631 
from gastric ulcer, 630 
from intestinal obstruction, 
631 
etiology of, 628 
hemorrhage in, 630 
morbid anatomv of, 629 
pathology of, 629 
perforation in, 629 

symptoms of, 630 
prognosis in, 631 
symptoms of, 629 
treatment of, 632 
gastric, 579. See Gastric ulcer. 

in typhoid fever, 36 
intestinal, in paratyphoid fever, 59 
peptic, 579 
perforating, of foot, in locomotor 

ataxia, 964 
of stomach, 579 
Ulceration, laryngeal, in typhoid fever, 42 

of oesophagus in typhoid fever, 35 
Ulcerative appendicitis, 617 
endocarditis, 485 
pharyngitis, 554 
stomatitis, 546 
Ulcus ventriculi, 579 
Uncinaria Americana, 888 

duodenale, 886 
Uncinariasis, 887 
anaemia in, 890 
Charcot-Leyden crystals in, 890 
definition of, 887 
diagnosis of, 891 
etiology of, 888 
frequency of, 888 



INDEX 



1131 



Uncinariasis, morbid anatomy of, 890 

pathology of, 890 

prophylaxis of, 889 

symptoms of, 890 

treatment of, 892 
Undulant fever, 245 
Uraemia, 720 

amaurosis in, 722 

convulsive type of, 721 

definition of, 720 

diagnosis of, 723 

from heatstroke, 723 
.from opium poisoning, 723 

etiology of, 720 

hemiplegia in, 722 

insomnia in, 722 

latent, 722 

mania in, 722 

monoplegia in, 722 

odor in, 722 

paralytic form of, 722 

pathology of, 720 

prognosis in, 723 

symptoms of, 721 

treatment of, hot pack in, 724 
Uraemic apoplexy, 923 
Uric acid diathesis, 746 
Urinary secretion, disorders of, 737 
Urine acetone in, tests for, 799, 800 

in acute diffuse nephritis, 701 

albumin in, 741 
tests for, 742 

albumose in, 746 

in beriberi, 256 

blood in, 738 

in cholelithiasis, 679 

in chronic interstitial nephritis. 712 
parenchymatous nephritis, 706 

chyle in, 744 

in croupous pneumonia, 153 

in diabetes insipidus, 807 
mellitus, 795 

haemoglobin in, 739 

indican in, 745 

melanin in, 746 

oxalates in, 745 

phosphates in, 745 

pus in, 744 

in renal calculus, 735 

in rheumatic fever, acute, 199 

in smallpox, 77 

sugar in, tests for, 799 

suppression of, 737 

in scarlet, fever, 101 

uric acid in, 746 

in yellow fever, 216 
Urticaria in acute rheumatic fever, 201 
Uterus, tuberculosis of, 342 



VACCINATION, 88 
method of, 88 
in smallpox, 73, 88 
Vaccine lymph, glycerinated, 89 
Vaccinia. 88 



Vaccinia in man, primary, 89 

secondary, 89 
Vagus nerve, disease of, 1030 
Valvular endocarditis, 482 
Varicella, 90 

definition of, 90 

diagnosis of, 92 

from smallpox, 92 

eruption in, 91 

erysipelas in, 92 

etiology of, 90 

incubation in, 90 

nephritis in, 92 

prognosis in, 92 

symptoms of, 90 

treatment of, 92 
Varicose aneurysm, 534 

groin glands in filariasis, 896 
Variola, 70. See Smallpox. 

fulminans, 81 

pustulosa hemorrhagica, 81 
Varioloid, 82 
Vascular goitre, 749 

Venesection in pulmonary emphysema, 419 
Venous sinuses, thrombosis of, 946 

thrombosis in croupous pneumonia, 
162 
Ver macaque, 912 
Verrucous endocarditis, 482 
Verruga, 360 

definition of, 360 

distribution of, 360 

etiology of. 361 

incubation of, 361 

joints in, 361 

Peruviana, 360 

prognosis in, 362 

symptoms of, 361 

treatment of, 362 
Vertebrae, disease of, 993 
diagnosis of, 994 
prognosis in, 994 
symptoms of, 994 
treatment of, 994 

malignant growths of, 994 
Vertigo, 1029 

in brain tumor, 933 
Vesical crises in locomotor ataxia, 962 

tuberculosis, 340 
Vesicular stomatitis, 546 
Violinists' cramp, 1072 
Visceroptosis, 632 
Visual tract. 1016 
Volvulus, 627 

prognosis of, 627 

symptoms of, 627 

treatment of, 627 
Vomiting, cyclic, 607 

Von Graefe's sign in exophthalmic goitre, 
753 



w 



ATER-HAMMER pulse in aortic re- 
gurgitation, 511 
infection by, in typhoid fever, 18 



1132 



INDEX 



Weber's syndrome in brain tumor, 934 

Weil's disease, 352 

Weisses blut, 780 

Westphal's symptom in locomotor ataxia, 

961 
Wet brain, 846 
Whipworm, 900 
White flux, 242 
Whooping-cough, 119 

amblyopia in, 122 

bacillus pertussis Eppendorf in, 119 

bronchopneumonia in, 122 

conjunctival hemorrhages in, 122 

complications of, 122 

definition of, 119 

diagnosis of, 123 

distribution of, 119 

duration of, 121 

emphysema in, 122 

etiology of, 119 

frequency of, 119 

glandular enlargement in, 122 

incubation in, 120 

in measles, 113 

morbid anatomy of, 120 

mortality in, 123 

paralysis in, 122 

paroxysm of, 120 

pathology of, 120 

physical signs in, 121 

pneumothorax in, 122 

prognosis in, 123 

symptoms of, 120 

treatment of, 123 

bronchitis tent in, 123 

vomiting in, 122 
Widal test in typhoid fever, 48 
Winckel's disease, 786 
"Wooden tongue," 274 
Wool-sorters' disease, 257 
Word blindness, 931 

deafness, 931 
Worm, beef-, 901 

guinea-, 896 

hook-, 888 

Medina, 896 

pin-, 885 

pork-, 901 

ring-, 909 

round-, 884 

screw-, 911 
H 



Worm, seat-, 885 

thread-, 885 

whip-, 900 
Wounds of heart, 481 
Wrist-drop in lead poisoning, 853 
Writers' cramp, 1072 
Wryneck, 1033 

congenital, 1033 

spasmodic, 1033 

spurious, 1034 

XEROSTOMIA, 551 



Y 



AWS, 358 

Yellow atrophy of liver, acute, 670 
fever, 212 

albuminuria in, 216 

apoplectiform type of, 216 

blood in, 214 

cardiac changes in, 214 

convulsions in, 215 

definition of, 212 

diagnosis of, 217 

from dengue, 217 

from malarial haemoglo- 

binuric fever, 217 
from pernicious malarial 
fever 217 

etiology of, 212 

gastric changes in, 215 

haematemesis in, 605 

headache in, 215 

intermittent changes in, 216 

jaundice in, 216 

morbid anatomy of, 214 

mortality of, 217 

nephritic changes in, 215 

pain in, 215 

pathology of, 214 

prevention of, 212 

prognosis of, 217 

prophylaxis of, 214 

remission in, 215, 216 

respiration in, 215 

symptoms of, 215 

tongue in, 216 

treatment of, 218 

urine in, 216 

vomiting in, 216 



IRB >u 



®t 



K 




